Protein folding and clearance networks sense and respond to misfolded and aggregation-prone proteins by activating
cytoprotective cell stress responses that safeguard the proteome against damage, maintain the health of the cell, and
enhance lifespan. Surprisingly, cellular proteostasis undergoes a sudden and widespread failure early in Caenorhabditis
elegans adulthood, with marked consequences on proteostasis functions later in life. These changes in the regulation of
quality control systems, such as chaperones, the ubiquitin proteasome system and cellular stress responses, are controlled
cell-nonautonomously by the proliferation of germline stem cells. Here, we review recent studies examining changes in
proteostasis upon transition to adulthood and how proteostasis is modulated by reproduction onset, focusing on C. elegans.
Based on these and our own findings, we propose that the regulation of quality control systems is actively remodeled
at the point of transition between development and adulthood to influence the subsequent course of aging.
Keywords: Aging, Autophagy, Caenorhabditis elegans, Chaperones, Folding, Germline stem cells, Misfolding, Ubiquitin
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