Formation and function of dauer ascarosides in the nematodes Caenorhabditis briggsae and Caenorhabditis elegans

Abstract

The biosynthetic pathways and functions of ascaroside signaling molecules in the nematode Caenorhabditis elegans have been studied in order to better understand complex, integrative developmental decision-making. Although it is known that ascarosides play multiple roles in the development and behavior of nematode species other than C. elegans, these parallel pheromone systems have not been well-studied. Here, we show that ascarosides in the nematode Caenorhabditis briggsae are biosynthesized in the same manner as C. elegans and act to induce the alternative developmental pathway that generates the stress-resistant dauer lifestage. We show that ascr#2 is the primary component of crude dauer pheromone in C. briggsae; in contrast, C. elegans dauer pheromone relies on a combination of ascr#2, ascr#3, and several other components. We further demonstrate that Cbr-daf-22, like its C. elegans ortholog Cel-daf-22, is necessary to produce short-chain ascarosides. Moreover, Cbr-daf-22 and Cel-daf-22 mutants produce an ascaroside-independent metabolite that acts antagonistically to crude dauer pheromone and inhibits dauer formation.

Neuronal IL-17 controlsC. elegansdevelopmental diapause through CEP-1/p53

“…S1c, d). Dauer larvae can be identified by their growth arrest and distinct morphology characterized by specialized cuticular structures called alae, a constricted pharynx, arrested germ line, decreased pharyngeal pumping rates, and detergent (1% SDS) resistance (3)(4)(5)(6)(7)(8)(9). ilc-17.1(syb5296)X dauer larvae displayed all these features (Supplementary Fig.…”

“…1g). This suggested that the role of ILC-17.1 signaling in dauer might be related to food, a prominent modulator of the dauer decision (3)(4)(5)(6)(7)(8)(9), and that the ILC-17.1 ligand, and perhaps not the ILCR-2 receptor per se, could be responsive to the food signals.…”

“…During metazoan development, nutrient availability is coordinated with the division, growth and metabolic activity of individual cells through cell-cell communication. This is also the case in the invertebrate C. elegans, a free-living bacterivore, which displays a dramatic developmental plasticity to ensure that its growth and reproduction match available resources (1)(2)(3)(4)(5)(6)(7)(8)(9)(10). When C. elegans larvae hatch under optimal conditions (at 20°C, low population densities, on abundant food) they develop continuously into reproducing adults.…”

“…However, if they hatch under suboptimal conditions, such as in the paucity of food, at high population densities, or high ambient temperatures, larvae implement an alternative developmental program and arrest as quiescent, stress-resistant larvae called 'dauer' larvae. Dauer larvae display metabolic and organismal phenotypes specialized for dispersal and survival, and can remain arrested in this state for months to resume development into reproductive adults when favorable conditions return (1)(2)(3)(4)(5)(6)(7)(8)(9)(10). Previous studies have identified molecular pathways that mediate the dauer decision, showing that growth promoting molecules like insulins, transforming β growth factor (TGFβ/DAF-7) and lipid based dafachronic acid hormones are released by sensory neurons and other cells to license continued development; adverse environments inhibit these growth promoting signals and trigger dauer arrest (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11).…”

“…Dauer larvae display metabolic and organismal phenotypes specialized for dispersal and survival, and can remain arrested in this state for months to resume development into reproductive adults when favorable conditions return (1)(2)(3)(4)(5)(6)(7)(8)(9)(10). Previous studies have identified molecular pathways that mediate the dauer decision, showing that growth promoting molecules like insulins, transforming β growth factor (TGFβ/DAF-7) and lipid based dafachronic acid hormones are released by sensory neurons and other cells to license continued development; adverse environments inhibit these growth promoting signals and trigger dauer arrest (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11). A number of quantitative trait loci (QTL) also modulate dauer (12).…”