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First published online 20 February 2008
doi: 10.1242/dev.014969

Development 135, 1259-1269 (2008)
Published by The Company of Biologists 2008
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CDC-25.1 stability is regulated by distinct domains to restrict cell division during embryogenesis in C. elegans

Michaël Hebeisen and Richard Roy*

Department of Biology, McGill University, Montreal, Quebec, H3A 1B1, Canada.

* Author for correspondence (e-mail: richard.roy{at}mcgill.ca)

Accepted 29 January 2008

Cdc25 phosphatases are key positive cell cycle regulators that coordinate cell divisions with growth and morphogenesis in many organisms. Intriguingly in C. elegans, two cdc-25.1(gf) mutations induce tissue-specific and temporally restricted hyperplasia in the embryonic intestinal lineage, despite stabilization of the mutant CDC-25.1 protein in every blastomere. We investigated the molecular basis underlying the CDC-25.1(gf) stabilization and its associated tissue-specific phenotype. We found that both mutations affect a canonical β-TrCP phosphodegron motif, while the F-box protein LIN-23, the β-TrCP orthologue, is required for the timely degradation of CDC-25.1. Accordingly, depletion of lin-23 in wild-type embryos stabilizes CDC-25.1 and triggers intestinal hyperplasia, which is, at least in part, cdc-25.1 dependent. lin-23(RNAi) causes embryonic lethality owing to cell fate transformations that convert blastomeres to an intestinal fate, sensitizing them to increased levels of CDC-25.1. Our characterization of a novel destabilizing cdc-25.1(lf) intragenic suppressor that acts independently of lin-23 indicates that additional cues impinge on different motifs of the CDC-25.1 phosphatase during early embryogenesis to control its stability and turnover, in order to ensure the timely divisions of intestinal cells and coordinate them with the formation of the developing gut.

Key words: cdc-25.1, lin-23, F-box, β-TrCP, Intestine, Hyperplasia, Cell fate, Embryogenesis, C. elegans


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