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L1 arrest, daf-16/FoxO and nonautonomous control of post-embryonic development.

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Date
2016-04
Authors
Kaplan, Rebecca EW
Baugh, L Ryan
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Abstract
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.
Type
Journal article
Subject
FoxO
IGF
L1 arrest
L1 diapause
aging
daf-12
daf-16
dauer
dbl-1
insulin
Permalink
https://hdl.handle.net/10161/13271
Published Version (Please cite this version)
10.1080/21624054.2016.1175196
Publication Info
Kaplan, Rebecca EW; & Baugh, L 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 https://hdl.handle.net/10161/13271.
This is constructed from limited available data and may be imprecise. To cite this article, please review & use the official citation provided by the journal.
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Scholars@Duke

Baugh

L. Ryan Baugh

Professor of Biology
The Baugh Lab is interested in phenotypic plasticity and physiological adaptation to variable environmental conditions. We are using the roundworm C. elegans to understand how animals adapt to starvation using primarily genetic and genomic approaches. We are studying how development is governed by nutrient availability, how animals survive starvation, and the long-term consequences of starvation including adult disease and transgenerational epigenetic inheritance.
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