Epidermal Remodeling in Caenorhabditis elegans Dauers Requires the Nidogen Domain Protein DEX-1

Genetics: A Periodical Record of Investigations Bearing on Heredity and Variation

Caroline Beshers^2¹  Meera V. Sundaram^3²  Cagla Unal^2³  Jennifer D. Cohen^3⁴  Kristen M. Flatt^1⁵ 

[1] Department of Crop Sciences, University of Illinois at Urbana-Champaign, Illinois 61801-4730^2;Department of Crop Sciences, University of Illinois at Urbana-Champaign, Illinois 61801-4730^4;Department of Genetics, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania 19104-6145^3;Program in Neuroscience, University of Illinois at Urbana-Champaign, Illinois 61801-4730;Program in Neuroscience, University of Illinois at Urbana-Champaign, Illinois 61801-4730^1

关键词: polyphenism;    cuticlin;    SNED1;    tectorin;    DYF-7;    extracellular matrix;   

DOI  :  10.1534/genetics.118.301557

学科分类：医学（综合）

来源: Genetics Society of America

【 摘 要 】

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.

【 授权许可】

CC BY