Abstract
Caenorhabditis elegans enter an alternate developmental stage called dauer in unfavorable conditions such as starvation, overcrowding, or high temperature. Several evolutionarily conserved signaling pathways control dauer formation. DAF-7/TGFβ and serotonin, important ligands in these signaling pathways, affect not only dauer formation, but also the expression of one another. The heterotrimeric G proteins GOA-1 (Gαo) and EGL-30 (Gαq) mediate serotonin signaling as well as serotonin biosynthesis in C. elegans. It is not known whether GOA-1 or EGL-30 also affect dauer formation and/or daf-7 expression, which are both modulated in part by serotonin. The purpose of this study is to better understand the relationship between proteins important for neuronal signaling and developmental plasticity in both C. elegans and humans. Using promoter-GFP transgenic worms, it was determined that both goa-1 and egl-30 regulate daf-7 expression during larval development. In addition, the normal daf-7 response to high temperature or starvation was altered in goa-1 and egl-30 mutants. Despite the effect of goa-1 and egl-30 mutations on daf-7 expression in various environmental conditions, there was no effect of the mutations on dauer formation. This paper provides evidence that while goa-1 and egl-30 are important for normal daf-7 expression, mutations in these genes are not sufficient to disrupt dauer formation.
Highlights
Under unfavorable environmental conditions, developing Caenorhabditis elegans enter an alternative stage called dauer
It is possible that additional G proteins such as GOA-1 and EGL-30 could primarily affect dauer formation or daf-7 expression through altering the morphology of ASI
To first determine whether ASI morphology was affected by mutations in either goa-1 or egl-30, gross neuronal structure was visualized using DiD
Summary
Under unfavorable environmental conditions, developing Caenorhabditis elegans enter an alternative stage called dauer. The dauer stage is reversible, and larvae resume development when environmental conditions improve (reviewed in [1]). Dauer formation is controlled in part by the DAF-7/TGFblike signaling pathway ([2] and reviewed in [1]). DAF-7 is expressed in the ASI sensory neurons and is required during larval development to inhibit dauer formation [3,4]. Environmental cues such as starvation and high temperature that trigger dauer formation downregulate daf-7 expression [3]. While several genes are required for normal daf-7 expression [5,6,7], the signaling pathways that control daf-7 expression and its sensitivity to environmental signals are still not well understood
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