Abstract
Animals can adapt to dynamic environmental conditions by modulating their developmental programs. Understanding the genetic architecture and molecular mechanisms underlying developmental plasticity in response to changing environments is an important and emerging area of research. Here, we show a novel role of cAMP response element binding protein (CREB)-encoding crh-1 gene in developmental polyphenism of C. elegans. Under conditions that promote normal development in wild-type animals, crh-1 mutants inappropriately form transient pre-dauer (L2d) larvae and express the L2d marker gene. L2d formation in crh-1 mutants is specifically induced by the ascaroside pheromone ascr#5 (asc-ωC3; C3), and crh-1 functions autonomously in the ascr#5-sensing ASI neurons to inhibit L2d formation. Moreover, we find that CRH-1 directly binds upstream of the daf-7 TGF-β locus and promotes its expression in the ASI neurons. Taken together, these results provide new insight into how animals alter their developmental programs in response to environmental changes.
Highlights
Animals exhibit phenotypic traits whose expression can be influenced by environmental signals, including temperature, food availability, and crowding
These results reveal that cAMP response element binding protein (CREB) modulates developmental plasticity by repressing L2d entry in the presence of rich food sources and abundant ascr#5, via direct regulation of daf-7 transforming growth factor-β (TGF-β) expression in the ascr#5-sensing ASI neurons
Flp-8p::gfp was expressed in the AAP-TRN of daf-7 mutant larvae (S2 Fig). These results suggest that the onset of flp-8p:: gfp expression in the AVM neurons and possibly the ALM and PLM neurons can be used as a marker for the L2d stage
Summary
Animals exhibit phenotypic traits whose expression can be influenced by environmental signals, including temperature, food availability, and crowding These signals are sensed, processed, and integrated by the nervous system, and govern appropriate developmental and/or behavioral phenotypes through effecting local and systemic changes in gene expression and/or endocrine signals. Population density and food supply determine wing development (winged vs wingless) of the pea aphid (A. pisum) via ecdysone signaling [1] This extreme form of phenotypic plasticity is referred to as polyphenism—the development of alternate and distinct phenotypes in animals of the same genotype—and is found across taxa [2,3]. Hatched L1/L2 larvae of C. elegans sense and integrate environmental signals, including food availability, temperature, and the abundance of pheromones (a population density indicator) to determine whether to undergo normal reproductive development into the L3 larval stage, or arrest at an alternate L3 stage, known as dauer. The signals and molecules that promote the L1-to-L2d developmental transition are not well understood
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