#Pseudogenic

[ace-paradox]

Coining a -tive term I've been using.

Could not find a term that even remotely fit my experience, therfore I made a new one:

Faketive

A Faketive is a headmate who was pretended to be real before they became an actual member of the system.

This may include, but isn't limited to:

- Headmates initially pretended by a system who went on to become an acctual member of the system.

- Pretended headmates by singlets due to misunderstanding, curiosity, or external pressures to be a system.

- Headmates of Pseudogenic or Fakergenic systems

- Any Headmates with a source rooted in faking or lying about plurality.

- All headmates who feel they were once pretended by their headmate(s)

Faketives, recognizing their growth from a made-up identity to an acknowledged part of the system.

Related Terms:

Faketives may share characteristics with autojects, OCtives, or Mostives, especially when the fabricated identity originates within the system itself.

They may be related to roleplaytives or dramatitives if they were initially used to simulate scenarios or perform roles.

If stemming from an identity created under false pretenses (e.g., the system pretending to be someone else), they may align with Mendaxgenic origins.

Coined by me

requested by me

[immult]

The first session went well! The party was sent to investigate some eldritch horrors, failed some wis saves and got to experience horrifying visions! I even snuck in a psuedo imogen character in your honor!

FOR ME? thanks kindly pardner. there is now an imogen who lives in somebody's campaign (npc pseudogen counts!). like literally that's one more imogen than the last time i checked and i think that's AMAZING. glad it went well for yall (and terrible for the PCs).

[neosciencehub]

Our Research Targets as Many Traits of Cancer as Possible Through Pseudogenes

Our Research Targets as Many Traits of Cancer as Possible Through Pseudogenes @neosciencehub #neosciencehub #science #research #pseudogenes #cancer #NSH #EMBL #NCI #NIH #biology #Genomics #healthcare #DNA #oesophagel #IISER #AI #NCI #

Meet GovadaPravallika, a promising mind who has pursued her Masters in Science from the esteemed Indian Institute of Science Education and Research (IISER), Pune, one of only six such institutions in India. Currently, she is delving deeper into the realm of Cancer Biology and Genomics for her PhD. She took a leap in her world of genetics and genomics and published a radical research- “Stage II…

[cytgen]

Abstract Tandemly arranged repetitive regions (repeats) that encode 5S rRNA (5S rDNA) are an indispensable component of eukaryotic genomes. Typically, 5S rDNA repeats within a genome are very similar due to the concerted nature of the evolution of this type of repeats. Each 5S rDNA repeat consists of an evolutionarily conserved coding sequence (CDS) and a variable intergenic spacer (IGS). 5S rDNA is a popular model for studying the molecular evolution of repetitive sequences, and the high rate of IGS mutations determines its wide use in phylogenetic analysis of closely related taxa. Nevertheless, 5S rDNA remains unexplored for many groups of higher plants, especially for the Plumbaginaceae family. Some taxa of this family are endemic to southern Ukraine and listed in the Red Book. However, their taxonomic status is controversial, and its clarification requires the use of molecular phylogenetic methods. In this work, we examined the molecular organization of 5S rDNA for representatives of four genera of the tribe Limonieae, the largest in the family Plumbaginaceae. It was shown that the CDS of 5S rDNA of representatives of the genera Limonium, Armeria, and Ceratolimon possess single mutations that do not affect the formation of the secondary structure of 5S rRNA. In contrast, in the genomes of Goniolimon species, in addition to functionally normal 5S rDNA repeats, numerous pseudogenes were found that do not evolve in a concerted manner and contain numerous mutations in the CDS that disrupt the secondary structure of 5S rRNA. A significant phylogenetic distance between representatives of the subgenera Pteroclados and Limonium of the genus Limonium indicates that Pteroclados can be considered a separate genus. The high rate of molecular evolution makes 5S rDNA IGS a convenient tool for the reconstruction of phylogenetic relationships within the studied genera of the tribe Limonieae and the barcoding of Ukrainian endemics of the genus Limonium.

Keywords: 5S rDNA genetic polymorphism molecular evolution and phylogeny repetitive sequences pseudogenes Armeria Ceratolimon Goniolimon Limonium

[mleprae]

leprosy out of all bacteria known to man places 2nd in bacteria with the most pseudogenes (genes that are useless and have no function). Most bacteria have around <5% pseudogenes, and that's a generous number! Leprosy has around 40-48%, few theories are thrown around as to why it has so many pseudogenes and why it doesn't Get Rid of It already!! My favorite one is that the reason why it's holding onto all this junk is that it MIGHT be useful at some point, like a hoarder... gene hoarder.... BAD gene hoarder

[owlservice]

Perhaps the most striking example of this loss of olfactory receptor genes can be seen in the cetaceans—whales and dolphins. The ancestors of these animals were terrestrial mammals, something like hippos; about 40 million years ago they began to return to the sea, and now they are entirely aquatic, although they remain air-breathers and therefore cannot smell under water. This means that the only time a whale or dolphin can smell is during those split seconds when it surfaces, exhales and then rapidly inhales. In cetaceans, around 68 per cent of DNA sequences that can be identified as olfactory receptor genes are pseudogenes. This suggests that olfaction plays a limited role in the survival of these animals, and that their olfactory genes can accumulate mutations without harming an animal’s chances of reproduction.

Smell (AVSI) by Matthew Cobb

We need to start throwing bath bombs in the ocean to preserve the cetacean olfactory receptor gene lineage

[sophieinwonderland]

how do you feel about the divide between the tulpamancy and the wider endo community? i keep seeing posts that wish for "more systems that piss people off" and list off obscure origins like firpergenic and pseudogenic, but not a mention of tulpas, even though we bear half of all the hate coming from sysmeds.

I see "pro-endo" posts that censor us as t*lpagenic, i see posts insisting that we have to leave our communities and start calling ourselves willogenic or other terms they came up with, otherwise we deserve to be the endos' scapegoats. i see posts from transplurals rejecting any mention of tulpamancy techniques that could help them and separating themselves from tulpamancy, even though i and i'm sure many others have had similar experiences of hating being a singlet and changing that with tulpamancy

Is this it? Is this all the discourse is ever going to be? I wish the kids would realise that they'll never win if they don't stick with their most controversial, and i wish we didn't have to defend both our own existence and theirs at the same time

I think the divide is overstated. There's a small handful of pro endos who are against the term tulpa. And they do tend to be rather vocal about it.

I mean, you do a search for "#pro endo #anti tulpa" in the tags and you'll see most are just people intentionally crosstagging to reach the other side. Tags are obviously not the only things that matter since not everyone tags their stuff as anti tulpa. But still, I just don't see this mentality that much outside of a very few pro endo blogs.

And at that, many of these anti-tulpa pro-endo blogs are people who have been in sysmed circles and picking up their talking points from them. Either "originally pro endo but fell into anti endo circles later" or "reformed anti endo who absorbed anti endo talking point before making the change but still doesn't accept tulpas."

You look into a lot of these so-called pro-endo anti-tulpas who make anti-tulpa posts, and it's not long until you find them arguing that endogenic and pro endo systems aren't oppressed and should shut up about it.

Or calling the pro-endo community nasty because we're not polite enough to people fakeclaiming our existences and harassing us for being plural for non-trauma reasons.

I would hardly call the "endogenic systems exist but I hate their community and think they should shut up about being oppressed" camp pro endo.

To the extent that actual anti-tulpa pro-endos do exist, I do find it's pretty stupid. I think it shoots yourself in the foot on multiple fronts. As you mention, it separates them from valuable resources that can help their systems.

It also plays into sysmed misinformation meant to divide the community. It's the same exact thing that happened when transphobes spread the talking point that "Faegender" was appropriative to sew division in the trans community, and demonize people for using neo pronouns.

The other thing is... tulpamancy is being researched right now more than other sorts of plurality, in a scientific way. When the Stanford Tulpa Study is published, it's going to be super important to spread that as much as possible.

And I expect we'll also see future studies on tulpas that will be into the actual creation process, which will be amazing. Imagine if we had a longitudinal study demonstrating that singlets can create headmates from scratch! This would completely and utterly destroy all remaining sysmed talking points.

Any pro-endo systems not sharing studies like this because they don't like a word would, frankly, be harming all endogenic systems with their silence.

But like I said, these tend to be a very vocal minority. I don't worry about them or concern myself with them.

I also think as tulpa studies come out and are the main evidence showing that plurality can be induced at any age into singlets, many of the stragglers will end up falling in line. 🤷‍♀️

[cleverwordsandotherstuffilike]

Medical innovations and scientific advances at Harvard Medical School through the decades (Part 2 of 2)

1995 Triple-organ transplant; kidney disease blood glucose levels

1996 How cells sense oxygen; Alzheimer's treatments; immune system advances

1997 p73 gene; aspirin

1998 Adult live-donor liver transplant

1999 Fluorescent molecular probes

2000 Brain abnormalities associated with abuse and neglect

2001 Circadian clock

2002 Rheumatoid arthritis pathway; C-reactive protein

2003 Multi-drug-resistant tuberculosis treatment; source of pre-eclampsia

2004 Blood stem cells; protein transfer

2005 Prenatal nutrition; herpes vaccine candidate

2006 Cholesterol mechanism; DNA sequencing techniques

2007 Cellular switch; rheumatoid arthritis gene; brown-fat cell switch

2008 RIPKI inhibitors; metastatic melanoma remission

2009 LIN28 protein; RNA interference; cancer cells' starvation; brown fat

2010 Enhancer transcription

2011 Kidney failure markers; cancer cell vulnerability; global health care budget models

2012 Tumour suppressor gene p53; ancient migration; infectious disease diagnostics

2013 Cardiac hypertrophy reversal; cathepsin k pathways

2014 Hematopoietic stem cells; pancreatic stem cells

2015 Bioartificial replacement limb; PD-1 pathway; The Lancet Commission on Global Surgery; pseudogene; damaged protein disposal; multiple sclerosis; somatic mutations; deafness gene therapies

2016 Sigma-1 receptor structure; Zika vaccine candidate; circadian rhythm-bipolar disorder link; microbiome

2017 Unlocking the blood-brain barrier; deciphering the structure of a scissor like enzyme

2018 The 'graying' of T cells; From one cell, a detailed road map

2019 Finding herpes' Achilles' heel; viral peptides critical to natural HIV control

2020 How COVID causes loss of smell; obesity fuels tumour growth; heart muscle dysfunction

2021 SARS-CoV-2 vaccine; immune evasion; AI gene interpretation; radiation vulnerability

2022 Fruit fly cell atlas; viral infection on video; boot camp for immune cells

2023 How the brain senses infection; new origin of breast cancer; the microbiome and cancer immunotherapy

[pokemoncenter]

On Pokemon DNA

In all living things, there is a special polymer of nucleotides forming a double helix called Deoxyribonucleic Acid, or DNA. This is the basis of life. DNA is something akin to the instructions of life- It encodes instructions for cells and proteins to follow, and from that instruction, it builds the appropriate life form.

(I am aware that this is vastly oversimplified, however, I wish to put in an extremely basic understanding for those who left school to go on Pokemon journeys, and thus would not have even this knowledge base to work with. I will not be explaining each base or each role of each part. Please understand.)

DNA is passed down from parent to child. When two living beings conceive a child, the zygote receives half its DNA from its father and half from its mother, engaging in new combinations, before even factoring in mutations.

However, DNA is not perfectly efficient. Over time, transmission errors, mutations, and other such factors build up, and portions of the DNA do not code instructions. Some of this DNA has use- Even if it does not code anything itself, it may modify or instruct other DNA coding sequences. This is called non-coding DNA, or ncDNA.

However, there is further DNA- Fragments of ancient DNA that still gets passed down, or pseudogenes- that seem to do nothing at all. This is called 'junk DNA'. However, the study of ncDNA and junk DNA is rather limited, as because they are not actively encoding information, they are thought of as useless.

(There is a theory that Mewtwo is so different from all known records of Mew, not because Team Rocket intentionally augmented Mewtwo, but because they deemed the ncDNA as worthless and removed it from the genome.)

It is said that the human genome is as much as 99% ncDNA, and the active part that creates genes and creates the person is as small as 1%. That is, over our millions of years of evolutionary history, only 1% of what we still hold on to remains in use.

(Atavism, when a trait lost over the course of evolution suddenly returns via a mutation, is thought to involve the reactivation of some ncDNA. Such examples include humans growing tails, or a Torchic with teeth.)

However, while humans have as much as 99%, interestingly, Pokemon eclipse even that, with potential 99.99% of their DNA seeming to be ncDNA. The strange part is, this is true for most Pokemon- Regardless of its species or complexity, all Pokemon seem to have an incredible amount of ncDNA by any standards. The reason and method for this is currently unknown. Why Pokemon DNA genomes seem to be so long while so little of it is used, and why it is so consistent... Another mystery of Pokemon.

As mentioned above, I purposefully oversimplified things here to try to make it easier for those with no understanding or schooling in genetics to understand. However, I recognize I may have accidentally made some parts misleading or even incorrect in my attempts to simplify matters. If any experts on genetics wish to weigh in and add in your own thoughts and corrections, I would welcome this.

[lokiinmediasideblog]

A funny thing about me is that I read Anne Rice's Taltos while attending college and studying Biology, and it was fun seeing some old genomics theories in a book written in the 1990s. In Taltos they equate the size of a genome to an organism's complexity. It's the reason given as to why the Taltos has such powers and complexity over humans. This is not the case. And by that logic, some bacteria would be more complex than humans despite being single-celled organisms lacking a nucleus and organelles.

This excerpt is from the link above^^^:

Beyond Estimating the Number of Protein-Coding Genes

As with genome size, having more protein-coding genes does not necessarily translate into greater complexity. This is because the eukaryotic genome has evolved other ways to generate biological complexity. Much of this complexity derives from how the genome "behaves," or more precisely, how various genes are expressed.

Alternative splicing was the first phenomenon scientists discovered that made them realize that genomic complexity cannot be judged by the number of protein-coding genes. During alternative splicing, which occurs after transcription and before translation, introns are removed and exons are spliced together to make an mRNA molecule. However, the exons are not necessarily all spliced back together in the same way. Thus, a single gene, or transcription unit, can code for multiple proteins or other gene products, depending on how the exons are spliced back together. In fact, scientists have estimated that there may be as many as 500,000 or more different human proteins, all coded by a mere 20,000 protein-coding genes.

Scientists have since come across several other mechanisms that contribute to the eukaryotic genome's capacity to generate phenotypic complexity. These include RNA editing, trans-splicing, and tandem chimerism. RNA editing is the alteration of an mRNA molecule after transcription—for example, the modification of a cytosine to a uracil before an mRNA molecule is translated into a protein. The phenotypic consequences of RNA editing vary among genes and species. While sometimes detrimental (e.g., some RNA editing events have been associated with disease), those RNA editing events that lead to slight changes in protein structure could be selectively advantageous (Reenan, 2005). Trans-splicing is the splicing together of separate transcripts to form an mRNA molecule, as opposed to alternative splicing, which is the splicing together of exons from the same transcript. Tandem chimerism occurs when adjacent transcription units are transcribed together to form a single "chimeric" mRNA molecule (Parra et al., 2005).

Consider again those 60,000 protein-coding genes in Trichomonas vaginalis. If all of those 60,000 genes operated at the same level of complexity as the 20,000 or so genes in Homo sapiens, then shouldn't T. vaginalis be a much more complex organism than it is? As it turns out, its genes do not operate at that same level of complexity. For starters, few of the genes have any introns at all, which means that alternative splicing is not a major source of protein variation. Rather, scientists suspect the large number of genes—which, incidentally, is 10 times more than they expected they would find before they started the sequencing project—is due to duplication (Carlton et al., 2007). In other words, many of the genes are simply copies of each other. Furthermore, about half are believed to be "pseudogenes," or DNA sequences that are similar to functional protein-coding genes but have lost their protein-encoding capacities. Scientists still don't know why the T. vaginalis genome has so many genes, including so many defunct genes.

Organismal complexity is thus the result of much more than the sheer number of nucleotides that compose a genome and the number of coding sequences in that genome. Not only may one coding sequence encode a large number of separate protein products via alternative splicing, but many genomes are also rich with noncoding RNA sequences that work to coordinate gene expression. When one combines these elements with other regulatory elements, such as enhancers and promoters, as well as with potential sequences that remain uncharacterized, it becomes clear that while size is one component of organismal complexity, its contribution to that complexity is small.

[oh-okay-kay]

i think about this paper a lot. it discusses a *very* biological perspective (mainly through the lense of Ca2+ homeostasis and physiology), rather than a social perspective, on how gender differs from sex, and still comes to the conclusion that there are pretty much infinite genders, as well as occasionally discusses how being gay or bi or whatever is evolutionarily just as valid as being straight. super interesting

"It will be argued that it follows from the principles of Ca2+- physiology and homeostasis that all individuals of a sexually reproducing animal population have a personalized gender behaviour. Thus, subdividing gender-behaviours in hetero-, homo-, bi-, trans- etc. which all result from a differential use of the very same basic physiological principles, is too primitive a system that may yield false sociological interpretations."

"The logical, not to say self-evident answer given to: Why do many, in particular higher organisms produce sperm and eggs? usually is: That is the condition to have (chances for) a progeny and for being evolutionarily successful. Yet, this answer implies that testes and ovaries are aware of the reproduction-oriented drive the whole organism might have. This cannot possibly be the case: ovaries and testes do not plan for the future by producing gametes. According to the current status of evolutionary theory, there is no goal whatsoever in evolution."

"There is no generally accepted definition of gender, because the concept itself is not static but dynamic... the meaning of gender depends on who uses the word, in what context, and for what ends."

"If the reproduction-related behaviour would only be determined by the same set of genes that govern gonad formation and differentiation, there would probably only be heterosexuality and no homosexuality. But homosexuality, bisexuality, asexuality etc. do occur. Thus, the observed variability in behaviour must be caused by a more complex (set of) mechanism(s) than just the few genes that govern gonad differentiation."

"In such conditions, thus when gender behaviour becomes very personalized, the number of possible gender forms will near the number of all constituting individuals of the whole population. Thus in our own species there are as many different gender variants as there are individuals, 7 billion plus. But the total number of genes coding for proteins present in the human genome is only about 20,000. In addition, there are also some 10,000 pseudogenes, some genes can be subject to epigenetic modifications, and the junk DNA (that does not code for proteins) also has some regulatory functions. Even if all this is taken into account, the discrepancy 7 billion+ versus some 30,000+ genes and pseudogenes, illustrates that gender must have a physiological basis that enables a huge variability that can unfold while making use of only a limited number of genes."

"Because, many people believe that reproduction has been created or has come into existence with the goal of a progeny, gender variants that do not aim at a progeny, will be perceived as unnatural or, in a religious context, even as sinners. But reproductive archaeology teaches us that sexual reproduction did come into existence as the result of a sort of bacterial infection, not at all with the goal of producing a progeny in a novel way, namely by making use of special sex cells (sperm and eggs). Of course, heterosexuality is also in such a context a seemingly more successful form because it enables a progeny. However, this is a fortuitous coincidental feature, which does not imply any (in the case of humans) moral superiority: all gender forms have a cell-physiological basis. They are all variants of the same basic model. The supposedly better (in the long-term) form for the entire population, the heterosexual one, only seems better because it occurs in a much larger percentage of the population, and because most people erroneously think that the production of gametes and fertilization has come into existence in the course of evolution with the goal of producing a progeny."

"In conclusion: In this paper I advanced the physiology-based view that there are probably as many different gender variants as there are sexually reproducing individuals, and this not only in humans. Hence, there is no need to make subcategories in the gender variants with the purpose to install a moral hierarchy as they are all physiologically equal."

also, as an ace, the line "Thus in this view, sexual reproduction results from an evolutionary ancient bacterial-type infection, with sub-lethal effects. Thus it is a mild disease" is very funny

can’t stop thinking about my friend’s cishet partner who said last night that he doesn’t think anyone is the same gender. god-tier take.

[evoldir]

Fwd: Postdoc: UGent_Belgium.Two.PlantGenomeEvolution

Begin forwarded message: > From: evoldir@evol.biology.mcmaster.ca > Subject: Postdoc: UGent_Belgium.Two.PlantGenomeEvolution > Date: 11 January 2025 at 05:27:42 GMT > To: rdmpage@gmail.com > > > > > FWO-UGent funded bioinformatics postdocs - Unveiling the significance > of gene loss in plant evolution > > We are seeking two highly motivated postdoctoral researchers to join > our research team based in the Van de Peer lab, under the supervision of > Dr. Zhen Li, Assistant Professor at Ghent University/VIB Staff Scientist. > > The two positions are funded through an FWO research grant awarded to > Dr. Zhen Li and will focus on the evolutionary significance of gene loss > in shaping plant adaptation, speciation, and biological innovations. This > project aims to redefine our understanding of gene loss alongside gene > gain in plant evolution, focusing on developing novel genomic approaches > to analyze gene loss across diverse plant lineages and their evolutionary > consequences. To this end, the initial focus will be developing a novel > genomic approach integrating homolog identification and multiple genome > alignment to identify gene loss in plants and investigating its links > with species divergence and adaptive traits in various plant clades, > e.g., Orchidaceae, Poaceae, Solanaceae, Brassicaceae, and Fagales. > > Research Focus Areas > While the two positions will work closely together and share many > responsibilities, they have slightly different initial focus areas: > Position 1: Computational Genomics and Method Development > - Develop novel genomic frameworks for detecting gene loss in >  plant genomes > - Implement approaches to distinguish DNA deletion from pseudogenization > - Analysis of gene loss patterns across diverse plant lineages > - Explore graph-based algorithms for multiple genome alignment and >  ancestral karyotype reconstruction > > Position 2: Evolutionary Analysis and Network Biology > - Analysis of cross-species/-ecotype co-expression and gene >  regulatory networks > - Study of molecular mechanisms underlying how gene loss affects >  biological network rewiring > - Integration of phenotypic data with omics analysis > - Explore machine learning and network analysis methods > > We Offer > The VIB-UGent Center for Plant Systems Biology is a world-leading > science institution in Ghent, Belgium. Ghent University is among the top > 100 global universities according to several international rankings. > - A fully funded, full-time postdoctoral position for one year (with >  possibility of a two-year extension after positive evaluation) in a >  stimulating and supportive international research environment > - Access to state-of-the-art tools and computational infrastructure, >  including CPU/GPU clusters > - Opportunity to contribute to cutting-edge research in plant evolution >  and genomics > - Support for attending international conference and developing >  professional networks > - Comprehensive training in academic, technical, and career skills >  through VIB and Ghent University > > Motivated candidates are asked to apply online via the VIB application > procedure. > > A complete application file (English) should contain the following > documents: > - A cover/motivation letter (max. 2 pages) stating career goals, >  experience, and how these relate to your preferred position 1 and/or 2 > - A detailed CV, including a list of your scientific publications > - Contact information of at least two academic references > > For detailed information, please visithttps://jobso.id/ko16 > For inquiries about the positions, please mail to zhen.li@psb.vib-ugent.be > > Zhen Li

[immult]

Today is the day that pseudogen prepares the party for a boss fight that they decided they wanted to play but are almost certainly underprepared for

your pseudogen being an eshteross/keyleth/allura figure is making my heart squeeze. i know bona fide imogen would love nothing more than early retirement but i can dream.

good luck with the session don't crit too much against your players.

[neosciencehub]

Pseudogenes in Esophageal Carcinoma

Unveiling the Shadows: New Frontier in Cancer Biology Cancer research is continually evolving, branching into areas previously unexplored or deemed less significant. A prime example of this evolution is the study of pseudogenes and their impact on cancer, specifically esophageal carcinoma. How do the Pseudogenes Drive Cancer Progression in the Oesophagus? Pseudogenes are DNA sequences that…

[suresuresureaursure]

guys…I think we may have pseudogenic angst ocd

[mleprae]

I want to sooo desesperately believe that leprosy's pseudogenes actually encode for something but nobody has figured out how to 'activate' them, unfortunately it is more likely that those pseudogenes are just junk.... but leprosy keeps surprising us at every turn so.. maybe? maybe?