DOI: 10.1101/462713Nov 5, 2018Paper

Prolonged quiescence delays somatic stem cell-like division in Caenorhabditis elegans and is controlled by insulin signalling

BioRxiv : the Preprint Server for Biology
María OlmedoM. Artal-Sanz

Abstract

Cells can enter quiescence in adverse conditions and resume proliferation when the environment becomes favourable. Prolonged quiescence comes with a cost, reducing proliferation potential and survival. Interestingly, cellular quiescence also occurs in normal development, with many cells spending most of their lifetime at this state. Elucidating the mechanisms involved in surviving long-term quiescence and in maintenance of cellular proliferation potential will contribute to a better understanding of the process of tissue regeneration. Developmental arrest of C. elegans at the L1 stage is an emerging model for the study of cellular quiescence and reactivation. During arrest, L1 larvae undergo a process that shares phenotypic hallmarks with the ageing of the adult. Interestingly, insulin signalling, a prominent pathway in the regulation of ageing, also balances cell proliferation and activation of stress resistance pathways during quiescence, becoming a candidate regulator of proliferation potential. Here we report that prolonged L1 quiescence delays reactivation of blast cell divisions in C. elegans, leading to a delay in the initiation of postembryonic development. This delay is accompanied by increased inter-individual variabi...Continue Reading

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