L1 arrest, daf-16/FoxO and nonautonomous control of post-embryonic development.
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
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http://hdl.handle.net/10161/13271Published Version (Please cite this version)
10.1080/21624054.2016.1175196Publication Info
Kaplan, 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.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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Show full item recordScholars@Duke
L. Ryan Baugh
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.
Becky Kaplan
Student
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