Dauer

Abstract

In response to harsh environmental conditions, C. elegans larvae undergo dauer arrest at the second molt. The past decade has yielded many insights into the signaling pathways and the molecular mechanisms that govern this developmental transition. Dauer pheromone, the major physiologic signal promoting dauer arrest, has been purified, identified, and synthesized. The molecular identities of the vast majority of dauer regulatory genes isolated in initial genetic screens are now known. Physiologic ligands for DAF-12, a nuclear receptor that is the final common target of dauer regulatory pathways, have been identified. The discovery of the Hid (high temperature induction of dauer) phenotype and the results of enhancer screens have greatly expanded the repertoire of dauer regulatory genes. Genomic analysis of dauer arrest has highlighted the role of pathway crosstalk in dauer regulation. Nonetheless, critical questions remain about the mechanistic underpinnings of dauer arrest.

A size threshold governsCaenorhabditis elegansdevelopmental progression

“…Consistent with this, interfering with the oscillatory expression of certain heterochronic genes uncouples moult timing from completion of stage-specific development, causing major growth abnormalities [9,10]. Moreover, in the absence of food, L1 larvae can completely arrest development and survive for weeks without moulting or any other morphological changes [11]; L2 worms can also undergo a transition to a quiescent dauer form [12]. Despite the strong dependence of C. elegans growth and development on nutrition, we lack a mechanistic understanding of the cues that trigger moulting and developmental progression.…”

Genetic mapping of variation in dauer larvae development in growing populations of Caenorhabditis elegans

“…In the nematode Caenorhabditis elegans, dauer larvae are formed when conditions are unsuitable for growth and reproduction, with worms developing as dauer larvae in response to low food availability, high conspecific population density and high temperatures (Golden and Riddle, 1984;Hu, 2007). Dauer pheromone, a complex mix of structurally related ascarosides (Jeong et al, 2005;Butcher et al, 2007;Pungaliya et al, 2009;Park et al, 2012), is used by C. elegans to assess population density, with these ascarosides also acting to regulate aggregation, mate recognition and dispersal (Srinivasan et al, 2008;Harvey, 2009;Pungaliya et al, 2009;Izrayelit et al, 2012;Jang et al, 2012).…”

“…Dauer pheromone, a complex mix of structurally related ascarosides (Jeong et al, 2005;Butcher et al, 2007;Pungaliya et al, 2009;Park et al, 2012), is used by C. elegans to assess population density, with these ascarosides also acting to regulate aggregation, mate recognition and dispersal (Srinivasan et al, 2008;Harvey, 2009;Pungaliya et al, 2009;Izrayelit et al, 2012;Jang et al, 2012). Although there is an extensive and detailed understanding of the genetic pathways that specify dauer and non-dauer larval development in C. elegans (see Hu (2007) for a review), the ecology of the species is still poorly understood. Indeed, the natural habitat of C. elegans, rotting fruit, has been proposed only recently (Kiontke et al, 2011;Félix and Duveau, 2012).…”

New links between protein N-terminal acetylation, dauer diapause, and the insulin/IGF-1 signaling pathway inCaenorhabditis elegans

“…When challenged with high temperature, low nutrient availability, and high population density, C. elegans larvae enter dauer diapause, an alternate third larval stage that is stress resistant. Genetic studies of dauer formation led to the discovery of an evolutionarily conserved insulin/insulin-like growth factor (IGF-1) pathway (reviewed by Hu (2007) 3 ). The C. elegans insulin-like receptor tyrosine kinase, DAF-2, signals through a protein kinase cascade to inhibit the function of the FOXO transcription factor DAF-16.…”