L1 arrest, daf-16/FoxO and nonautonomous control of post-embryonic development.
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Post-embryonic development is governed by nutrient availability. L1 arrest, dauer formation and aging illustrate how starvation, anticipation of starvation and caloric restriction have profound influence on C. elegans development, respectively. Insulin-like signaling through the Forkhead box O transcription factor daf-16/FoxO regulates each of these processes. We recently reported that ins-4, ins-6 and daf-28 promote L1 development from the intestine and chemosensory neurons, similar to their role in dauer development. daf-16 functions cell-nonautonomously in regulation of L1 arrest, dauer development and aging. Discrepancies in daf-16 sites of action have been reported in each context, but the consensus implicates epidermis, intestine and nervous system. We suggest technical limitations of the experimental approach responsible for discrepant results. Steroid hormone signaling through daf-12/NHR is known to function downstream of daf-16 in control of dauer development, but signaling pathways mediating cell-nonautonomous effects of daf-16 in aging and L1 arrest had not been identified. We recently showed that daf-16 promotes L1 arrest by inhibiting daf-12/NHR and dbl-1/TGF-β Sma/Mab signaling, two pathways that promote L1 development in fed larvae. We will review these results on L1 arrest and speculate on why there are so many signals and signaling centers regulating post-embryonic development.
Published Version (Please cite this version)10.1080/21624054.2016.1175196
Publication InfoKaplan, RE; & Baugh, Ryan (2016). L1 arrest, daf-16/FoxO and nonautonomous control of post-embryonic development. Worm, 5(2). pp. e1175196. 10.1080/21624054.2016.1175196. Retrieved from http://hdl.handle.net/10161/13271.
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Associate Professor of Biology
We study nutritional control of development in the roundworm Caenorhabditis elegans. We are interested in the signaling pathways and gene regulatory mechanisms that enable the worm to reversibly arrest development and resist stress in response to starvation. We are also interested in epigenetic mechanisms that mediate transgenerational effects of starvation.
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