#phosphorylative

[selachii-lu]

i binged all of nqd recently but these are the doodles i sketched during season one. my designs def have changed since this but here’s what i originally imagined

[coollittleguys]

Man I love the Golgi apparatus.

Removal of Man? Addition of Gal?? Trans network??? Sign me up

[whats-in-a-sentence]

The systemic production of proteinase inhibitors in young tomato plants is triggered by a complex sequence of events (Figure 23.20):

Wounded tomato leaves synthesize prosystemin, a large (200 amino acids) precursor protein.

Prosystemin is proteolytically processed to produce the short (18 amino acids) polypeptide DAMP called systemin.

Systemin is released from damaged cells into the apoplast.

In adjacent intact tissue (phloem parenchyma), systemin binds to a pattern recognition receptor on the plasma membrane.

The activated systemin receptor becomes phosphorylated and activates a phospholipase A2 (PLA2).

The activated PLA2 generates the signal that initiates JA biosynthesis.

JA is then transported through the phloem to systemic parts of the plant by an unknown mechanism.

JA is taken up by target tissues and activates the expression of genes that encourage proteinase inhibitors.

"Plant Physiology and Development" int'l 6e - Taiz, L., Zeiger, E., Møller, I.M., Murphy, A.

[dykeyuu]

2 final exams day is OVER!! ended up with an A in chinese😋 and im reluctant to get my hopes up bc i felt great about the midterm and ended up just getting a 78 but secretly i feel like i mega slayed the signal transduction final

[lesbonoi]

bio class is just full of fucking words

[biology-geology-beaches-india]

[blueoaknx]

The Impact of High Fructose Corn Syrup on Mitochondrial Function

The Impact of High Fructose Corn Syrup on Mitochondrial Function:

Analysis

High fructose corn syrup (HFCS), a widely used sweetener derived from corn, has become a major component of the modern diet, especially in processed foods and sugary beverages. HFCS is composed of glucose and fructose in varying proportions, with HFCS-55 (55% fructose, 45% glucose) and HFCS-42 (42% fructose, 58% glucose) being the most common formulations. While the impact of HFCS on metabolic health has been widely discussed, recent studies have shown that it can also exert a detrimental effect on mitochondrial function. This technical analysis explores the biochemical mechanisms by which HFCS damages mitochondria, contributing to cellular dysfunction and a range of metabolic diseases.

Mitochondrial Physiology and Biochemical Function

Mitochondria are highly specialized organelles responsible for producing adenosine triphosphate (ATP), the primary energy currency of the cell, through oxidative phosphorylation (OXPHOS). This process occurs in the inner mitochondrial membrane and involves the electron transport chain (ETC) and ATP synthase. The mitochondria are also involved in regulating cellular metabolism, maintaining redox balance, calcium homeostasis, and apoptosis (programmed cell death). Mitochondrial dysfunction, characterized by impaired ATP production, altered mitochondrial dynamics (fusion/fission), and excessive reactive oxygen species (ROS) production, is a key factor in the pathogenesis of many chronic diseases, including obesity, insulin resistance, cardiovascular diseases, and neurodegenerative disorders.

Fructose Metabolism and Its Divergence from Glucose

The metabolism of fructose, particularly in the liver, diverges significantly from that of glucose, and it is this divergence that underpins much of the mitochondrial dysfunction associated with HFCS consumption. Unlike glucose, which is predominantly metabolized via glycolysis and the citric acid cycle (TCA cycle), fructose bypasses the rate-limiting step of glycolysis, catalyzed by phosphofructokinase-1 (PFK-1), and is instead phosphorylated by fructokinase to form fructose-1-phosphate. This rapid metabolism of fructose in the liver can overwhelm metabolic pathways and lead to the accumulation of intermediate metabolites such as dihydroxyacetone phosphate (DHAP) and glyceraldehyde, which can be further converted to fatty acids and triglycerides through de novo lipogenesis (DNL).

Excessive fructose consumption leads to the accumulation of triglycerides, particularly within hepatocytes, which is a hallmark of non-alcoholic fatty liver disease (NAFLD). The lipid accumulation in the liver, in turn, exacerbates mitochondrial dysfunction and oxidative stress, contributing to insulin resistance and a cascade of metabolic disorders.

Mechanisms of Mitochondrial Damage Induced by HFCS

Increased ROS Production

One of the most significant consequences of excess fructose metabolism is the elevated production of reactive oxygen species (ROS). ROS are byproducts of cellular respiration, primarily generated at complexes I and III of the electron transport chain. Under normal conditions, mitochondria have a robust antioxidant defense system, including enzymes like superoxide dismutase (SOD), catalase, and glutathione peroxidase, which help neutralize ROS. However, when cells are exposed to an overload of fructose, the liver mitochondria become overwhelmed, leading to excessive ROS generation.

Fructose metabolism increases the NADPH/NADP+ ratio, enhancing the activity of nicotinamide adenine dinucleotide phosphate (NADPH)-dependent oxidases such as NADPH oxidase (NOX), which further amplifies ROS production. These ROS cause oxidative damage to mitochondrial DNA (mtDNA), lipids in the mitochondrial membranes, and mitochondrial proteins. Such damage impairs mitochondrial function by decreasing mitochondrial membrane potential, disrupting the electron transport chain, and promoting mitochondrial fragmentation. Furthermore, mtDNA is particularly vulnerable to ROS due to its proximity to the electron transport chain and the lack of histone protection, leading to mutations that impair mitochondrial replication and protein synthesis.

Disruption of Mitochondrial Biogenesis

Mitochondrial biogenesis refers to the process by which new mitochondria are synthesized within a cell to meet the energy demands. This process is tightly regulated by several transcription factors, most notably peroxisome proliferator-activated receptor-gamma coactivator 1-alpha (PGC-1α). PGC-1α activates the transcription of nuclear and mitochondrial genes involved in energy metabolism, mitochondrial dynamics, and antioxidant defenses.

Fructose consumption has been shown to inhibit PGC-1α expression in both liver and skeletal muscle cells. Reduced PGC-1α levels lead to impaired mitochondrial biogenesis, which limits the ability of cells to adapt to increased energy demands. This is particularly concerning in tissues with high metabolic demands, such as muscle, heart, and liver, where impaired mitochondrial function can exacerbate energy deficits and lead to insulin resistance, fatty liver disease, and other metabolic disorders.

Mitochondrial Permeability Transition and Apoptosis

Chronic exposure to high levels of fructose can lead to mitochondrial permeability transition (MPT), a process in which the mitochondrial inner membrane becomes permeable to ions and small molecules, disrupting mitochondrial function. MPT is typically induced by excessive ROS production, calcium overload, or changes in the mitochondrial membrane potential. The opening of the mitochondrial permeability transition pore (MPTP) leads to the loss of mitochondrial membrane potential, uncoupling of oxidative phosphorylation, and the release of pro-apoptotic factors such as cytochrome c into the cytoplasm. This, in turn, activates the caspase cascade, promoting apoptosis.

In the context of HFCS-induced mitochondrial dysfunction, increased ROS and altered metabolic intermediates, such as ceramides, may trigger MPT and apoptotic pathways, leading to cell death and tissue damage. In tissues such as the liver and pancreas, this can exacerbate the pathological progression of fatty liver disease and insulin resistance.

Fatty Acid Accumulation and Impaired Beta-Oxidation

Excessive fructose consumption induces de novo lipogenesis (DNL) in the liver, leading to an increase in the synthesis of fatty acids, which are esterified into triglycerides and stored within hepatocytes. This accumulation of lipids can overwhelm the capacity of mitochondria to oxidize these fatty acids via beta-oxidation, leading to mitochondrial dysfunction. The accumulation of lipotoxic intermediates such as ceramides and diacylglycerols further impairs mitochondrial function by inhibiting key enzymes involved in mitochondrial energy production.

Moreover, the excess fatty acids can impair mitochondrial membrane fluidity, reducing the efficiency of oxidative phosphorylation. The lipid-induced mitochondrial dysfunction leads to further oxidative stress, creating a feedback loop that exacerbates the metabolic disturbances caused by high fructose intake.

Clinical Implications of HFCS-Induced Mitochondrial Dysfunction

The long-term consumption of HFCS has profound implications for human health, particularly in the context of metabolic diseases:

Insulin Resistance and Type 2 Diabetes: HFCS-induced mitochondrial dysfunction, particularly in liver and muscle cells, contributes to impaired insulin signaling and glucose homeostasis. As mitochondrial function declines, cells become less responsive to insulin, leading to insulin resistance, a precursor to type 2 diabetes.

Non-Alcoholic Fatty Liver Disease (NAFLD): The accumulation of fat in the liver, driven by increased fructose metabolism, leads to mitochondrial damage and dysfunction, which exacerbates the progression of NAFLD to non-alcoholic steatohepatitis (NASH), a more severe form of liver disease.

Cardiovascular Disease: Mitochondrial dysfunction in cardiomyocytes can impair ATP production, leading to reduced contractile function and the progression of cardiovascular disease. The increased oxidative stress and inflammatory mediators associated with mitochondrial damage also contribute to vascular injury and atherosclerosis.

Neurodegenerative Diseases: Impaired mitochondrial function in neurons, driven by high fructose intake, may contribute to neurodegenerative diseases such as Alzheimer's and Parkinson's disease, as mitochondria play a critical role in maintaining neuronal health.

Conclusion

High fructose corn syrup exerts a significant impact on mitochondrial function through several interconnected mechanisms. These include the increased production of reactive oxygen species (ROS), inhibition of mitochondrial biogenesis, induction of mitochondrial permeability transition, and the accumulation of toxic lipid intermediates. These disruptions in mitochondrial homeostasis contribute to the development of insulin resistance, non-alcoholic fatty liver disease, and other chronic metabolic diseases. Addressing the widespread consumption of HFCS and reducing dietary fructose intake could be crucial in mitigating mitochondrial dysfunction and preventing associated metabolic disease

[cytgen]

Abstract Protein kinases represent one of the largest eukaryotic enzyme superfamilies. However, only a few can directly phosphorylate tubulin and contribute to the modulation of the “tubulin code.” The authors previously confirmed the structural and functional homology of the plant protein kinase IREH1 and members of the mammalian MAST kinase family. Their participation in the regulation of the microtubule system in plant and animal cells was also experimentally confirmed. At the same time, the direct contribution of MAST/IRE to the “tubulin code” remains unclear. In the current study, based on bioinformatical and structural biology methods, the possibility of such an interaction was evaluated. The target sites of MAST/IRE-phosphorylation of tubulin were predicted based on similarity to the generalized specific profiles. Two potential MAST/IRE specific sites, conserved in human and Arabidopsis tubulins were selected: Thr73 (80) exists in most isotypes of α-tubulin and Ser115 was found in the majority of human and plant isotypes of β-tubulin. It was predicted that phosphorylation of the first site can affect the assembly of α/β-tubulin heterodimer, and phosphorylation of the second may affect the interaction between neighboring protofilaments of microtubules. The last site Ser433, was found in both γ-tubulin isotypes of A. thaliana, but it was absent in mammals. The external position of Ser433 in plant γ-tubulin allows for suggesting that phosphorylation of this amino acid can affect the structure of the γTuRC complex but it does not affect inner contacts of γTuSC and their interaction in the ring.

[otabekisautistic]

do you think oxidative phosphorylation feels good for the adp

[evil-jennifer-hamilton-wb]

Hear me out:

Would (Graphed using Desmos, created by me)

[asongoftearsandfandoms]

It is the year of our lord twenty twenty-four, how has no one made a sick remix of Oxidative Phosphorylation (song by Science Groove, 2004)

[tenth-sentence]

ATP is a phosphorylating agent (that is, it donates phosphates to other molecules) in many biochemical processes, where it acts as an energy source.

"Chemistry" 2e - Blackman, A., Bottle, S., Schmid, S., Mocerino, M., Wille, U.

[whats-in-a-sentence]

One of these experiments, carried out by Emerson, measured the quantum yield of photosynthesis as a function of wavelength and revealed an effect known as the red drop (Figure 7.12). (...) The observation that the overall quantum yield of photosynthesis is nearly independent of wavelength (see Figure 7.12) strongly suggests that such a mechanism exists.

"Plant Physiology and Development" int'l 6e - Taiz, L., Zeiger, E., Møller, I.M., Murphy, A.

[natrasharomanova]

absolutely losing my mind at this poem Hans Adolf Krebs included at the end of his paper about the tricarboxylic acid cycle

[biology-geology-beaches-india]

TSRNOSS. Page 225.