#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]

TSRNOSS, p 810.

[lakeeffectbitch]

So turns out that in ME/CFS all of your body’s cells are probably using the same energy production compensation methods as cancer cells. Fucking tracks lmao

[pxlpanic]

lil rant in the tags

will delete later jsbdjs

ps. didnt know there were max 30 tags wow

[blueoaknx]

Mitochondrial Dysfunction Drives Cognitive Decline

Introduction

Mitochondria, often referred to as the powerhouses of the cell, are crucial organelles responsible for energy production through adenosine triphosphate (ATP) synthesis. Beyond their well-known role in energy metabolism, mitochondria regulate a wide range of cellular processes, including calcium homeostasis, reactive oxygen species (ROS) generation, and apoptosis. When mitochondria malfunction, the consequences can be far-reaching, especially for energy-intensive organs like the brain. Recent research highlights mitochondrial dysfunction as a central factor in cognitive decline, contributing to neurodegenerative diseases such as Alzheimer’s, Parkinson’s, and Huntington’s disease. This article explores the mechanisms by which mitochondrial dysfunction impacts cognitive function and discusses potential therapeutic strategies.

The Brain's Energy Demands and Mitochondrial Function

The human brain, despite accounting for only about 2% of body weight, consumes approximately 20% of the body’s energy. Neurons, the primary cells of the nervous system, rely heavily on mitochondrial ATP to sustain synaptic activity, ion gradient maintenance, and neurotransmitter synthesis. Efficient mitochondrial function is critical for maintaining neuronal health and connectivity, which are foundational for learning, memory, and other cognitive processes.

Mechanisms of Mitochondrial Dysfunction in Cognitive Decline

Reduced ATP Production: Mitochondria produce ATP through oxidative phosphorylation (OXPHOS) in the electron transport chain (ETC). Damage to ETC components, often caused by genetic mutations or oxidative stress, can reduce ATP production. Energy-starved neurons may fail to maintain synaptic function, leading to cognitive impairments.

Excessive ROS Generation: While ROS are natural byproducts of mitochondrial activity and play roles in cell signaling, excessive ROS can damage mitochondrial DNA (mtDNA), proteins, and lipids. This oxidative damage exacerbates mitochondrial dysfunction, creating a vicious cycle that contributes to neuronal degeneration.

Impaired Calcium Regulation: Mitochondria help buffer intracellular calcium levels, which are critical for neurotransmitter release and synaptic plasticity. Dysfunctional mitochondria may fail to regulate calcium, leading to excitotoxicity—a condition where excessive calcium causes neuronal injury and death.

Mitochondrial Dynamics: Mitochondria constantly undergo fission (division) and fusion (joining) to adapt to cellular demands and maintain their integrity. Imbalances in these processes can result in fragmented or overly fused mitochondria, impairing their function and transport within neurons.

Mitochondrial Transport Defects: Neurons have long axons and dendrites that require efficient transport of mitochondria to regions of high energy demand, such as synaptic terminals. Dysfunction in mitochondrial transport mechanisms can disrupt synaptic activity and contribute to cognitive decline.

Mitochondrial Dysfunction in Neurodegenerative Diseases

Alzheimer’s Disease (AD): Mitochondrial dysfunction is a hallmark of AD. Amyloid-beta plaques and tau tangles, characteristic of AD, have been shown to impair mitochondrial function. Elevated ROS levels and reduced ATP production exacerbate neuronal loss and cognitive decline in AD.

Parkinson’s Disease (PD): PD is associated with mutations in genes like PINK1 and PARKIN, which regulate mitochondrial quality control. Impaired mitophagy—the process of removing damaged mitochondria���leads to their accumulation, contributing to dopaminergic neuron degeneration and motor as well as cognitive deficits.

Huntington’s Disease (HD): In HD, mutant huntingtin protein interferes with mitochondrial dynamics and function, resulting in energy deficits and increased oxidative stress. These mitochondrial abnormalities contribute to the progressive cognitive and motor decline observed in HD patients.

Diagnostic and Therapeutic Approaches

Biomarkers of Mitochondrial Dysfunction: Advances in molecular biology have identified potential biomarkers, such as altered mtDNA levels, ROS, and metabolites associated with mitochondrial pathways. These biomarkers can aid in early diagnosis and monitoring of neurodegenerative diseases.

Pharmacological Interventions:

Antioxidants: Compounds like coenzyme Q10, vitamin E, and MitoQ target mitochondrial ROS, reducing oxidative damage and preserving mitochondrial function.

Mitochondrial Biogenesis Enhancers: Agents like resveratrol and PGC-1α activators promote the production of new mitochondria and improve mitochondrial health.

Calcium Modulators: Drugs that stabilize calcium levels, such as memantine, may protect neurons from excitotoxicity.

Gene Therapy: Gene-editing tools like CRISPR/Cas9 offer potential to correct mtDNA mutations or enhance the expression of genes involved in mitochondrial quality control. For example, boosting PINK1 or PARKIN expression could improve mitophagy in PD.

Lifestyle Interventions:

Dietary Interventions: Ketogenic diets and intermittent fasting have been shown to enhance mitochondrial function by promoting efficient energy utilization and reducing ROS.

Exercise: Regular physical activity stimulates mitochondrial biogenesis and reduces oxidative stress, offering neuroprotective benefits.

Sleep Optimization: Adequate sleep is essential for mitochondrial repair and the clearance of damaged proteins, such as amyloid-beta.

Future Directions in Research

Understanding the interplay between mitochondrial dysfunction and cognitive decline opens new avenues for research and therapy. Emerging technologies, such as single-cell transcriptomics and advanced imaging, allow for detailed exploration of mitochondrial dynamics in neurons. Additionally, the development of mitochondria-targeted drugs and nanotechnologies holds promise for precise therapeutic interventions.

Conclusion

Mitochondrial dysfunction plays a pivotal role in driving cognitive decline and is implicated in the pathogenesis of various neurodegenerative diseases. Addressing mitochondrial health through targeted therapies, lifestyle modifications, and early diagnostic measures offers hope for mitigating cognitive impairments and improving quality of life. As our understanding of mitochondrial biology deepens, so too does the potential for innovative treatments that could transform the landscape of neurodegenerative disease management.

[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

[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.

[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)

[biology-geology-beaches-india]

TSRNOSS, p 619.