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Desynchronization between timers provokes transient arrest during C. elegans development

Romero-Exposito, F. J.; Moreno-Rivero, A.; Munoz-Barrera, M.; Garcia-Sanchez, S.; Rodriguez-Peris, F.; Gritti, N.; Sartor, F.; Merrow, M.; van Zon, J. S.; Mata-Cabana, A.; Olmedo, M.

2024-03-31 developmental biology
10.1101/2024.03.31.587169 bioRxiv
Show abstract

In multicellular organisms, developmental timers integrate internal and external cues to control numerous cellular processes that need to be temporally coordinated. The molting timer and the developmental timer run in parallel during C. elegans development. We reveal a novel state of transient arrest of the molting timer upon delay of the developmental timer. This means that synchronous development is not inherent but requires active synchronization of parallel timers. Additional timer variability, like that provoked by modulation of nutrient sensing pathways, increases desynchrony between these timers and consequently extends transient arrest. Mutation of the insulin receptor gene daf-2 reduces the speed of both timers but has a larger impact on the developmental timer, that then appears delayed relative to the molting timer. In this context, prolonged arrest of the molting timer provides a mechanism for resynchronization. TeaserActive resynchronization at specific checkpoints of two parallel timers controlling developmental events.

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