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 ). 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.
