Epidermal remodeling in Caenorhabditis elegans dauers requires the nidogen domain protein DEX-1

Kristen M. Flatt, Caroline Beshers, Cagla Unal, Jennifer D. Cohen, Meera V. Sundaram, Nathan E. Schroeder

Research output: Contribution to journalArticlepeer-review


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.

Original languageEnglish (US)
Pages (from-to)169-183
Number of pages15
Issue number1
StatePublished - Jan 2019


  • Cuticlin
  • DYF-7
  • Extracellular matrix
  • Polyphenism
  • SNED1
  • Tectorin
  • WormBook

ASJC Scopus subject areas

  • Genetics

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