C. elegans DAF-18/PTEN Mediates Nutrient-Dependent Arrest of Cell Cycle and Growth in the Germline

Masamitsu Fukuyama, Ann E. Rougvie, Joel H. Rothman

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104 Scopus citations


The molecular pathways that link nutritional cues to developmental programs are poorly understood. Caenorhabditis elegans hatchlings arrest in a dormant state termed "L1 diapause" until food is supplied. However, little is known about what signal transduction pathways mediate nutritional status to control arrest and initiation of postembryonic development. We report that C. elegans embryonic germline precursors undergo G2 arrest with condensed chromosomes and remain arrested throughout L1 diapause. Loss of the DAF-18/PTEN tumor suppressor bypasses this arrest, resulting in inappropriate germline growth dependent on the AGE-1/PI-3 and AKT-1/PKB kinases. DAF-18 also regulates an insulin/IGF-like pathway essential for longevity and dauer larva formation. However, DAF-16/FoxO, which is repressed by this pathway, is not required for germline arrest in L1 diapause. Thus, these findings indicate that quiescence of germline development during L1 diapause is not a passive consequence of nutrient deprivation, but rather is actively maintained by DAF-18 through a pathway distinct from that which regulates longevity and dauer formation.

Original languageEnglish (US)
Pages (from-to)773-779
Number of pages7
JournalCurrent Biology
Issue number8
StatePublished - Apr 18 2006

Bibliographical note

Funding Information:
We are grateful to C. Bargmann, Y. Bobbinec, J. Carlson, G. Gundersen, K. Kemphues, M. Maduro, G. Ruvkun, J. Schumacher, S. Strome, M. Yamashita, the C. elegans Genetic Center (CGC), and the C. elegans Knockout Consortium for valuable reagents and strains; M. Han, Y. Suzuki, R. Baugh, and P. Sternberg for sharing unpublished data; and members of the Rothman and Rougvie labs and the University of Minnesota Worm Community for discussion and encouragement. Some nematode strains were provided by the CGC, which is funded by the National Institutes of Health (NIH) National Center for Research Resources. M.F. was supported by a Postdoctoral Fellowship of the American Heart Association (AHA), Greater Midwest Affiliate during part of these studies. This work was supported by grants from the NIH (GM50227) and National Sciences Foundation (NSF) (IOB-0515682) to A.E.R. and the NIH (CA95943) and the March of Dimes Birth Defects Foundation to J.H.R.




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