To grow or not to grow: nutritional control of development during Caenorhabditis elegans L1 arrest.
Abstract
It is widely appreciated that larvae of the nematode Caenorhabditis elegans arrest
development by forming dauer larvae in response to multiple unfavorable environmental
conditions. C. elegans larvae can also reversibly arrest development earlier, during
the first larval stage (L1), in response to starvation. "L1 arrest" (also known as
"L1 diapause") occurs without morphological modification but is accompanied by increased
stress resistance. Caloric restriction and periodic fasting can extend adult lifespan,
and developmental models are critical to understanding how the animal is buffered
from fluctuations in nutrient availability, impacting lifespan. L1 arrest provides
an opportunity to study nutritional control of development. Given its relevance to
aging, diabetes, obesity and cancer, interest in L1 arrest is increasing, and signaling
pathways and gene regulatory mechanisms controlling arrest and recovery have been
characterized. Insulin-like signaling is a critical regulator, and it is modified
by and acts through microRNAs. DAF-18/PTEN, AMP-activated kinase and fatty acid biosynthesis
are also involved. The nervous system, epidermis, and intestine contribute systemically
to regulation of arrest, but cell-autonomous signaling likely contributes to regulation
in the germline. A relatively small number of genes affecting starvation survival
during L1 arrest are known, and many of them also affect adult lifespan, reflecting
a common genetic basis ripe for exploration. mRNA expression is well characterized
during arrest, recovery, and normal L1 development, providing a metazoan model for
nutritional control of gene expression. In particular, post-recruitment regulation
of RNA polymerase II is under nutritional control, potentially contributing to a rapid
and coordinated response to feeding. The phenomenology of L1 arrest will be reviewed,
as well as regulation of developmental arrest and starvation survival by various signaling
pathways and gene regulatory mechanisms.
Type
Journal articleSubject
developmental arrestdiapause
insulin-like signaling
starvation
stress resistance
Animals
Caenorhabditis elegans
Gene Expression Regulation, Developmental
Germ Cells
Humans
Insulin
Larva
Longevity
MicroRNAs
RNA Polymerase II
Signal Transduction
Starvation
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https://hdl.handle.net/10161/10400Published Version (Please cite this version)
10.1534/genetics.113.150847Publication Info
Baugh, L Ryan (2013). To grow or not to grow: nutritional control of development during Caenorhabditis elegans
L1 arrest. Genetics, 194(3). pp. 539-555. 10.1534/genetics.113.150847. Retrieved from https://hdl.handle.net/10161/10400.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
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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