First published online May 11, 2006
Development 133, 1106e (2006)
© The Company of Biologists Limited
Keeping C. elegans development on time
Postembryonic metazoan development is genetically programmed but its timing
can be modified by environmental factors. Because sensory neurons detect these
cues, Ruaud and Bessereau are studying the role of the nervous system in the
temporal regulation of postembryonic C. elegans development. They now report
that nicotinic receptor activation caused by exposure to DMPP, a
nicotinic-receptor agonist, delays development in the second larval stage (L2)
of C. elegans but does not affect the timing of moulting (see
p. 2211). As a
result, the larvae cannot make a proper L3 cuticle in time and they die at the
L2/L3 moult. The researchers report that development and moulting can be
resynchronised and that DMPP-induced lethality can be avoided by forcing the
worms into a previously unrecognised L2 diapause (arrest in development).
Further results indicate that UNC-63, a nicotinic acetylcholine-receptor
subunit, and DAF-12, a nuclear hormone receptor that regulates larval entry
into L3 diapause, are both components of a neuroendocrine pathway that
controls developmental timing in L2 in C. elegans.
Related articles in Development:
- Activation of nicotinic receptors uncouples a developmental timer from the molting timer in C. elegans
- Anne-Françoise Ruaud and Jean-Louis Bessereau
Development 2006 133: 2211-2222.
[Abstract]
[Full Text]
