ArticlebioRxiv : the preprint server for biology2025
Box C/D snoRNPs and MDT-15/MED15 regulate mitochondrial surveillance via fatty acid metabolism.
Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Multicellular organisms constantly encounter biotic and abiotic stressors that threaten to disrupt their homeostasis. To counteract this, they have evolved a series of conserved defense networks which monitor organellar function and the accumulation of aberrant molecular signals. As mitochondrial dysfunction can lead to a variety of pathologies, including metabolic impairment, neurodegeneration, cardiovascular disease, cancer, and sensitivity to bacterial infections, understanding these mitochondrial surveillance pathways is crucial. Previous research in our lab established that one such pathway, the Ethanol Stress and Response Element (ESRE), was activated by a broad range of stresses, including exposure to the Gram-negative, opportunistic human pathogen
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