Abstract
Phenotypic plasticity is a critical component of an organism’s ability to thrive in an ever-changing environment. The free-living nematode, Caenorhabditis elegans, adapts to unfavorable environmental conditions by pausing reproductive development and entering a stress-resistant larval stage known as dauer. The transition into dauer is marked by vast morphological changes – including remodeling of epidermis, neurons and muscle. Though many of these dauer-specific traits have been described, the molecular basis of dauer-specific remodeling is still poorly understood. Here we show that the nidogen-domain containing protein DEX-1 functions downstream of the dauer decision to facilitate stage-specific tissue remodeling during dauer morphogenesis. DEX-1 was previously shown to regulate sensory dendrite formation during embryogenesis. We find that DEX-1 is also required for the proper remodeling of the stem cell-like epidermal seam cells and maintenance of seam cell quiescence during dauer. dex-1 mutant dauers lack distinct lateral cuticular alae during dauer and have increased sensitivity to sodium dodecyl sulfate (SDS). Furthermore, we find that DEX-1 mediated seam cell remodeling is required for proper dauer mobility. We show that DEX-1 acts cell autonomously in the seam cells during dauer and that dex-1 expression during dauer is regulated through DAF-16/FOXO-mediated derepression. Finally, we show that dex-1 interacts with a family of zona pellucida-domain encoding genes to regulate dauer-specific epidermal remodeling. Taken together, our data indicates that DEX-1 plays a central role in C. elegans epidermal remodeling during dauer.
