#that’s because A pairs with U (Uracil)

[bambeebirdie]

Have some goofy Valentine’s Day cards I made

[junhuiste]

experi-meant to be ⋆ park wonbin

pairing: wonbin x gn reader

tags/warnings: fluff, cursing, college au, laboratory environment, one mention of baking, 1600 words

a/n: i meant to publish this on valentine’s day since i had lab that day but i never finished it lol. there’s some microbio lab procedure jargon so like this is what streaking plates is if you want a visual lmfaoao. this is my first published work in like three years it feels weird haha + i might change my layout/header for fics but for now i’ll keep the same layout i've had for past fics

wonbin believes U are the uracil to his adenine—you should always be paired together.

| seunghan: dude 

| seunghan: lowkey i can’t come to lab bc my car won’t fucking start so i’ll have to make it up next week :\ but taehyun and his partner would probably be willing to help you out with calculations and clean up hopefully

Wonbin pants heading up the stairs into the classroom lab, cheeks immediately pink as he’s made a spectacle amongst everyone already sitting and tuned into the TA’s pre-lab lesson. Sighing as he processes Seunghan’s text, Wonbin turns to the drawing of bacterial growth curves on the whiteboard but is soon after preoccupied with the fact that there is no Taehyun on a stool. There’s just your backside entirely in front of him. 

Taehyun is one to set up all his materials before the TA even steps foot through the lab door so if he isn’t here now then that means—

“Guess you’re stuck with me for today.” 

Wonbin tries to swallow but it gets stuck halfway down his throat and is about to go into a choke type cough frenzy when he surprises himself and softly clears his throat instead. His thoughts are all just stuck there—in the middle of his esophagus, begging for them to travel back up to his brain so he has enough stamina to stick it through the four hour class. 

“No hate to him because Taehyunnie’s a tad faster at getting through the steps, so you know, we’re usually out thirty minutes early, but I can promise you I’m better at calculations. And I’m more precise with measurements,” you let out a small giggle before setting your backpack on the floor next to Wonbin’s.

The commotion of pipettes being thrown onto the surface, glass tubes clinking, and sneakers squeaking rushing to obtain their samples is right away drowned out in Wonbin’s ears by the sight of you perched atop the stool a mere few inches away from him. He tries to keep his chest from heaving at bay by taking his notebook out of his backpack and reviewing the method for today’s class. The solution is only short lived though, promptly taking notice of how you gather materials from the drawer while simultaneously reading through your own notebook. 

Every Tuesday and Thursday, Wonbin assumes his seat in the third to last row of his Virology lecture, close enough to the door that he can be among the first to leave as soon as “see you guys next time” leaves Professor Choi’s lips. He longs for the day (ideally it would be quite before the last week of classes but realistically that’s the best he has to offer for now) that he musters up just the slightest bit of courage to join you and Taehyun in the second row, where Seunghan also occasionally accompanies you two. It’s only the third week of this semester, but perhaps the sixth course of his over the past three years Wonbin’s seen you in. From Biochemistry to Rhetoric 2, he has never taken place at a desk next to yours. 

Wonbin’s always aching to know how you’d answer everything he could ever ask you, be it the attendance quiz question or your weekend plans—what time you usually roll out of bed, whether or not you stroll to the local farmer’s market near campus, if you’re spending Saturday with a special someone. He needs to hear you laugh at Taehyun’s cynicism about college. He needs to hear it up close, not having to strain his ear when he’s fifteen rows behind when you crack up at your friend during the five minute break Professor Choi gives the class. 

But Wonbin will take what he can get for now, and if that’s helping you fulfill your wish of completing the lab procedure as quickly as possible, he’ll do it. 

“I can do the calculations for us,” you begin, “would you mind getting our mutant strains at the front of the class and streak the Petri dishes?” 

Wonbin nods almost too enthusiastically and curses at himself for seeming embarrassingly desperate in front of you. Sure, he’d like to muster up the courage to ask you out, but today he’ll try to take it one step at a time.

When Wonbin returns with new plates to grow your bacteria on and two tubes filled with your bacterial strains, you scoot your chair closer to his to later show the finished calculations. He catches a whiff of your light perfume and almost falls out of his own chair. 

As he’s setting up the Bunsen burner for sterilization, you chuckle, “you know the real reason Taehyun’s not here today is because he left town last night to get a head start on the extravagant romantic weekend he has planned with Gaeul.”

“If there’s one way to use our one free unexcused absence, that’ll do it,” Wonbin replies. 

“Do you have any plans for Valentine’s Day, Wonbin? I mean if you did I just hope you wouldn’t leave me early like Taehyun did,” your eyes meet his for a brief second before flitting back to your notebook.

Wonbin’s grip on the matchstick to light the burner loosens. He just barely catches himself before the match could fall from his hand onto the lab bench. What he needed to get a grip on was his fucking sanity—he almost set the classroom on fire because his heart instead is aflame for yours. 

Taking a breath, Wonbin exhales when the flame turns to blue, finally lighting the Bunsen burner. 

“Nope, no plans,” he briefly turns to you. There’s a beat and he considers that asking you back would seem too forward, but he does it anyway. 

Upon seeing your grin before you open your mouth, he turns his attention right back to the tubes and plates in front of him. 

It’s so over. 

For a second Wonbin’s relieved, because he thinks he can actually get through the next two hours without overthinking his micro movements in front of you. Now that it’s over for him, maybe he can actually pay attention to the way the metal loop he’s holding makes contact with the jelly-like agar inside the plastic plate and not disappoint Seunghan with the results. However, it’s not realistic because even still, Wonbin takes note of all your beauty and remains completely bewitched.

“Honestly I wish...I mean Minjeong, Yunjin and I are gonna do a rom-com binge and bake desserts…but you know…not any plans with someone like that…” 

Your temporary lab partner tries to hide his smile and nods silently as he continues switching between spreading bacteria on the plate with the metal loop and then sterilizing the loop in the blue flame. 

The rest of lab goes smoothly as Wonbin tries to quell the embers within him for the time remaining. There’s forty minutes left but technically to you Wonbin knows time is dashing away and it should feel like there’s what but only ten minutes left to do everything. Your pair was a few steps ahead of the others, just like how it would be when Taehyun accompanied you every week. 

Wonbin has been psyching himself up the past two hours to finally ask you out but currently he’s stuck in his head and just can’t seem to get it out. Does he chase you after you’ve stepped foot out of the lab or should he leave you be? Or maybe he can try next week. He’ll keep telling himself that until there’s one day of instruction left and then he won’t see you for three months and then he’ll lament the entire summer to Seunghan that he didn’t say shit. 

He can do that…or just rip the bandage off at an agonizing speed. 

The last Petri dish that Wonbin holds is being wrapped in parafilm to prevent contamination. He’d been going through the motions of the procedure while simultaneously not paying attention to his surroundings, at his own self’s behest. You’ve already cleaned the entire lab bench and he doesn’t notice until he hears “see you in Virology,” and suddenly you’re slinging your backpack over your shoulder. 

It’s now or next week…or never—wait you know that Wonbin’s in your Virology class? What you said is ringing in his ears and it hits him all at once.

Petri dishes in hand and turning around, Wonbin freezes in his tracks.

“Um…”

Your eyebrows furrow.

“Do you want to hang out tomorrow?” his own mouth betrays him and suddenly it’s all coming out much too quickly for his liking. 

You’re about to answer but before you can even get a word in, “I-I don’t mean to interfere with your plans with your friends but uh, if you wanted to do something like that I’m down.”

Your lips press into a line and Wonbin is about to pass out from the threatening fluorescent classroom lights. 

“Park Wonbin…are you asking me out on a date?” He can practically feel his sweat melting the parafilm tape off and a vision of him dropping the Petri dishes in front of you, cracking open and shattering, exposing E.coli to everyone in the room flashes before him. He blinks once and calms his vice grip on the plates. 

“Yes. Yes I am asking you out on a date,” Wonbin looks down at your sneakers, not knowing where else to shift his gaze to. 

“Well, I’ll see you tomorrow then,” you smirk, slinging the other strap of your backpack over your other shoulder and saluting.

Park Wonbin swears his heart is on fire and does a backflip off a fifty foot cliff. A curve forming on his lips, he smiles slightly waving with the plates still in his hand, “see ya…”

You halt your forward movement and turn back around, “Wonbin?” he perks up again, “you should sit next to me in lecture on Tuesday.”

[smoll-tangerine]

[a/n]: i somehow couldn't find this ask anymore (it probably got deleted) but thankfully, i had it saved on a google doc! i'm slowly going back to writing the remaining requests from my one-year anniversary event! to the user who sent me this request, thank you so much for your support!! i see that you have deactivated but i hope that somehow, you'll find your way back to this request of yours! also, yay, my first haechan request! i'm not too familiar with him/his character, but i hope you guys willl enjoy this nonetheless!!

lee donghyuck/lee haechan: character unlocked!

PAIRING. haechan x female reader GENRES. romcom, fluff, college!au PROMPT. "i'm always flirting with you. keep up." WORDS. 683

You were breathless by the time you got to the hospital, slightly feeling guilty that you couldn’t make it on time to see your boyfriend head in for his colonoscopy. 

Both of you were practically adults now, only a year left before you two graduate from college, and yet he could still act like such a child. Especially when he found out that you were going to be late for his appointment.

But then he stopped whining when he found out that you were going to be late only because you decided to attend the class – the one he was missing due to his appointment – and take notes for him so that he didn’t miss anything. 

“Hi,” you greeted the receptionist. “I’m the guardian for Lee Donghyuck? He had a colonoscopy at 3pm.” 

Her eyes lit up in what seemed to be amusement and motioned the door behind you. “Ah, so you’re the girlfriend he was telling everyone about. He should be coming out soon. Get ready.” 

Your brows furrowed in confusion, wondering what exactly should you be getting ready for. 

The second she finished her sentence, you saw Haechan come out with the hospital staff pushing him to his room. 

“Donghyuck!” you exclaimed happily. 

Your boyfriend seemed drowsy, probably the lingering after-effects of the anaesthesia. You had to hold your laughter back from how goofy he looked, especially combined with the hospital gown and the messy hair. 

“Who are you?” he asked as he smacked his lips a few times. 

You frowned at his question. “Are you really asking me who I am?” 

“Mhm, yeah.” He hummed and then giggled. “You’re pretty.” 

Oh, you wished you could film this moment and show it to the rest of the boys. Renjun would  totally make fun of him for this. But you also wanted to keep this moment to yourself. Was that selfish of you? 

“Can I have your number?” 

“You already have my number,” you answered, slightly annoyed, but also amused. 

“Stop lying. I don’t have your number.” 

“Donghyuck, I’m your girlfriend. I’m pretty sure that my number is on your phone somewhere.” 

“You’re my girlfriend?” Donghyuck gasped, almost exaggeratedly. “Wait, where’s my phone. I need to make sure that it’s true.” 

“How about I’ll give your phone back when you’re feeling a bit better, yeah?” 

“I’m feeling awesome, though?” 

“I bet you do.” You snorted and patted him on his head. “Stay here while I get your discharge papers, alright?” 

“Can’t you bring me with you?” 

You looked him up-and-down with a side-eye. “In your current state? Yeah, no. Why do you want to stick to me so much? Just be a good boy and stay in your bed until the anaesthesia wears off.” 

Donghyuck pouts, his bottom lip jutting out in disappointment. “Is it so wrong of me to want to be next to my girlfriend? I guess I’m a sugar because I stick to you like glue-cose.” 

You made a face of disgust and apprehension. “Babe, that was so bad. It wasn’t even funny.” 

But that didn’t stop him from dropping another line on you. “I wish I were adenine so that I could be paired up with YOU. Get it? Like adenine is paired with uracil, and uracil’s symbol is the letter ‘U?’” 

You sighed through your nose. 

“Oh, oh, I got a better one! If I were an enzyme, I would be a helicase so I can unzip your gene,” he said and looked super proud. 

Was this how he was able to seduce you and ask you out? 

“Are you really flirting with me, right now? In this state?” you asked him while pinching his cheeks. 

While you were slightly unimpressed by his choice of pick-up lines, you still somehow found him pretty endearing. 

“I’m always flirting with you. Keep up.” 

You shook your head and left to grab his discharge papers. 

You regretted just the slightest for not filming him. 

But Renjun’s cry of anguish when he found out that you didn’t film Donghyuck at a moment of weakness completely made up for it.

[doomed-jester]

My favorite thing about Homestuck is that all the chumhandles have initials made up of G, C, A and T, the four "letters" that make up DNA base pairs.

The notable exceptions are John's ectoBiologist handle, (justified because he was originally ghostyTrickster but changed it) and the cherubs, whose handles use the letter U. This is clever because uracil (U) replaces thymine (T) in RNA.

Considering the importance of DNA to the story, and the presence of a guardian named G-CAT, you'd think this would be something the fandom would discuss more or more frequently carry over to OC chumhandles.

[forthewomenonly]

Permit me to restructure the periodic table of elements and I would place U and I together.

- 💀

I wish I was adenine, then I could get paired with U. Get it? Because in RNA (Ribonucleic acid), adenine (A) makes a “base pair” with uracil (U).

[tomtenadia]

Be my Cytosine

Rowaelin month day 12 - delayed love confession

Ok, today’s title is a weird one. If you have a knowledge of basic biology you will know that DNA has four nucleobases called Adenine (A), Guanine (G), Cytosine (C) and Thymine (T). You should also know that C always pairs with G and A pairs with T but in RNA A cheats on T with Uracil. This should help to understand the confession at the end. In the fic Rowan is a geneticist... ( a field your truly finds extremely fascinating).

Apologies for the biology lesson. I felt I had to give an explanation for the weirdness of the title which is, by the way, also a play on the phrase Be my valentine...

Anyway... enjoy it!

Aelin was at the pub waiting for Rowan. He had texted her to meet him at their pub. She had a tiring day at work and was more than happy to finish off the day at the pub with her best friend.

Aelin was a high school teacher and Rowan was a scientist. He worked in a lab as a geneticist.

They had friends in common, and they met through them but their beginnings had been turbulent. The man had confessed he hated her guts and she had admitted she was not his fan either. The animosity had lasted for about a year. Then something shifted and slowly their relationship settled and they became friends. Until the she broke up with Chaol, he kicked her out of the flat and Rowan had been the first one to offer her his spare bedroom. So they became flatmates and the friendship blossomed even further to the point she could now call him her best friend.

What she had never had the guts to tell him was that she had been in love with him for a while now. But she had kept it to herself. They lived together and it might complicate everything between them. So she had pined in silence. Not even her friends knew about her secret.

*

Rowan was looking forward to meet Aelin at the pub. He had big news and she was the first person he wanted to share it with.

The job offer had been the culmination of years spent on books, his PhD years spent in labs day in and day out and then his currently living in a lab. but all of the sacrifices had finally paid off. He had been offered the position as a lead scientist in Doranelle as a part of the research team at the country’s most prestigious hospital. It was the opportunity of a lifetime.

He had spent the day in a daze.

Now he was driving and he hoped she would be happy for him.

Once at the pub he parked and finally walked in. He scanned the venue and finally spotted her blonde hair. She was sitting at a table with two pints in front of her.

“I got your favourite as soon as you told me you were five minutes out. Still nice and cold.

They clinked their glasses and Aelin took a huge gulp of her beer.

“Long day at work?” He mused at the avidity with which she drank the first gulp.

“Teenagers and their drama…” she explained “and on top of that, parents who think they can tell you how to do the job that you have been doing for the past ten years.”

“Just tell them to fuck off.”

“Says the man who works all day with petri dishes and DNA. They at least don’t talk back to you.”

Rowan chuckled “DNA mutating might be its way to tell me to fuck off.”

Aelin snorted so hard at the joke, while she was taking a sip that she had inhaled a bit of the beer and was now coughing after the drink went down the wrong pipe.

Rowan patted her back and she coughed a bit more.

“Are you okay?”

Aelin nodded “sorry I just imagined a DNA strand unfolding and in cartoon style morph back into a middle finger in the microscope.”

This time was the turn of Rowan to laugh. She loved that dynamic of theirs. She had even brushed up on some of her high school biology to make jokes. Once for Samhain she had dressed up as a Punnett square. Rowan had laughed for then minutes, then went and corrected it, saying that the combinations were incorrect.

Rowan cleared his voice and the atmosphere shifted all of a sudden “I got a big news today.”

Aelin grinned “Spill you heterozygote beans, Whitethorn.”

“I got a job offer.” He admitted, taking a sip of his beer “An hospital in Doranelle has offered me a lead scientist position for their project on genetic mutations. They read all my papers on a specific disease and its onset. Now they want me to work in one of their state of the art labs.”

Aelin gasped. That was an incredible opportunity. She knew how hard he had worked to get where he was and the job offer was the reward for all the time he had sacrificed and personal life as well. He and Lyria had dated for a couple of years until she left him because he was more dedicated to her job than her.

And if a part of Aelin was elated for him, the other, the selfish one, was hurting. He would leave. He would have a brand new successful life in Doranelle. Away from her. It hurt.

“Ro, that is absolutely amazing,” she hugged him hard and tried to hide the ache in her heart. 

“I will need to leave in two weeks. I can move the lease of the flat to your name, I— ”

Aelin shushed him “let’s just celebrate tonight.” He nodded and toasted to a new adventure.

*

Two weeks later

Aelin had begged Rowan to let her drive him to the airport. He had tried to convince her that he was happy to take a taxi, but Aelin had been stubborn and now she was helping him unload his luggage from the trunk of her car.

Her heart was racing. The previous night she had cried herself to sleep. The idea of him leaving her for good was killing her.

She accompanied him to check-in and forced herself to calm the tears that were now threatening to spill.

And when he started walking to the security area, the place where she knew she’d have to eventually say good bye to him, she froze.

Rowan noticed she had stopped “What’s wrong, fireheart?”

Aelin looked up at him, tears finally broke free “I love you.” She sobbed. “Rowan Whitethorn, I love you. You are the C to my G.” She let out a wet chuckle “not A since it cheats on T with U.”

Rowan laughed.

“What I am trying to say is that is you. Only you. And I know it’s the wrong time because you are going away to your dream job, but I had to tell you.” She was now sobbing and Rowan pulled her to his chest “you are the most amazing woman I ever met and I don’t deserve you.” He pulled back but kissed her on the forehead “be happy, Aelin.”

And he slowly walked away from her. Aelin watched at him disappear through the barriers. Never looking back. Aelin cried and cried. She stared at the screen watching the message switching from Boarding Now to Gate closed. She sat on a chair in the waiting are and let her desperation take over.

*

It was half an hour later when she heard a voice call her name. She hadn’t moved from her chair, she just could not leave.

It couldn’t be. He was on a plane.

She stood and turned and saw Rowan standing near the chair with his duffel bag on his shoulder.

“Rowan?” She breathed, her voice shaken by sobs “the plane.”

“I got off the plane.” He chuckled “and pissed off a lot of people since now they have to unload my luggage.”

“You got off the plane.”

He nodded again and took a step to her “I sat at my seat and all I could think was your confession. And realised that I have been an idiot.” He took her hand “I love you, Aelin. You are as well the C to my G. It took me almost to take off to realise it but better late than never.”

Aelin threw herself in his arms and he held her tight “and where else will I find a woman who uses genetics for a love declaration? That was super hot.” Aelin chuckled while inhaling the scent of pine and snow that was so typically him “what about your job?”

Rowan shrugged “my boss was quite gutted at losing me. I guess they will be happy when I phone tomorrow and tell them that I am happy to go back if they still want me.”

“But—” Rowan shushed her with a kiss.

“No buts, I have no regrets. This is the right choice.” And he kissed her.

A few minutes later a voice called him “Mr Whitethorn.” He turned and saw an airport attendant carrying his luggage.

“Thank you, and I am sorry.”

The man grunted something and walked away.

Aelin grabbed one of the bags and his hand and they walked out.

“Let’s be clear, I blame oxytocin.”

Rowan stopped and pulled her to him and then lifted Aelin in his arms, not caring about all the hundreds of people around them.

“I love you, Aelin Galathynius.”

[blog-cosmosuniverse1]

What Can Go Wrong?

What Can Go Wrong?

One key take-home from the Nature Reviews Drug Discovery article5 cited above is that replacing rare codons “must be used judiciously,” as rarer codons can have slower translation rates and a slowed-down rate is actually necessary to prevent protein misfolding.

The spike protein is the toxic part of the virus responsible for the most unique effects of the virus, such as the blood clotting disorders, neurological problems and heart damage. To expect the COVID shot to not produce these kinds of effects would be rather naïve.

A (adenine) and U (uracil) in the third position are rare, and the COVID shots replace these A’s and U’s with G’s (guanine) or C’s (cytosine). According to Seneff, this switch results in a 1,000-fold greater amount of spike protein compared to being infected with the actual virus.

What could go wrong? Well, just about anything. Again, the shot induces spike protein at levels unheard of in nature (even if SARS-CoV-2 is a “souped up” manmade concoction), and the spike protein is the toxic part of the virus responsible for the most unique effects of the virus, such as the blood clotting disorders, neurological problems and heart damage.

So, to expect the COVID shot to not produce these kinds of effects would be rather naïve. The codon switches might also result in protein misfolding, which is equally bad news. As explained by Seneff in our previous interview:

“The spike proteins that these mRNA vaccines are producing … aren’t able to go into the membrane, which I think is going to encourage it to become a problematic prion protein. Then, when you have inflammation, it upregulates alpha-synuclein [a neuronal protein that regulates synaptic traffic and neurotransmitter release].

So, you're going to get alpha-synuclein drawn into misfolded spike proteins, turning into a mess inside the dendritic cells in the germinal centers in the spleen. And they're going to package up all this crud into exosomes and release them. They’re then going to travel along the vagus nerve to the brainstem and cause things like Parkinson's disease.

So, I think this is a complete setup for Parkinson's disease ... It's going to push forward the date at which someone who has a propensity towards Parkinson's is going to get it.

And it's probably going to cause people to get Parkinson's who never would have gotten it in the first place — especially if they keep getting the vaccine every year. Every year you do a booster, you bring the date that you're going to get Parkinson's ever closer.”

Immune Dysfunction and Viral Flare-Ups

Other significant threats include immune dysfunction and the flare-up of latent viral infections, which is something Mikovits has been warning about. In our previous interview, she noted:

“We use poly(I:C) [a toll-like receptor 3 agonist] to signal the cell to turn on the type I interferon pathway, and because [the spike protein your body produces in response to the COVID shot] is an unnatural synthetic envelope, you're not seeing poly(I:C), and you're not [activating] the Type I interferon pathway.

You've bypassed the plasmacytoid dendritic cell, which combined with IL-10, by talking to the regulatory B cells, decides what subclasses of antibodies to put out. So, you've bypassed the communication between the innate and adaptive immune response. You now miss the signaling of the endocannabinoid receptors …

A large part of Dr. [Francis] Ruscetti’s and my work over the last 30 years has been to show you don't need an infectious transmissible virus — just pieces and parts of these viruses are worse, because they also turn on danger signals. They act like danger signals and pathogen-associated molecular patterns.

So, it synergistically leaves that inflammatory cytokine signature on that spins your innate immune response out of control. It just cannot keep up with the myelopoiesis [the production of cells in your bone marrow]. Hence you see a skew-away from the mesenchymal stem cell towards TGF-beta regulated hematopoietic stem cells.

This means you could see bleeding disorders on both ends. You can't make enough firetrucks to send to the fire. Your innate immune response can't get there, and then you've just got a total train wreck of your immune system.”

We’re now seeing reports of herpes and shingles infection following COVID-19 injection, and this is precisely what you can expect if your Type I interferon pathway is disabled. That’s not the end of your potential troubles, however, as these coinfections could accelerate other diseases as well.

For example, herpes viruses have been implicated as a trigger of both AIDS6 and myalgic encephalomyelitis7 (chronic fatigue syndrome or ME-CFS). According to Mikovits, these diseases don’t appear until viruses from different families partner up and retroviruses take out the Type 1 interferon pathway. Long term, the COVID mass injection campaign may be laying the foundation for a rapidly approaching avalanche of a wide range of debilitating chronic illnesses.

Are COVID Shots Appropriately Optimized?

As noted in the Vaccines article cited earlier, the codon optimization in the Pfizer and Moderna shots could be problematic:8

“As mammalian host cells attack unmodified exogeneous RNA, all U nucleotides were replaced by N1-methylpseudouridine (Ψ). However, Ψ wobbles more in base-pairing than U and can pair not only with A and G, but also, to a lesser extent, with C and U.

This is likely to increase misreading of a codon by a near-cognate tRNA. When nucleotide U in stop codons was replaced by Ψ, the rate of misreading of a stop codon by a near-cognate tRNAs increased.

Such readthrough events would not only decrease the number of immunogenic proteins, but also produce a longer protein of unknown fate with potentially deleterious effects …

The designers of both vaccines considered CGG as the optimal codon in the CGN codon family and recoded almost all CGN codons to CGG … [M]ultiple lines of evidence suggest that CGC is a better codon than CGG. The designers of the mRNA vaccines (especially mRNA-1273) chose a wrong codon as the optimal codon.”

The paper also points out the importance of vaccine mRNA to be translated accurately and not merely effectively, because if the wrong amino acids are incorporated, it can confuse your immune system and prevent it from identifying the correct targets.

Accuracy is also important in translation termination, and here it comes down to selecting the correct stop codons. Stop codons (UAA, UAG or UGA), when present at the end of an mRNA coding sequence signals the termination of protein synthesis.

According to the author, both Pfizer and Moderna selected less than optimal stop codons. “UGA is a poor choice of a stop codon, and UGAU in Pfizer/BioNTech and Moderna mRNA vaccines could be even worse,” she says.

What Health Problems Can We Expect to See More Of?

While the variety of diseases we may see a rise in as a result of this vaccination campaign are myriad, some general predictions can be made. We’ve already seen a massive uptick in blood clotting disorders, heart attacks and stroke, as well as heart inflammation.

More long term, Seneff believes we’ll see a significant rise in cancer, accelerated Parkinson's-like diseases, Huntington's disease, and all types of autoimmune diseases and neurodegenerative disorders.

Mikovits also suspects many will develop chronic and debilitating diseases and will die prematurely. At highest risk, she places those who are asymptomatically infected with XMRVs and gammaretroviruses from contaminated conventional vaccines. The COVID shot will effectively accelerate their death by crippling their immune function. “The kids that are highly vaccinated, they're ticking time bombs,” Mikovits said in my May 2021 interview.

What Are the Options?

While all of this is highly problematic, there is hope. From my perspective, I believe the best thing you can do is to build your innate immune system. To do that, you need to become metabolically flexible and optimize your diet. You’ll also want to make sure your vitamin D level is optimized to between 60 ng/mL and 80 ng/mL (100 nmol/L to 150 nmol/L).

I also recommend time-restricted eating, where you eat all your meals for the day within a six- to eight-hour window. Time-restricted eating will also upregulate autophagy, which may help digest and remove spike protein. Avoid all vegetable oils and processed foods. Focus on certified-organic foods to minimize your glyphosate exposure.

Sauna therapy may also be helpful. It upregulates heat shock proteins, which can help refold misfolded proteins. They also tag damaged proteins and target them for removal.

[biostudyblog]

Molecular Genetics

DNA has not always been the accepted building block of genes and inherited material. Until the 1950′s, this role was believed to be filled by proteins.

The Search For Inheritable Material

In 1927, Griffith discovered bacterial transformation, which is the ability of bacteria to change their genetic makeup by absorbing foreign DNA molecules from other bacterial cells and incorporating the DNA into their own.

Then, in 1944, Avery, MacLeod, and McCarty published their findings that the molecule that Griffith’s bacteria was transferring was DNA. 

In 1952, Hershey and Chase proved that it was DNA and not proteins that were the molecules of inheritance. They tagged bacteriophages (viruses that target bacteria) with radioactive isotopes, tagging the protein coat and DNA with different materials. They discovered that when the bacteria were infected with the virus, it was only the radioactive isotope they had tagged the DNA with that showed up.

Rosalind Franklin continued work started by Maurice Wilkins, and by carrying out X-ray crystallography analysis of DNA, found that DNA was a helix. Unfortunately, although her work was the essential backbone to Watson and Crick’s later discovery that DNA is a double helix, she didn’t get credit and was not named in the Nobel Prize.

Meselson and Stahl proved Watson and Crick’s hypothesis that DNA replicates in a semiconservative fashion. In order to prove this, they cultured bacteria in containing heavy nitrogen. They then moved them into a container with light nitrogen. The bacteria could replicate and divide once, and the new bacterial DNA had one heavy strand and one light strand, proving their hypothesis correct.

Structure of DNA

DNA is a double helix and looks like a twisted ladder

DNA has two complementary strands running in opposite sides from each other.

It’s a polymer with repeating units called nucleotides.

Each nucleotide has a 5 carbon sugar (deoxyribose), a phosphate molecule, and a nitrogenous base

There are four possible nitrogenous bases: The purines adenine, and guanine, and the pyrimidines thymine and cytosine. A goes with T and C goes with G.

The nucleotides of opposite chains are bound by hydrogen bonds.

DNA Replication in Eukaryotes

DNA replication is the process of making a perfect replica of the original DNA strand. Semi-conservative replication shows that the two new molecules of DNA have one old strand and one new strand. 

Replication occurs during interphase

DNA polymerase catalyzes the replication of new DNA. It also proofreads each new DNA strand, fixing errors to minimise mutations.

DNA unzips at the hydrogen bonds connecting its two strands.

Each strand of DNA serves as a template for the new strand, based on the base-pairing rules.

Every time DNA replicates, some nucleotides on the end are lost. To prevent this from causing a problem, their DNA has nonsense repeating nucleotide sequences called telomeres.

Structure of RNA

RNA is a single-stranded helix.

It is a polymer, like DNA made of repeating units of nucleotides

It has ribose, a phosphate and a nitrogenous base

RNA does not have Thymine. Instead, it has Uracil. A pairs with U, C pairs with G.

There are 3 kinds: mRNA (messenger RNA) tRNA (transfer RNA) and rRNA (ribosomal RNA)

mRNA: Carries messages from DNA in the nucleus to the cytoplasm during protein synthesis. The nucleotides on mRNA are called codons.

tRNA: Carries amino acids to the mRNA to form a polypeptide. They have triplet nucleotides that are complementary to those of mRNA. These are called anticodons.

rRNA: Is structural. Makes up the ribosome, along with proteins

Protein Synthesis

There are 3 main steps to protein synthesis: transcription, RNA processing, and translation.

Transcription

Transcription is the process where DNA makes RNA. It is facilitated by RNA polymerase and takes place in the nucleus. The triplet codes on DNA are transcribed into codon sequences in the mRNA. 

If the sequences in DNA triplets is: AAA TAA CCG GAC

The codons will look like this: UUU AUU GGC CUG  (remember RNA does not have Thymine)

RNA Processing

After transcription, the initial transcript is processed and edited by enzymes, who remove introns (noncoding sequences of RNA). The remaining exons are pieced back together to form the final transcript. The now shorter mRNA leaves the nucleus

Translation of mRNA Into Protein

Translation is the conversion of mRNA into an amino acid sequence. 

It occurs in the ribosome. Amino acids in the cytoplasm are carried by tRNA to the codons of the mRNA strand according to the base-pairing rules (think of it as trying to put a puzzle together.)

Some tRNA molecules can bind to two or more codons. For example, there are 4 separate sequences who code for the single amino acid: Serine.

Gene Regulation

Cells are not constantly synthesizing all the peptides it can make, as otherwise, the excess proteins would harm the bodies homeostasis. What this means is that the cells need to be able to turn their genes off sometimes. While this process is not well understood in humans, in bacteria it is a much more simple process, and much better understood. 

The operon is the key to gene regulation. It is a cluster of functional genes, along with the “switches” that turn them on and off. There are two kinds. The Lac or inducible operon is normally turned off until it is actively triggered by something in the environment. The other is the repressible operon, which is always turned on unless it is actively turned off.

On the operon, there is the promoter. This is the binding site of RNA polymerase. RNA polymerase always needs to bind to DNA before transcription happens, so the promoter is the equivalent of an on the switch. There is also the operator, which is the binding site for the repressor, which turns of the Lac operon. The TATA box helps RNA polymerase bind to the promoter

Mutations

Mutations are changes in genetic material. They are spontaneous and random. They can be caused by mutagenic agents, toxic chemicals, and radiation. They are often given a bad name, however, they are essential for natural selection.

Point Mutation

A point mutation is the most simple form of a mutation. It is a base pair substitution, where one nucleotide becomes another. The effects of this can be seen when trying to read a sentence.

THE FAT CAT SAW THE DOG ------ THE FAT CAT SAW THE HOG

The change isn’t too dramatic, and the sentence is still legible, albeit having a different meaning

Insertion and Deletion

Insertion and deletion cause much more dramatic changes. They occur when one nucleotide is lost, or an extra nucleotide is added to the sequence. These are also known as frameshift mutations.

Insertion:

THE FAT CAT SAW THE DOG --- TTH EFA TCA TSA WTH EDO G

Deletion:

THE FAT CAT SAW THE DOG--- HEF ATC ATS AWT HED OG

Chromosome Mutations

I went over chromosome mutations more in detail in my classical genetics post, so I’ll do a brief overview of some terms here. 

Aneuploidy is a condition where someone has an abnormal number of chromosomes. Someone who is intersex is an aneuploid because of a chromosomal mutation that gave them an abnormal number of sex chromosomes. 

The condition of having more chromosomes than average is called polyploidy. People with down syndrome are polyploids. More specifically, they have trisomy-21, meaning instead of 2 chromosome 21′s, they have 3.

These mutations are caused by nondisjunction when homologous pairs do not separate properly during meiosis.

It is important to know that chromosomal mutations do not always have disastrous effects. People with aneuploidy still live extremely fulfilled lives, and some don’t just learn to live, become happy with how they were born. 

The Human Genome

A genome is an organism’s genetic material. The human genome contains around 3 billion base pairs of DNA and 20,000 genes. 97% of that DNA does not code for protein production. Some of this DNA are regulatory sequences controlling gene expression, some are pseudogenes, which are former genes which accumulate over time. DNA is still very elusive, and scientists learn new things about it every day. Maybe one day, a scientist will read this blog, shaking his head at how wrong we were today.

Genetic Engineering and Recombinant DNA

Recombinant DNA is the act of taking DNA from two sources and combining them into one cell. This is the foundation of genetic engineering and biotechnology. Two pieces of this massive subject are gene therapy and environmental cleanup. The hope with gene therapy is that scientists may figure out how to insert functioning genes into humans to replace their nonfunctioning ones. Success could mean a cure for cystic fibrosis and sickle cell anaemia. Along with this, microbes could be engineered to decontaminate harmful chemicals at mining sites. GMO’s could be modified 

However, the safety of genetic engineering. GMO’s, in particular, have become a major talking point. One major concern is that GMO’s will accidentally be introduced to the wild which could have major impacts on the ecosystems surrounding farmland.

Restriction Enzymes

Restriction enzymes are essential for scientists who work with DNA. They cut DNA at recognition sequences or sites. They are referred to as molecular scissors. The pieces of DNA that result from the cuts are called restriction fragments.

Gel Electrophoresis

Gel electrophoresis is the act of separating large molecules of DNA based on their rate of movement through an agarose gel in an electric field. The smaller the molecule of DNA, the faster it travels. Before being placed in the gel, the DNA is prepared with restriction enzymes, providing small enough molecules for the scientists to work with.

Polymerase Chain Reaction

Discovered in 1985, a PCR is a cell free, an automated technique that rapidly copies or amplifies DNA. This is great for forensic science, where small pieces of DNA can be expanded, and then compared.

[amorarisa]

Fenton: *texts Gandra* If I had to choose between DNA and RNA, I'd choose RNA because it has U in it.

Gandra: *texting*

Fenton: *stares at his mobile impatiently*

Gandra: You can't just choose one! They are both necessary for life! And what does uracile have to do with that choice?

Gandra: Oh...

Gandra: Were you trying to flirt with me?

Fenton: I wasn't trying, I WAS flirting with you.

Fenton: Sorry, I suck at it.

Gandra: *texting*

Fenton: *ready to accept his fate as forever single*

Gandra: I wish I was adenine so I could get paired with U.

Fenton: ...

Fenton: Marry me?

[tommyru]

Hereditary alterations: the different reasons as well as types

Did you recognize that all humans share 99.9% of their genetic information? This implies our originality depends on the staying 0.1%, which varies between people as well as identifies our physical characteristics (phenotype), as well as just how we react to environmental aspects.

Wish to find out even more? In this short article we delve into the different sorts of genetic alterations which can happen in the genome, along with how scientific knowledge as well as services have advanced because the publication of the entire sequence of the human genome in 2003.

Key Concepts

In order to comprehend the possible genetic modifications that create our "originality", we must clarify a couple of vital ideas. As we clarified in "Genes and also chromosomes: just how do they identify our life as well as our wellness?" and also other write-ups on our blog site, DNA stands for Deoxyribonucleic Acid, a complicated particle discovered in the center of the huge bulk of our body's cells.

DNA lugs the guidelines for the production as well as procedure of our body's cells: from the colour of our hair to the genetic diseases we may develop.

The DNA sequence is stood for in a streamlined method according to the nucleotide base:

Adenine (A).

Thymine (T).

Guanine (G).

Cytosine (C).

The nucleotides are therefore distinguished by their base, and the DNA sequence is represented in a simplified way according to the nucleotide base as A, T, C or G. DNA's structure has 2 corresponding nucleotide strands, which bind in a details way: A with T as well as C with G, and also develop the nucleotide base pairs of DNA. Both chains are wrapped around each other to create a dual helix.

Central dogma of molecular biology.

DNA has the instructions, yet it can not accomplish all the functions that happen in the body alone. Proteins are in charge of executing these functions, and the process whereby we obtain from DNA to a protein is caught by the central conviction of molecular biology. In the DNA sequence we can discover specific areas known as genes, which contain the info for creating healthy proteins. These healthy proteins execute details functions in the body.

There is a whole mechanism within the cells to guarantee that this process is executed properly. Initially, the DNA is transcribed right into carrier RNA (mRNA) in the cell center. In this procedure the T (thymine) nucleotide is changed by U (Uracil) in the mRNA (single-stranded) leaving the center and, thanks to unique structures called ribosomes, it is converted right into healthy protein which is formed by a series of amino acids.

But ... if RNA is developed with a mix of 4 bases as well as healthy proteins are created with a combination of 20 various amino acids, just how does translation work?

The response hinges on the genetic code laid out in the 1960s, for which RW Holley, G Khorana and also MW Nirenberg were awarded the Nobel Prize for medication. In the mRNA series the nucleotides read in threes, forming a codon that is translated right into a details amino acid, as displayed in the table listed below. These "signals" or codons inscribe the amino acids that will certainly form the proteins. Amongst these, there are 4 special signals:.

AUG: marks the start of the translation.

UAA, UAG, UGA: these are the stop codons, which indicate that the translation is total.

Lastly, what is the distinction in between genome as well as exome?

The whole collection of DNA in an organism is called the genome. For human beings, the genome contains greater than 6 billion nucleotides. As a matter of fact, if we took the entire DNA sequence of a solitary cell and also stretched it out, it would certainly more than 2 metres long. Yet of those 6 billion nucleotides, just a tiny component (about 2%) are presently understood to consist of protein-forming information, that little fraction being the exome. For that reason, we define the exome as the coding area of the DNA, while the rest of the DNA makes up non-coding regions, which do not have details for healthy protein synthesis. So if it does not code for proteins, what is the function of non-coding DNA? For a long time, it was considered to be "scrap DNA", nonetheless, scientific advancements have actually disclosed that non-coding DNA has numerous functions, one of the most important of which is to regulate the expression of various other genetics.

So, having reached this factor ...

What are hereditary alterations?

Any change in the DNA series can modify the hereditary code and also for that reason might modify the synthesis of the healthy protein that it inscribes.

For example, if we consider the hereditary code table, the CAA codon is translated into the amino acid glutamine, while AAA is converted right into lysine, so the change of one nucleotide for one more (C for A) changes the composition of the healthy protein, which might harm its function. But, if the change is to UAA, rather than giving rise to glutamine, this is a stop codon, so it quits healthy protein synthesis.

Consequently, the medical importance of a hereditary modification will certainly depend upon where it occurs, i.e. whether it takes place in the coding area (exome) or not, and additionally whether the change leads to an extreme change in healthy protein synthesis and also consequently its function in the body.

What type of changes might take place?

The instance shown over is an alternative, as one nucleotide is exchanged for one more, yet there are other sorts of genetic modifications, even more typically:.

Substitution: exchanges one base for one more.

Removal: removal of a collection of bases.

Duplication: duplication of a section of bases.

Inversion: inversion of the order of a series of bases.

Why do hereditary alterations happen?

There are 2 primary reasons for genetic modifications:.

Exterior, environmental variables.

Inner, hereditary aspects.

Mostly all of the cells in the body are on a regular basis replaced. To do this, the cells split into two child cells. Mistakes can take place during this department process, leading to hereditary changes. Exterior variables such as tobacco or the sunlight's radiation, amongst several others, raise the probability of such errors occurring. We call these somatic anomalies, since they only affect the cell in which the mistake has occurred, and also they are not handed down to offspring.

Nevertheless, hereditary changes can likewise exist from birth. If the egg or the sperm cell has a hereditary error, this will certainly be transferred to the zygote and will consequently show up in all its cells, because all the cells of the "new" human being stem from that "initial" cell. It is also feasible for the change to occur throughout embryogenesis (the transformation procedure from zygote to embryo), even if it does not appear in the sex cells. In both situations these modifications are called germline mutations, and also people that have them can pass them on their spawn.

Hereditary alterations, mutations and also polymorphisms.

Mutations.

I make sure you've heard of anomalies, and you probably have a negative association with the term. There is a factor for this, given that anomalies are hereditary alterations that take place in less than 1% of the population and also are connected to a higher danger of establishing an illness.

For example, you have actually possibly become aware of the BRCA1 genetics. This gene's function is to correctly manage cellular division in order to stop tumors. An anomaly in this gene causes unchecked cellular division, which enhances the danger of creating a tumour. Extra exactly, people that have a BRCA1 anomaly have a 46% -87% danger of developing bust cancer in their life time.

Polymorphisms.

Polymorphisms are hereditary modifications that occur in greater than 1% of the populace. Most polymorphisms are what is known as single nucleotide polymorphism or SNP, implying that the genetic alteration just affects the exchange of one nucleotide for an additional. Today there are numerous known SNPs distributed throughout the genome. Actually, it is approximated that there is 1 SNP for every 100 to 1,000 bases (A, T, G, C) throughout the genome.

SNPs are responsible for 90% of things that distinguish us from one another, i.e. they determine most hereditary variability in between individuals. Phenotypic traits, i.e. noticeable functions such as eye colour and also height, which separate us from each various other, are identified by genetic polymorphisms. Most SNPs are discovered in non-coding regions (98% of DNA) as well as do not straight affect health. Various other SNPs situated in coding areas (2% of DNA) can influence various aspects of a private, such as a greater sensitivity to a certain multifactorial illness, whose growth is affected by both genetic as well as ecological variables.

Genetic variation, the trick to evolution.

Thus, these genetic variations that most of us have in our genetics are what make us unique. If there were no hereditary variation, there would be no evolution either, since the origin of all hereditary variation are anomalies, i.e. stable and also genetic modifications (in successive generations) in the genes. Anomalies raise genetic diversity, yet do not have a flexible objective, because they take place by chance.

Each types has a various anomaly price, regulated by natural selection to make sure that it can deal with the duality of security and also change integral to any kind of atmosphere, in a well balanced means.

Would you like to understand what defines you genetically?

The first draft of the human genome sequence was released at the beginning of the 21st century. The Human Genome Task was carried out between 1990 as well as 2003, as well as it involved numerous global institutions. With an initial budget plan of 3 billion bucks, the task's objective was to figure out the entire sequence of the human genome, in other words, to acquire all the linear message comprising the series of As, Ts, Cs and also Gs that comprise DNA.

These scientific developments ushered in the genomic era in biology and also medicine as well as allowed us to develop the series of the human recommendation genome, i.e. the sequence of a common genome where we can currently evaluate a person's genome.

Now you know why people have different physical qualities, show even more capacity for a specific sport, or perhaps have a greater danger of struggling with a certain illness. All of it relies on that 0.1% that makes us special. Having the ability to discover these genetic alterations in a preventative means is important if we want to adapt our way of life based on our genetics and also therefore improve our quality of life.

That is feasible here at BGI China. Discover more concerning yourself and improve your life and also the lives of those around you. The BGI China genetics examination series your entire genome and also shows you about various genetic facets of your wellness.

Something that appeared like sci-fi just a few years ago is currently a fact which is at your fingertips, supplying you with accessibility to important info and also preventative and customised medicine.

Click to know more about BGI gene test products if you are interested.

[nonchalanttoh]

The sides as nucleotide bases

“Let me know if i lose you…”

Ok, so I’m sitting in Bio 100 and we are learning about DNA replication. DNA is made of nucelotides. Nucleotides have a sequence of bases that determines a whole bunch stuff.

The bases are Adenine, Thymine, Guanine, and Cytosine.

There are 4 of them. I was like, “wow thats the same number as OG sanders sides. Let’s pair them to make the bases’ names more memorable.”

My thought process was as follows:

Cytosine © -> Virgil because both names stick out to me

Thymine (T) -> Patton because both their names kinda fit in with the rest but also don’t (i.e. Patton is the only one ending with -on but it still fits with the -an)

Adenine (A) -> Logan because Adenine is complimentary to Thymine (they bind together) and because logicality

Guanine (G) -> Roman because the -an ending for Roman and Logan can correlate with the -nine ending AND Guanine and Cytosine are complimentary and they bind together, ergo prinxiety

So here’s what we got:

DNA = A -> T and C -> G

Logan -> Patton and Virgil -> Roman

(and vice versa)

Seem to work out well, doesnt it? BUT WAIT… theres more.

When doing its thing, DNA is translated into RNA, and RNA has it’s own set of rules. Instead of Thymine, Adenine is compatible with a different base called Uracil (U). Uracil takes the place of Thymine and serves a similar purpose, it’s just a different base. Sound familiar?

T (Patton) is replaced with U. Sounds like Uracil would be a good Deceit to me.

I originally thought that Thymine would be Patton based soley on the name. This makes it even better.

So,

DNA = A -> T and C -> G

Logan -> Patton and Virgil -> Roman

And

RNA = A -> U and C -> G

Logan -> Deceit (pretending to be Patton) and Virgil -> Roman

Now you know a bit about molecular biology and you can remember my bit by relating it to the Sanders Sides. Thank you for your time.

[art-now-germany]

Genetic code (Portraiture New Generation)!- Original..., Igor Bajenov

Genetic code (Portraiture New Generation)!........ New in Service Investment Type Please -Company by Russ & Luxury -Gallery itself without foreign mediation the Perfecte Auctions Photo Art (unique / original) ..... which will cost a fortune in 5-8 years every time Art Auction Worldwide! ....... Take more favorable to buy the opportunity and you save real Money. Printed on Luxury Photo Paper 310 gr/m. Comes with certificate of authenticity numbered and signed. A representation of the genetic code (Code-sun): In the sequence from the inside outwards is a base triplet of mRNA (as read from 5 'to 3') assigned to one of the twenty amino acids canonical here marked or a stop codon. As genetic code which is referred to, with a deposited in the sequence of base pairs of the DNA double strand genetic material after it has been rewritten in the nucleotide sequence of an RNA single strand, can then be translated into the amino acid sequence of the polypeptide chain of a protein. This genetic code is the same for all known species of organisms in the Broad. It assigns a triplet of three consecutive nucleobases of nucleic acids - the so-called codon - in each case a certain proteinogenic amino acid to. The translation, called translation, takes place on the ribosomes in the cytosol of a cell. They form as specified by the sequence of nucleotides of a mRNA, the sequence of amino acids of a peptide by assigned to each codon on the anticodon of a transfer ribonucleic acid (tRNA) a particular amino acid, and this is connected with the previous one. In this manner, a certain predetermined information is transferred in the form of a peptide chain, which then folds the particular form of a protein. The more complex creatures, however, the higher the proportion of genetic information seems to be, which is not translated into proteins. A considerable portion of non-coding DNA is indeed transcribed into RNA but not translated. These non-coding RNA species transcriptome serve a diverse regulation of numerous cellular processes - so the transcription itself, as well as the possible translation, also a possible DNA repair, and moreover particular epigenetic marks of DNA fragments and i.a. various functions of the immune system. An example of the pairing of the codon on an mRNA with the complementary anticodon of a tRNA, here loaded with alanine tRNAAla whose anticodon fits GCC. The transfer ribonucleic acids, tRNAs, contained in a prominent place a loop of the cloverleaf-like molecule a characteristic nucleotide triplet which distinguishes them from each other. It consists of three nucleotides corresponding to nucleotides of a particular codon in that they are complementary to these and form a tripartite anticodon respectively. Codon-anticodon match basenpaarend and them is the same specific amino acid associated. A tRNA is loaded each with the amino acid that for the right to their anticodon codon stands. In this way, by the specific binding of an amino acid to a tRNA with a specific anticodon, that is the sign of a particular amino acid, the codon translated into the genetically coded amino acid. Strictly speaking, the genetic code is therefore already included in the structure of the different tRNA species: For each one tRNA molecule contains such a structured amino acid-binding site, that because only those amino acid is bonded, corresponding to its anticodon according to the genetic code. Upon binding to its tRNA is an amino acid for the biosynthesis of proteins on the ribosome available, so it can be added next link in the polypeptide chain - if the anticodon of tRNA matches a codon in the predetermined nucleotide sequence of the mRNA. Representation of the transcription of genetic information from a DNA portion in an RNA transcript, then where U stands instead of T. As a prerequisite for this protein synthesis of the DNA segment of a gene must first be in a ribonucleic acid (RNA) can be rewritten (transcription). It can in eukaryotic cells to certain parts of hnRNA selectively removed (splicing) or modified afterwards (RNA editing); then this preliminary pre-mRNA is further processed to the final mRNA that is finally exported from the cell nucleus. Because only at the ribosomes, which may be present in the cytosol in free space or are connected to the endoplasmic reticulum, are then linked using the mRNA template of the amino acids matching the codon tRNAs together to form a polypeptide. This process by which the information of a gene is expressed in the form of a protein (gene expression), thus results from a series of steps. Here, the main processes are distinguished as (1) transcription - a portion of the DNA of the genome is transcribed by RNA polymerase in RNA - and (2) post-transcriptional modification - an RNA transcriptome is altered - and (3) Translation - a mRNA is on ribosome translates into a polypeptide. This can be followed (4) still connect a posttranslational modification - a polypeptide of the proteome is changed. The processes up to the synthesis of a protein are also summarized as translation, since it is only in protein synthesis, the reaction of the triplet-sequences of a DNA into an amino acid sequence is clear. The actual application of the genetic code, namely the translation of a nucleotide sequence into an amino acid with reference to the codons or of the anticodon, already takes place in the binding of an amino acid at their tRNA by the respective aminoacyl tRNA synthetase, so in the preparation of amino acids for their possible assembly in a protein. A few base triplet not encode an amino acid. As such, they carry no meaning in this sense, they are also called nonsense codons; this result in translation to a stop, the finished protein synthesis, and are therefore called also stop codons. All organisms use the basic features of the same genetic code. The basic most commonly used version is specified in the following tables. These indicate which amino acids are encoded by one of 43 = 64 possible codons commonly, or which codon is translated into one of the 20 canonical amino acids. So is, for example, the codon GAU for the amino acid Asp (aspartic acid), and Cys (cysteine) is encoded by codons UGU and UGC. The bases indicated in the table are adenine, guanine, cytosine and uracil nucleotides of the mRNA; in nucleotides of DNA on the other hand occurs on thymine instead of uracil.

https://www.saatchiart.com/art/Painting-Genetic-code-Portraiture-New-Generation-Original/462428/3172230/view

[aburameshin]

Síntese Proteica

Protein synthesis is the protein production mechanism determined by DNA, which takes place in two phases called transcription and translation .

The process takes place in the cytoplasm of cells and also involves RNA , ribosomes, specific enzymes and amino acids that will form the sequence of the protein to be formed.

Stages of gene or genetic expression.

In summary, DNA is "transcribed" by messenger RNA (mRNA) and then the information is "translated" by ribosomes (ribosomal RNA compounds and protein molecules) and by the transporter RNA (tRNA), which carries the amino acids, whose sequence will determine the protein to be formed.

Gene expression

The steps in the protein synthesis process are regulated by genes. Gene expression is the name of the process by which the information contained in genes (the DNAsequence ) generates gene products, which are RNA molecules (in the gene transcription stage) and proteins (in the gene translation stage).

Genetic Transcription

In this first phase, the DNA molecule opens, and the codes present in the gene are transcribed to the RNA molecule. The RNA polymerase enzyme binds to one end of the gene, separating the DNA strands and the free ribonucleotides to pair with the DNA strand that serves as a template.

The sequence of the nitrogenous bases of the RNA exactly follow the sequence of bases of the DNA, according to the following rule: U with A (Uracil-RNA and Adenine-DNA), A with T (Adenine-RNA and Thymine-DNA), C with G (Cytosine-RNA and Guanine-DNA) and G with C (Guanine-RNA and Cytosine-DNA).

What determines the beginning and end of the gene to be transcribed are specific sequences of nucleotides, the beginning is the promoter region of the gene and the end is the terminal region . The RNA polymerase fits into the promoter region of the gene and goes to the terminal region.

Genetic Translation

The polypeptide chain is formed by the union of amino acids according to the nucleotide sequence of the mRNA. This mRNA sequence , called a codon , is determined by the base sequence of the DNA strand that served as a template. Thus, protein synthesis is the translation of information contained in the gene, which is why it is called gene translation.

Genetic Code: Codons and Amino Acids

There is a correspondence between the sequence of nitrogenous bases, which make up the codon of the mRNA, and the associated amino acids that is called the genetic code . The combination of broken bases form 64 different codons to which correspond 20 types of amino acids that will make up proteins .

See in the figure below the circle of the genetic code, which must be read from the middle outwards, so for example: the codon AAA is associated with the amino acid lysine (Lys), GGU is glycine (Gly) and UUC is phenylalanine (Phe).

Genetic Code Circle. The codon AUG, associated with the amino acid Methionine, is initiation and codons UAA, UAG and UGA without associated amino acids, are stop.

The genetic code is said to be "degenerate" because many of the amino acids can be encoded by the same codon, such as the serine (Ser) associated with the codons UCU, UCC, UCA and UCG. However, there is the amino acid Methionine associated with only one AUG codon , which signals the start of translation , and 3 stop codons(UAA, UAG and UGA) not associated with any amino acid, which signal the end of protein synthesis .

Formation of the Polypeptide Chain

Schematic representation of the association between the ribosome, tRNA and mRNA, for protein formation.

Protein synthesis begins with the association between a tRNA, a ribosome and an mRNA. Each tRNA carries an amino acid whose sequence of bases, called anticodon , corresponds to the codon of the mRNA.

The tRNA carrying a methionine, guided by the ribosome, binds to the mRNA where the corresponding codon (AUG) is located, initiating the process. Then it turns off and another tRNA turns on bringing in another amino acid.

This operation is repeated several times forming the polypeptide chain, whose sequence of amino acids is determined by the mRNA. When the ribosome finally reaches the region of the mRNA where there is a stop codon, the end of the process is determined.

[chromoscience]

DNA to RNA Transcription Process

Image by Arek Socha from Pixabay OpenStax Anatomy and Physiology DNA is housed within the nucleus, and protein synthesis takes place in the cytoplasm, thus there must be some sort of intermediate messenger that leaves the nucleus and manages protein synthesis. This intermediate messenger is messenger RNA (mRNA), a single-stranded nucleic acid that carries a copy of the genetic code for a single gene out of the nucleus and into the cytoplasm where it is used to produce proteins. There are several different types of RNA, each having different functions in the cell. The structure of RNA is similar to DNA with a few small exceptions. For one thing, unlike DNA, most types of RNA, including mRNA, are single-stranded and contain no complementary strand. Second, the ribose sugar in RNA contains an additional oxygen atom compared with DNA. Finally, instead of the base thymine, RNA contains the base uracil. This means that adenine will always pair up with uracil during the protein synthesis process. Gene expression begins with the process called transcription, which is the synthesis of a strand of mRNA that is complementary to the gene of interest. This process is called transcription because the mRNA is like a transcript, or copy, of the gene’s DNA code. Transcription begins in a fashion somewhat like DNA replication, in that a region of DNA unwinds and the two strands separate, however, only that small portion of the DNA will be split apart. The triplets within the gene on this section of the DNA molecule are used as the template to transcribe the complementary strand of RNA. A codon is a three-base sequence of mRNA, so-called because they directly encode amino acids. Like DNA replication, there are three stages to transcription: initiation, elongation, and termination.

In the first of the two stages of making protein from DNA, a gene on the DNA molecule is transcribed into a complementary mRNA molecule. Source: OpenStax Anatomy and Physiology Stage 1: Initiation. A region at the beginning of the gene called a promoter—a particular sequence of nucleotides—triggers the start of transcription. Stage 2: Elongation. Transcription starts when RNA polymerase unwinds the DNA segment. One strand, referred to as the coding strand, becomes the template with the genes to be coded. The polymerase then aligns the correct nucleic acid (A, C, G, or U) with its complementary base on the coding strand of DNA. RNA polymerase is an enzyme that adds new nucleotides to a growing strand of RNA. This process builds a strand of mRNA. Stage 3: Termination. When the polymerase has reached the end of the gene, one of three specific triplets (UAA, UAG, or UGA) codes a “stop” signal, which triggers the enzymes to terminate transcription and release the mRNA transcript. Before the mRNA molecule leaves the nucleus and proceeds to protein synthesis, it is modified in a number of ways. For this reason, it is often called a pre-mRNA at this stage. For example, your DNA, and thus complementary mRNA, contains long regions called non-coding regions that do not code for amino acids. Their function is still a mystery, but the process called splicing removes these non-coding regions from the pre-mRNA transcript. A spliceosome—a structure composed of various proteins and other molecules—attaches to the mRNA and “splices” or cuts out the non-coding regions. The removed segment of the transcript is called an intron. The remaining exons are pasted together. An exon is a segment of RNA that remains after splicing. Interestingly, some introns that are removed from mRNA are not always non-coding. When different coding regions of mRNA are spliced out, different variations of the protein will eventually result, with differences in structure and function. This process results in a much larger variety of possible proteins and protein functions. When the mRNA transcript is ready, it travels out of the nucleus and into the cytoplasm.

In the nucleus, a structure called a spliceosome cuts out introns (noncoding regions) within a pre-mRNA transcript and reconnects the exons. Source: OpenStax Anatomy and Physiology Source: Referrals: https://www.reddit.com/r/RNA/ Read the full article

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What is CRISPR-Cas9? The revolutionary gene-editing tech explained

Until very recently if you wanted to create, say, a drought-resistant corn plant, your options were extremely limited. You could opt for selective breeding, try bombarding seeds with radiation in the hope of inducing a favourable change, or else opt to insert a snippet of DNA from another organism entirely.

But these approaches were long-winded, imprecise or expensive – and sometimes all three at the same time. Enter CRISPR. Precise and inexpensive to produce, this small molecule can be programmed to edit the DNA of organisms right down to specific genes.

The development of cheap, relatively easy gene-editing has opened up a smorgasbord of new scientific possibilities. In the US, CRISPR-edited long-life mushrooms have already been approved by authorities while elsewhere researchers are toying with the idea creating spicy tomatoes and peach-flavoured strawberries.

But the game-changing technology could have the biggest impact when it comes to human health. If we could edit out the troublesome mutations that cause genetic diseases – such as haemophilia and sickle-cell anaemia – we could put an end to them altogether. The path for human gene-editing is littered with controversies and tough ethical dilemmas, however, as the news in late 2018 that – against all ethical guidance – a Chinese scientist had secretly created the first gene-edited babies.

Here’s everything you need to know about the complex and sometimes controversial technology driving the gene-editing revolution.

What is CRISPR?

CRISPR evolved as a way for some species of bacteria to defend themselves against viral invaders. Each time they faced a new virus, bacteria would capture snippets of DNA from that virus’ genome and create a copy to store in its own DNA. “They gather a set of sequences that they’ve been exposed to,” says Malcolm White, a biologist at the University of St Andrews, “these [bacteria] essentially carry a little library in their genome.”

To stick with the library analogy, these snippets of viral DNA were like little books – each one containing the data that allowed the bacterium to recognise and quickly kill off a virus next time it invaded. And in-between these chunks of useful DNA there are slightly less useful chunks of repetitive DNA keeping them separate – like a kind of molecular bookend.

These repeating segments of DNA are what gives CRISPR its name – Clustered Regularly Interspaced Short Palindromic Repeat – but it’s really the bits between these repeats that make CRISPR so useful. These useful bits are, somewhat unhelpfully, called spacers, and each one contains a reference to the DNA of a virus the bacteria (or its ancestors) had come across in the past. When a previously unseen virus attacks the bacterium, it adds another spacer to its library of previous attacks.

When a virus from that same species attacks again, the spacer corresponding to that virus’ genome swings into action. It’s a bit like the way that our own immune systems can recognise a flu virus if we’ve had that year’s flu vaccine. The spacer sequence is turned into RNA – a molecule that contains messages from DNA – and hunts down the corresponding piece of viral DNA. Once it finds it, an enzyme attached to the RNA string acts as a pair of biological scissors, cutting the target DNA and rendering the virus harmless.

You might have heard this system referred to as CRISPR-Cas9 as well as just plain CRISPR. In this case, the Cas9 bit refers to the enzyme used to cut the target DNA. “We can programme [Cas9] very easily to target one DNA sequence and to be very specific so it won’t cut anything that’s even similar in sequence,” says White. There can be other kinds of enzymes involved in gene-editing – Cas12 and Cpf1 for example – but all of them work in the same basic way.

How does it work?

Of course, all this is only useful if you’re a bacterium. So how do we turn an anti-virus defence mechanism into something that could let us edit human genomes at will?

Rather than relying on bacteria to create the molecules for them, scientists have worked out how to create their own versions of the CRISPR molecules in the lab. To start with, they need to work out the section of DNA that they want to target. For a condition sickle-cell anaemia, which is caused by a fault in a single gene, this is relatively easy, since we’ve already sequenced the gene that causes this disease and so know exactly the genetic code that we’re trying to target.

The banana is dying. The race is on to reinvent it before it’s too late

Before we get down to the business of unzipping and chopping up DNA, it’s worth getting to grips with the basics of how DNA is structured. Holding together the familiar DNA double-helix are four different nitrogen bases: adenine (A), thymine (T), guanine (G) and cytosine (C). The ordering of these bases determines everything about us, genetically-speaking. Eye colour, how tall we’re likely to be, whether we’re susceptible to certain diseases, it’s all written out in base pairs in our genetic code.

Like teeth on a zipper, these bases always pair up with their complementary base. A always pairs with T while G always pairs with C, over and over again until you’ve got to the three billion base pairs that make up the human genome.

But DNA isn’t much use staying locked up in a double helix – it needs to get that information out there and into the cell where it can be used to create proteins, which are the building blocks of pretty much everything in our bodies. To do to this, DNA unzips itself, breaking apart those base pairs until they’re flapping about in the cell.

These flapping, momentarily unpaired base pairs match up with short segments of RNA which contain their own own bases. RNA shares three bases with DNA – G, C and A – but T is alway replaced by U (uracil). Similar base-pairing rules apply, so an exposed DNA G base will pair with an RNA C base while a DNA A base will pair with a U. If you have an exposed DNA sequence of GAC, for example, you’ll end up with an RNA sequence of CUG.

Scientists use these basic principles to create their own CRISPR molecules which, as we pointed out above, are short stretches of RNA. All you need to do is open up a stretch of interesting-looking DNA – like the bit that contains the mutation that leads to sickle-cell anaemia – and build the complementary RNA sequence, with DNA-chopping enzyme attached. It’s a bit like starting with one side of a zipper and using that to build the corresponding but opposite side of the zipper that neatly fits into it.

Once you’ve got your CRISPR molecules, you need them to get your target cell. Luckily, viruses love nothing more than injecting stuff into other cells, so popping CRISPR molecules into otherwise benign viruses is one particularly useful way of introducing CRISPR into cells that’s already been put to work with in numerous studies involving mice.

Now CRISPR-Cas9 can really get to work. The Cas9 enzyme starts by unzipping bits of the DNA double helix while the RNA molecule sniffs its way along the exposed base pairs looking for a perfect match. Once the perfect match is found, Cas9 cuts out the troublesome gene before repairing the remaining bits of DNA. Other enzymes can add in insert genes instead of deleting them, but the basic process of unzipping, recognising and editing remains the same across different CRISPR molecules.

What is CRISPR used for?

CRISPR is particularly attractive to the agricultural industry, which is always looking for a way to engineer disease- and weather-resistant crops which will increase yields and, subsequently, their profit margins. In October 2015, plant biologists at Pennsylvania State University in the US presented US Department of Agriculture (USDA) regulators with button mushrooms that had been edited so they go brown a lot more slowly than normal mushrooms.

A year later, the USDA confirmed that the same mushrooms would be cultivated and sold without having to pass through the agency’s regulatory process for genetically-modified foods. Now, non-browning mushrooms are hardly the most thrilling foodstuff, granted, but this USDA is a pretty big deal because it hints that CRISPR-edited crops might be able to sidestep some of the environmental backlash levelled at GMO crops.

And it’s not just mushrooms getting the CRISPR love. In Australia, one scientist has already used CRISPR to make bananas resistant to a deadly fungus threatening to decimate the world’s crop of the fruit, while others are working on using the technology to create naturally decaffeinated coffee or finally engineer the perfect tomato.

Timeline: When was CRISPR discovered?

2005

After characterising CRISPR in 1993, Francisco Mojica at the University of Alicante in Spain became the first to hypothesise that the DNA sequences were part of bacteria’s adaptive immune system.

2007

Scientists at Danisco, a Danish food research firm, proved experimentally that CRISPR was part of a bacterial immune system and that Cas9 inactivates the invading virus.

2011

Emmanuelle Charpentier’s group at Umeå University in Sweden demonstrates the role of tracerRNA in guiding Cas9 to its cellular target.

2012

Emmanuelle Charpentier and Jennifer Doudna at the University of California, Berkeley simplify the CRISPR system by fusing together different elements into a single, synthetic guide

Although the agricultural world provides some of the furthest-along examples of CRISPR in action, the stakes are much higher when it comes to human health. Animal studies are already underway to use CRISPR to tackle sickle-cell anaemia and haemophilia – two promising candidates for CRISPR-treatment because they’re determined by a relatively small number of mutations. In the case of sickle-cell anaemia, the condition is caused by just the mutation of a single base pair in one gene.

The more genes involved in a condition, the harder it becomes to use CRISPR as a potential solution. “There are not many human diseases where only one gene is mutated,” says White. Certain cancers, for instance, are linked to multiple mutations in different genes, and often the link between genetic mutations and cancer risk are poorly understood so there’s no guarantee that – even if we could use CRISPR to fix faulty genes – that’d it’d be any kind of panacea for cancer.

Why is CRISPR controversial?

Late last year, He Jiankui, a researcher the Southern University of Science and Technology in Shenzhen shocked the scientific world when he claimed responsibility for the world’s first CRISPR-edited human beings. He reportedly took embryos from couples where the  father was HIV-positive and the mother HIV-negative and used CRISPR to edit the gene controlling a protein channel that HIV uses to enter cells.

The experiment – which was detailed in a YouTube video, not a peer-reviewed journal – was widely condemned by scientists. “It’s been widely acknowledged that the science is not yet ready for clinical application,” says Sarah Chan, a bioethicist and director of the Mason Institute for Medicine, Life Sciences and the Law at the University of Edinburgh said at the time. “More has to be done to resolve uncertainties, and to try and understand the risks.”

Although the He study does violate clear ethical boundaries, it does raise one of the big ethical conundrums when it comes to CRISPR. The problem is that it’s not that easy to use CRISPR to change your genome once you’re an adult – you’d need to find some way of introducing the molecules to every single target cell.

This is perhaps achievable for conditions like sickle-cell anaemia, where you only need to change the DNA in red blood cells. By using CRISPR to edit bone marrow – where red blood cells are produced – you might be able to target a relatively small percentage of cells and still fix the condition.

But if you want to change a person’s entire genome, you need to edit their DNA when they’re little more than a tiny cluster of cells. This leads to all kinds of ethical issues. Why stop at identifying and chopping out genetic diseases, for instance, if we could also tweak an embryo’s DNA so the resulting baby was more likely to be intelligent, or good-looking?

“What if we wanted to change future life span, or intelligence, or Alzheimer’s disease potential or whether they go bald when they get to middle age,” says White. “Societies going to have to come to terms with what we want – it’s not up to scientists.”

Although human gene-editing raises some of the biggest ethical questions, things aren’t an awful lot clearer when it comes to agriculture. In July 1018, the European Court of Justice threw the future of gene-edited crops into doubt when it confirmed that CRISPR-edited crops would not be exempt from existing regulations limiting the cultivation and sale of genetically-modified crops.

Crops that have been genetically-modified – usually by inserting a gene from one organism into another – have long been sidelined in Europe, despite their popularity in other parts of the world. Despite a scientific consensus that GM foods are safe to eat, headlines warning of ‘frankenfood’ and lobbying from environmental groups helped keep GM crops away from human consumption.

But agricultural advocates for CRISPR hoped that the new gene-editing technology would provide an opportunity to redress this balance. The ECJ ruling means that any CRISPR-edited food that is to be grown or sold in the EU must pass stringent safety tests that non-edited crops (or crops made using certain techniques like radiation mutation) do not have to face. For now, at least, one of the biggest barriers facing CRISPR isn’t science, but public relations.

More great stories from WIRED

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– Glasgow cured violence by treating it as a health epidemic

– Upgrade your sound with our guide to the best headphones

– The best Black Mirror episodes ranked

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New Post has been published on Biology Dictionary

New Post has been published on https://biologydictionary.net/nucleic-acid/

Nucleic Acid

Nucleic Acid Definition

Nucleic acid is the chemical name for the molecules RNA and DNA. The name comes from the fact that these molecules are acids – that is, they are good at donating protons and accepting electron pairs in chemical reactions – and the fact that they were first discovered in the nuclei of our cells.

Nucleic acids are large molecules made up of strings, or “polymers,” of units called “nucleotides.” All life on Earth uses nucleic acids as their medium for recording hereditary information – that is nucleic acids are the hard drives containing the essential blueprint or “source code” for making cells.

For many years, scientists wondered how living things “knew” how to produce all the complex materials they need to grow and survive, and how they passed their traits down to their offspring.

Scientists eventually found the answer in the form of DNA – deoxyribonucleic acid – a molecule located in the nucleus of cells, which was passed down from parent cells to “daughter” cells.

When DNA was damaged, or passed on incorrectly, the scientists found that cells did not work properly. Damage to DNA would cause cells and organisms to develop incorrectly, or be so badly damaged that they simply died.

Later experiments revealed that another type of nucleic acid – RNA, or ribonucleic acid – acted as a “messenger” that could carry copies of the instructions found in DNA. Ribonucleic acid was also used to pass down instructions from generation to generation by some viruses.

Today, scientists know that the source code for cells is quite literally written in nucleic acids. Genetic engineering changes organisms’ traits by adding, removing, or rewriting parts of their DNA – and subsequently changing what “parts” the cells produce.

A sufficiently skilled genetic “programmer” can create the instructions for a living cell from scratch using the nucleic acid code. Scientists did exactly that in 2010, using an artificial DNA synthesizer to “write” a genome from scratch using bits of source code taken from other cells.

All living cells on Earth “read” and “write” their source codes in almost exactly the same “language” using nucleic acids. Sets of three nucleotides, called triplets, can code for any given amino acid, or for the stop or start of protein production.

Other properties of nucleic acids may influence DNA expression in more subtle ways, such as by sticking together and making it harder for transcription enzymes to access the code they store.

The fact that all living cells on Earth “speak” almost the same genetic “language” supports the idea of a universal common ancestor – that is, the idea that all life on Earth today started with a single primordial cell whose descendants evolved to give rise to all modern living species.

From a chemical perspective, the nucleotides that are strung together to create nucleic acids consists of a five-carbon sugar, a phosphate group, and a nitrogen-containing base. The image below shows structural drawings of the four DNA and the four RNA nitrogenous bases used by living things on Earth in their nucleic acids.

It also shows how the sugar-phosphate “backbones” bond at an angle that creates a helix – or a double helix in the case of DNA – when multiple nucleic acids are strung together into a single molecule:

Difference of DNA and RNA

DNA and RNA are both polymers of nucleotides. The term “polymer” comes from “poly” for “many” and “mer” for parts, referring to the fact that each nucleic acid is made of many nucleotides.

Because nucleic acids can be made naturally by reacting inorganic ingredients together, and because they are arguably the most essential ingredient for life on Earth, some scientists believe that the very first “life” on Earth may have been a self-replicating sequence of amino acids that was created by natural chemical reactions.

Nucleic acids have been found in meteorites from space, proving that these complex molecules can be formed by natural causes even in environments where there is no life.

Some scientists have even suggested that such meteorites may have helped create the first self-replicating nucleic acid “life” on Earth. This seems possible, but there is no firm evidence to say whether it is true.

Function of Nucleic Acids

By far the most important function of nucleic acids for living things is their role as carriers of information.

Because nucleic acids can be created with four “bases,” and because “base pairing rules” allow information to be “copied” by using one strand of nucleic acids as a template to create another, these molecules are able to both contain and copy information.

To understand this process, it may be useful to compare the DNA code to the binary code used by computers. The two codes are very different in their specifics, but the principle is the same. Just as your computer can create entire virtual realities simply by reading strings of 1s and 0s, cells can create entire living organisms by reading strings of the four DNA base pairs – A, T, C, and G.

As you might imagine, without binary code, you’d have no computer and no computer programs. In just the same way, living organisms need intact copies of their DNA “source code” to function.

The parallels between the genetic code and binary code has even led some scientists to propose the creation of “genetic computers,” which might be able to store information much more efficiently than silicon-based hard drives. However as our ability to record information on silicon has advanced, little attention has been given to research into “genetic computers.”

Because the DNA source code is just as vital to a cell as your operating system is to your computer, DNA must be protected from potential damage. To transport DNA’s instructions to other parts of the cell, then copies its information are made using another type of nucleic acid – RNA.

It’s these RNA copies of genetic information which are sent out of the nucleus and around the cell to be used as instructions by cellular machinery.

Nucleic acids and similar molecules can also be used by cells for other purposes. Ribosomes – the cellular machines that make protein – and some enzymes are made out of RNA.

The fact that RNA can act both as hereditary material and an enzyme strengthens the case for the idea that the very first life might have been a self-replicating, self-catalyzing RNA molecule.

Nucleic Acid Structure

Because nucleic acids can form huge polymers which can take on many shapes, there are several ways to discuss the “structure of nucleic acid”. It can mean something as simple as the sequence of nucleotides in a piece of DNA, or something as complex as the way that DNA molecule folds and how it interacts with other molecules.

Please refer to our Nucleic Acid Structure article for more information.

Polymer of Nucleic Acids

As mentioned above, a “polymer” is a molecule that is made up of smaller parts. “Poly” means “many,” while “mer” means “part.”

When you hear doctors or scientists talking about “nucleic acids,” they almost always mean polymers. RNA and DNA are both typically strands of many nucleotides strung together.

Single nucleotides are usually referred to as just that – nucleotides. The term “nucleic acid” as well as the terms “RNA” and “DNA” are usually reserved for polymers of many nucleic acid monomers strung together.

Monomer of Nucleic Acids

The monomers of nucleic acids are molecules called nucleotides. These molecules are fairly complex, consisting of a nitrogenous base plus a sugar-phosphate “backbone.”

When our cells join nucleotides together to form the polymers called nucleic acids, it bonds them by replacing the oxygen molecule of the 3′ sugar of one nucleotide’s backbone with the oxygen molecule of another nucleotide’s 5′ sugar.

This is possible because the chemical properties of nucleotides allow 5′ carbons to bond to multiple phosphates. These phosphates are attractive bonding partners for the 3′ oxygen molecule of the other nucleotide’s 3′ oxygen, so that oxygen molecule pops right off to bond with the phosphates, and is replaced by the oxygen of the 5′ sugar. The two nucleotide monomers are then fully linked with a covalent bond through that oxygen molecule, turning them into a single molecule.

Nucleotides are the monomers of nucleic acids, but just as nucleic acids can serve purposes other than carrying information, nucleotides can too.

The vital energy-carrying molecules ATP and GTP are both made from nucleotides – the nucleotides “A” and “G,” as you might have guessed.

In addition to carrying energy, GTP also plays a vital role in G-protein cell signaling pathways. The term “G-protein” actually comes from the “G” in “GTP” – the same G that’s found in the genetic code.

G-proteins are a special type of protein that can cause signaling cascades with important and complex consequences within a cell. G-proteins are turned “on” or “off” by the phosphorylation of GTP.

Quiz

1. Which of the following is NOT a reason why some scientists think the first life might have been made of RNA? A. RNA nucleotides can be created spontaneously by natural processes. B. RNA can carry hereditary information, just like DNA. C. RNA can form enzymes that can catalyze chemical reactions, just like proteins. D. None of the above.

Answer to Question #1

D is correct. All of the above are reasons why some scientists think RNA may have been the first life form!

2. If there are only four base pairs of RNA and DNA, then why do we list five? (A, G, C, T, and U?) A. Uracil is not a true nucleotide. B. Uracil is the RNA equivalent of Thymine. C. Uracil and Thymine are interchangeable. D. None of the above.

Answer to Question #2

B is correct. Uracil is the RNA equivalent of Thymine. Although there are tiny chemical differences between the two, U and T can play the same role in base pair hydrogen bonding. The four DNA base pairs are A, T, C, and G, while the four RNA base pairs are A, U, C, and G.

3. Why might the “handedness” of our nucleic acids be important? A. Left-handed nucleic acids might take up more room in our cells than right-handed ones. B. The handedness of one’s nucleic acids determines whether you’re left-handed or right-handed. C. Some enzymes can only interact with molecules that have the correct “handedness” for their active sites. D. None of the above.

Answer to Question #3

C is correct. While “handedness” in molecules has nothing to do with whether your right or left hand is dominant, it can determine whether your enzymes can interact with the molecule. Enzymes might interact very differently with the right-handed vs. left-handed version of a molecule.

References

Lodish, H. F. (2016). Molecular cell biology. New York, NY: Freeman.

Mansfield, M. L., & Ballanco, J. (2011). A Model for the Evolution of Nucleotide Polymerase Directionality. PLOS. Retrieved from http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0018881

Qin, K., Dong, C., Wu, G., & Lambert, N. A. (2011). Inactive-state preassembly of Gq-coupled receptors and Gq heterotrimers. Nature Chemical Biology, 7(10), 740-747. doi:10.1038/nchembio.642