The proteostasis network （PN） is essential for proteome function and cellular health. In aging, failure of the PN increases protein misfolding and aggregation and the risk for neurodegenerative diseases. For metazoans, such as C. elegans, the PN is regulated cell non-autonomously by cell-cell communication. Our studies have shown that the organismal heat shock response （HSR） for expression of molecular chaperones and other components of the PN is regulated by neuronal serotoninergic signaling, and that cholinergic signaling across the synaptic junction regulates muscle cell proteostasis. Further, that communication between intestine, muscle and neurons by transcellular chaperone signaling can boost chaperone production in distal tissues to enhance proteostasis. During aging, the HSR declines dramatically by germline signaling to the soma at reproductive maturity by placement of repressive chromatic marks at HS gene loci. The relationship with reproduction is observed by communication from the extracellular vitelline layer of the fertilized embryo to the uterus to trigger a parental protective response dependent upon DAF-16 in the vulva and HSF-1 in somatic tissues for stress resilience. These observations lead us to propose that the events of aging are genetically regulated and directly relevant to the stability and functionality of the proteome and cellular stress resilience, and that reproduction and progeny health has a strong influence on organismal stress resilience and proteostasis.

日時	2020年3月2日（月）13:00 ～14:30（12:45開場）
場所	京都産業大学 15号館1階15102セミナー室
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主催・ 世話人	京都産業大学生命科学部 タンパク質動態研究所　永田　和宏