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Koshkin, S.

Publications and source records attributed to Koshkin, S..

2 recordsLinked to original sources

Color-dependent foraging in C. elegans integrates chromoprotein photosensitization with bacterial metabolic cues

Animals rely on color to navigate complex environments, yet how eyeless organisms use chromatic information to guide food choice remains poorly understood. Here, we show that Caenorhabditis elegans exhibits robust color dependent foraging driven by microbial chromophores, preferentially consuming red while avoiding blue chromoprotein expressing bacteria across bacterial backgrounds and wild isolates. This discrimination persists in darkness and independently of photoreceptor, revealing a mechanism beyond canonical photoreception. Purified chromoproteins and bacterial metabolite fractions independently reproduce preference, demonstrating complementary chromatic and post ingestive metabolic cues. Mechanistically, blue chromoproteins generate singlet oxygen, producing oxidative stress and remodeling bacterial tryptophan and pterin metabolism, whereas red food promotes serotonin production and feeding-associated neuropeptide signaling. Disrupting serotonin biosynthesis or neuropeptide processing abolishes color preference. Together, our findings reveal a previously unrecognized, novel sensory strategy in which wavelength-selective pigment photochemistry transforms microbial color into metabolic information that is integrated through gut brain neuroendocrine signaling to guide foraging behavior in an eyeless animal.

molecular biology↗

BRD4-mediated epigenetic regulation of endoplasmic reticulum-mitochondria contact sites is governed by the mitochondrial complex III

Inter-organellar communication is critical for cellular metabolic homeostasis. One of the most abundant inter-organellar interactions are those at the endoplasmic reticulum and mitochondria contact sites (ERMCS). However, a detailed understanding of the mechanisms governing ERMCS regulation and their roles in cellular metabolism are limited by a lack of tools that permit temporal induction and reversal. Through unbiased screening approaches, we identified fedratinib, an FDA-approved drug, that dramatically increases ERMCS abundance by inhibiting the epigenetic modifier BRD4. Fedratinib rapidly and reversibly modulates mitochondrial and ER morphology and alters metabolic homeostasis. Moreover, ERMCS modulation depends on mitochondria electron transport chain complex III function. Comparison of fedratinib activity to other reported inducers of ERMCS revealed common mechanisms of induction and function, providing clarity and union to a growing body of experimental observations. In total, our results uncovered a novel epigenetic signaling pathway and an endogenous metabolic regulator that connects ERMCS and cellular metabolism.

cell biology↗