The nidogen-domain protein DEX-1 is necessary for the Caenorhabditis elegans dauer morphology and behavior

Flatt, Kristen M.

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https://hdl.handle.net/2142/106193 Copy

Description

Title

The nidogen-domain protein DEX-1 is necessary for the Caenorhabditis elegans dauer morphology and behavior

Author(s)

Flatt, Kristen M.

Issue Date

2019-11-25

Director of Research (if dissertation) or Advisor (if thesis)

Schroeder, Nathan

Doctoral Committee Chair(s)

Schroeder, Nathan

Committee Member(s)

• Juraska, Janice
• Brieher, William
• Vidal-Gadea, Adres

Department of Study

Neuroscience Program

Discipline

Neuroscience

Degree Granting Institution

University of Illinois at Urbana-Champaign

Degree Name

Ph.D.

Degree Level

Dissertation

Keyword(s)

• polypheniesm
• cuticlin
• extracellular matrix
• neuromuscular
• remodeling
• plasticity

Abstract

The ability to modify a given phenotype to adapt to the external environment (i.e. phenotypic plasticity) is a critical component of an organism’s ability to survive unfavorable conditions. The free-living nematode, Caenorhabditis elegans is an excellent example of phenotypic plasticity. When exposed to unfavorable conditions, C. elegans halts reproductive development and enters an alternative developmental stage called dauer. Dauer larvae undergo extensive tissue remodeling, including changes to the outer cuticle, muscle, and nervous system. Although several morphological and behavioral traits of the dauer larvae have been described, the molecular mechanisms underlying dauer-specific tissue remodeling have remained poorly understood. This work provides evidence that the nidogen domain-containing protein DEX-1 facilitates the stage-specific tissue remodeling observed during dauer morphogenesis. DEX-1 was previously shown to function as a secreted extracellular matrix protein that regulates sensory dendrite formation during embryogenesis. However, we found an alternative developmental role for DEX-1. Specifically, we show that DEX-1 is also required for remodeling of the stem-cell like hypodermal seam cells and formation of the cuticular lateral alae. Further, we found that DEX-1 is necessary for proper dauer mobility, and may function as a component of the neuromuscular system to facilitate dauer locomotion behaviors. We show that dex-1 is secreted from the seam cells, but functions locally in a cell-autonomous manner to facilitate dauer morphogenesis. dex-1 expression during dauer is also regulated through DAF-16/FOXO-mediated transcriptional activation. Finally, we show that dex-1 genetically interacts with a family of zona pellucida-domain genes to regulate seam cell remodeling and alae formation. Taken together, this work shows that DEX-1 is an extracellular matrix component that plays a critical role in C. elegans tissue plasticity during dauer formation.

Graduation Semester

2019-12

Type of Resource

text

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http://hdl.handle.net/2142/106193

Copyright and License Information

Copyright 2019 Kristen Flatt

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