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posted by Fnord666 on Monday March 09 2020, @05:15AM   Printer-friendly
from the cellular-SOS dept.

Arthur T Knackerbracket has found the following story:

Mitochondria cannot autonomously cope with stress and must instead call on the cell for help. Molecular geneticists at LMU have identified the long-sought signaling pathway which enables the organelles to do so.

Mitochondria are membrane-bounded intracellular organelles that supply the energy needed to power the biochemical operations required for cell function and survival. The energy is provided in the form of a compound called ATP, which can be hydrolyzed by specific enzymes to drive chemical reactions. When mitochondria are subjected to stress—owing to the accumulation of misfolded proteins, for example—their functional capacities are diminished. Degradation of mitochondrial function can have serious consequences for the affected cells, and potentially for the whole organism. In order to activate protective measures, mitochondria must transmit a distress signal into the surrounding cytosol. In a paper that appears in the leading scientific journal Nature, researchers led by Professor Lucas Jae at the LMU Gene Center now report that they have characterized the elusive signaling pathway that triggers the response to mitochondrial stress in human cells. Mitochondrial dysfunction is at the root of many serious disorders, and functional deterioration of these organelles is regarded as a major component of the aging process. The new findings are therefore of considerable significance in the search for new therapeutic approaches to the treatment of age-related diseases.

[...] According to the authors, these findings might open up new opportunities for therapeutic regulation of cellular stress responses. These could be relevant for conditions that are associated with mitochondrial malfunction—including debilitating, age-related neurodegenerative disorders, such as Parkinson's disease. Recently, drugs have been developed that can globally shut down the ISR. Although not tailored to a specific type of ISR-inducing stress, such compounds have been shown to have positive effects on cognition and learning in mice. However, unspecific inhibition of the ISR might also have undesirable effects, as the ISR, for instance, also mediates antiviral protection during infection. "In an alternative scenario, the cellular response to mitochondrial stress could be selectively modulated by manipulating the factors we have now identified," says Jae.

More information: Evelyn Fessler et al. A pathway coordinated by DELE1 relays mitochondrial stress to the cytosol, Nature (2020). DOI: 10.1038/s41586-020-2076-4


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  • (Score: 1) by anubi on Monday March 09 2020, @05:52PM

    by anubi (2828) on Monday March 09 2020, @05:52PM (#968563) Journal

    Sounds to me like how prions screw up the metabolic machinery.

    --
    "Prove all things; hold fast that which is good." [KJV: I Thessalonians 5:21]