Abstract

Phenotypic plasticity is a critical component of an organism’s ability to thrive in a 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. Although 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 facilitates 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 proper remodeling of the stem cell-like epidermal seam cells. dex-1 mutant dauers lack distinct lateral cuticular alae during dauer and have increased sensitivity to sodium dodecyl sulfate. Furthermore, we find that DEX-1 is required for proper dauer mobility. We show that DEX-1 is secreted from the seam cells during dauer, but acts locally in a cell-autonomous manner. We find that dex-1 expression during dauer is regulated through DAF-16/FOXO–mediated transcriptional activation. Finally, we show that dex-1 acts with a family of zona pellucida domain-encoding genes to regulate dauer-specific epidermal remodeling. Taken together, our data indicate that DEX-1 is an extracellular matrix component that plays a central role in C. elegans epidermal remodeling during dauer.

Highlights

  • TO survive changing environments, organisms modify their phenotype

  • We found that dex-1(ns42) mutants produce dauers that are defective in radial shrinkage, leading to a “dumpy dauer” phenotype (Figures 1C and 2A)

  • The dauer stage of C. elegans is an excellent example of a polyphenism, where distinct phenotypes are produced by the same genotype via environmental regulation (Simpson et al 2011)

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Summary

Introduction

TO survive changing environments, organisms modify their phenotype (i.e., phenotypic plasticity). Under unfavorable environmental conditions, C. elegans larvae arrest their development at the second larval molt and enter the stress-resistant dauer stage (Cassada and Russell 1975; Golden and Riddle 1984). Dauer-specific stress resistance is likely facilitated by several morphological changes that occur during dauer formation. (E and F) Transmission electron micrograph showing lateral alae (arrows) of a wild-type dauer (E) and dex-1(ns42) mutant dauer (F). Radial shrinkage and alae formation are regulated by a set of lateral hypodermal seam cells (Singh and Sulston 1978; Melendez et al 2003). Seam cell function and remodeling are critical for proper dauer morphology and increased environmental resistance. If the animal enters dauer diapause, the seam cells shrink and stop dividing (Melendez et al 2003; Karp and Ambros 2012)

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