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The LIN-3 gene of the nematode C. elegans is the vulval-inducing signal

Citation

Hill, Russell James (1994) The LIN-3 gene of the nematode C. elegans is the vulval-inducing signal. Dissertation (Ph.D.), California Institute of Technology. doi:10.7907/8z98-jj03. https://resolver.caltech.edu/CaltechTHESIS:05082013-083718323

Abstract

The development of the vulva of the nematode Caenorhabditis elegans is induced by a signal from the anchor cell of the somatic gonad. Activity of the gene lin-3 is required for the Vulval Precursor Cells (VPCs) to assume vulval fates. It is shown here that lin-3 encodes the vulval-inducing signal.

lin-3 was molecularly cloned by transposon-tagging and shown to encode a nematode member ofthe Epidermal Growth Factor (EGF) family. Genetic epistasis experiments indicate that lin-3 acts upstream of let-23, which encodes a homologue of the EGF-Receptor.

lin-3 transgenes that contain multiple copies of wild-type lin-3 genomic DNA clones confer a dominant multivulva phenotype in which up to all six of the VPCs assume vulval fates. The properties of these trans genes suggest that lin-3 can act in the anchor cell to induce vulval fates. Ablation of the gonadal precursors, which prevents the development of the AC, strongly reduces the ability of lin-3 transgenes to stimulate vulval development. A lin-3 recorder transgene that retains the ability to stimulate vulval development is expressed specifically in the anchor cell at the time of vulval induction.

Expression of an obligate secreted form of the EGF domain of Lin-S from a heterologous promoter is sufficient to induce vulval fates in the absence of the normal source of the inductive signal. This result suggests that Lin-S may act as a secreted factor, and that Lin-S may be the sole vulval-inducing signal made by the anchor cell.

lin-3 transgenes can cause adjacent VPCs to assume the 1° vulval fate and thus can override the action of the lateral signal mediated by lin-12 that normally prevents adjacent 1° fates. This indicates that the production of Lin-3 by the anchor cell must be limited to allow the VPCs to assume the proper pattern of fates of so 3° 3° 2° 1° 2° 3°.

Item Type:Thesis (Dissertation (Ph.D.))
Subject Keywords:Biology
Degree Grantor:California Institute of Technology
Division:Biology
Major Option:Biology
Thesis Availability:Public (worldwide access)
Research Advisor(s):
  • Sternberg, Paul W.
Thesis Committee:
  • Anderson, David J.
  • Benzer, Seymour
  • Lipshitz, Howard D.
  • Zinn, Kai George
  • Rothenberg, Ellen V.
Defense Date:October 1993
Record Number:CaltechTHESIS:05082013-083718323
Persistent URL:https://resolver.caltech.edu/CaltechTHESIS:05082013-083718323
DOI:10.7907/8z98-jj03
Default Usage Policy:No commercial reproduction, distribution, display or performance rights in this work are provided.
ID Code:7672
Collection:CaltechTHESIS
Deposited By: Benjamin Perez
Deposited On:08 May 2013 16:05
Last Modified:19 Apr 2021 22:38

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