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Epidermal Remodeling in Caenorhabditis elegans Dauers Requires the Nidogen Domain Protein DEX-1
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....
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Genetics Society of America
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6325711/ https://www.ncbi.nlm.nih.gov/pubmed/30409788 http://dx.doi.org/10.1534/genetics.118.301557 |
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author | Flatt, Kristen M. Beshers, Caroline Unal, Cagla Cohen, Jennifer D. Sundaram, Meera V. Schroeder, Nathan E. |
author_facet | Flatt, Kristen M. Beshers, Caroline Unal, Cagla Cohen, Jennifer D. Sundaram, Meera V. Schroeder, Nathan E. |
author_sort | Flatt, Kristen M. |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-6325711 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Genetics Society of America |
record_format | MEDLINE/PubMed |
spelling | pubmed-63257112020-01-01 Epidermal Remodeling in Caenorhabditis elegans Dauers Requires the Nidogen Domain Protein DEX-1 Flatt, Kristen M. Beshers, Caroline Unal, Cagla Cohen, Jennifer D. Sundaram, Meera V. Schroeder, Nathan E. Genetics Investigations 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. Genetics Society of America 2019-01 2018-11-01 /pmc/articles/PMC6325711/ /pubmed/30409788 http://dx.doi.org/10.1534/genetics.118.301557 Text en Copyright © 2019 Flatt et al. Available freely online through the author-supported open access option. This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Investigations Flatt, Kristen M. Beshers, Caroline Unal, Cagla Cohen, Jennifer D. Sundaram, Meera V. Schroeder, Nathan E. Epidermal Remodeling in Caenorhabditis elegans Dauers Requires the Nidogen Domain Protein DEX-1 |
title | Epidermal Remodeling in Caenorhabditis elegans Dauers Requires the Nidogen Domain Protein DEX-1 |
title_full | Epidermal Remodeling in Caenorhabditis elegans Dauers Requires the Nidogen Domain Protein DEX-1 |
title_fullStr | Epidermal Remodeling in Caenorhabditis elegans Dauers Requires the Nidogen Domain Protein DEX-1 |
title_full_unstemmed | Epidermal Remodeling in Caenorhabditis elegans Dauers Requires the Nidogen Domain Protein DEX-1 |
title_short | Epidermal Remodeling in Caenorhabditis elegans Dauers Requires the Nidogen Domain Protein DEX-1 |
title_sort | epidermal remodeling in caenorhabditis elegans dauers requires the nidogen domain protein dex-1 |
topic | Investigations |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6325711/ https://www.ncbi.nlm.nih.gov/pubmed/30409788 http://dx.doi.org/10.1534/genetics.118.301557 |
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