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Reversible suppression of autophagy in a mouse model reveals neuronal resilience.

Japanese researchers created a unique mouse model in which autophagy could be rapidly switched off and restarted using doxycycline. Just four weeks after autophagy was stopped, protein aggregates accumulated in neurons, protein and RNA composition was disrupted, axonal swellings appeared, and the animals developed motor and cognitive impairments.
However, the next stage of the experiment proved most unexpected: after autophagy was restored, most of these changes disappeared. Neurons were cleared of toxic debris, synapse and axon structure was restored, and the mice again successfully passed memory and motor coordination tests.
This study demonstrates that even after significant disruption of cellular homeostasis, nervous tissue retains significant potential for recovery if intracellular degradation mechanisms are reactivated.
If you clutter your house for too long and don't throw out everything that's broken, it will seem like it's no longer fit for habitation. But: clean it, tidy it up, and it'll be as good as new 😀

#science #cellular_biology #neurology #brain #autophagy #biology

science.org/doi/10.1126/scienc…

Metal-driven chemical reaction in deep sea may explain origin of life | Science | AAAS

Phosphate—a simple molecule composed of phosphorus and four oxygen atoms—is a cornerstone of biochemistry: it binds nucleotides into DNA chains and is involved in energy storage in the form of ATP. However, its chemical properties are paradoxical—it dissolves extremely poorly in water and reacts poorly, making it an unlikely candidate for a key player in the origin of life.

Evolutionary biologist William Martin of Heinrich-Heine-Universität offers an elegant solution to this paradox. He believes that the key step—the incorporation of phosphate into organic chemistry—occurred not in the primordial "soup," but at the bottom of the ocean, in hydrothermal vents, where minerals and metals acted as catalysts, replacing enzymes. His team tested this hypothesis experimentally and found that palladium (and to a lesser extent nickel) effectively catalyzes the addition of phosphate to key biomolecules—ribose, glucose, creatine, and AMP—at concentrations close to intracellular levels. Critically, all the necessary ingredients for this reaction are present in serpentinizing hydrothermal vents; the rocks there contain both nickel and palladium, as well as phosphite itself, and their porous structure creates a huge surface area for catalytic reactions.

#evolution #science #origin_of_life #geothermal_vents
science.org/content/article/me…

Age and early life adversity shape epigenome heterogeneity across tissues in macaques | Science

Different tissues and organs age at different rates, each individually.
Researchers measured DNA methylation profiles—chemical markers that change with age and reflect environmental influences—in 14 different macaque tissues. Analysis of age-related changes revealed striking heterogeneity: although methylation shifted toward certain average values ​​in each tissue over the years, the direction and magnitude of these shifts varied greatly between organs. Only a small number of epigenetic markers aged synchronously across the body, while most changes were tissue-specific. This means that standard blood tests, often used as "aging clocks," reflect only a fraction of the overall picture. Within a single individual, age-related changes in different tissues were more coordinated than between individuals, but this coordination decreased with age—tissues began to age "out of sync," with this heterogeneity evident from early life.
A study of the effects of early adversity (primarily maternal loss) revealed an unexpected contrast. Unlike age-related changes, which were tissue-specific, the effects of early stress manifested as a coordinated response throughout the entire organism: the same DNA regions exhibited similar methylation changes in most tissues, with the most pronounced changes occurring in immune and endocrine organs and tissues with long-lived cells. Moreover, different forms of stress (for example, maternal loss or drought) primarily affected different sets of genetic loci, suggesting the existence of multiple molecular pathways through which adversity leaves its mark on the genome.
Thus, the study demonstrates a fundamental difference: aging is a disintegrative, tissue-specific process, whereas early life trauma leaves a coordinated, systemic imprint that, although overlapping with age-related targets, acts through different mechanisms, shaping the organism's aging trajectory in its own way.

#science #biology #methylation #aging #news #genetics

science.org/doi/10.1126/scienc…

These ‘master’ proteins protect us from deadly mutations — and could inspire new drugs.
Our genome is full of potentially dangerous mutations, which in most cases show no signs of harm. This paradox is explained by the existence of special "buffer" proteins that mask the harmful effects of genetic changes. A key role among these is played by the well-known heat shock protein HSP90, which acts as a molecular chaperone, helping other proteins fold into the correct three-dimensional structure even in the presence of mutations that could otherwise disrupt this process. Essentially, HSP90 serves as a kind of "fuse," allowing the body to accumulate latent genetic potential that can be activated when needed. Disabling the HSP90 gene in flies leads to massive developmental abnormalities, as if releasing the entire accumulated burden of latent mutations.
Modern research has identified a number of other buffer genes, including proteins involved in chromatin organization. During heat stress, such as during a fever, HSP90 reserves can be depleted, and then hidden problems begin to manifest.
Thus, the evolutionary and medical significance of buffer proteins extends far beyond basic biology. On the one hand, they form a "silent" genetic reserve that can suddenly be released when environmental conditions change (for example, during global warming), generating new adaptive traits and accelerating evolution. On the other hand, understanding these mechanisms opens up therapeutic possibilities.
However, I can't even begin to imagine how a single protein could correct the infinite variety of mutations in an infinite variety of protein topologies. I assume it only works with proteins of a certain topology and corrects only specific mutations, for example, at the site of an alpha helix fold—correcting it will restore the correct folding—or simply tightening up anything that's slipping, judging by its shape, or something similar.

nature.com/articles/d41586-026…

#science #science_news #chaperones #heat_shock_proteins #mutations #biology #HSP90