Questions, Feedback & Help
Send us an email and we'll get back to you ASAP. Or you can read our Frequently Asked Questions.
  • page settings
  • hide sidebar
  • show empty fields
  • layout
  • (too narrow)
  • open all
  • close all
Resources » Paper

Raich WB et al. (1997) International C. elegans Meeting "CHARACTERIZATION OF zen-4, A MUTATION THAT SPECIFICALLY DISRUPTS VENTRAL ENCLOSURE"

  • History

  • Referenced

  • Tree Display

  • My Favorites

  • My Library

  • Comments on Raich WB et al. (1997) International C. elegans Meeting "CHARACTERIZATION OF zen-4, A MUTATION THAT SPECIFICALLY DISRUPTS VENTRAL ENCLOSURE" (0)

  • Overview

    Status:
    Publication type:
    Meeting_abstract
    WormBase ID:
    WBPaper00022644

    Raich WB, Rothman JH, & Hardin JD (1997). CHARACTERIZATION OF zen-4, A MUTATION THAT SPECIFICALLY DISRUPTS VENTRAL ENCLOSURE presented in International C. elegans Meeting. Unpublished information; cite only with author permission.

    The hypodermis of C. elegans forms as six rows of cells on the dorsolateral surface of the embryo. In a process known as ventral enclosure, the hypodermal sheet spreads bilaterally from the dorsal surface, ultimately meeting and establishing adherens junctions at the ventral midline. Laser ablation studies and treatment with a variety of cytoskeletal inhibitors demonstrate that ventral enclosure is a necessary prerequisite for the subsequent elongation of C. elegans into the vermiform shape achieved at hatching. In an effort to identify the molecular players involved in hypodermal enclosure, we are in the process of characterizing a zygotic lethal mutation called zen-4 required for this process. Immunostaining with the monoclonal antibody MH27, which recognizes a component of the adherens junction, indicates that the correct number of hypodermal cells are generated in homozygous zen-4 embryos. Time-lapse Nomarski movies demonstrate that the hypodermal cells begin to migrate ventrally; however, they cease their migration less than halfway towards the ventral midline. After a variable interval, the hypodermal cells retract towards the dorsal surface, where they remain as a hypodermal patch. Elongation of the zen-4 embryos is completely blocked, presumably as a consequence of the enclosure failure. The mutation has been mapped the right arm of chromosome IV between unc-44 and bli-6, and the mutation fails to complement the deficiency nDf41. Attempts to rescue the mutation by germline transformation are underway, and we are actively screening for additional zen-4 alleles.

    Affiliation:
    - Cellular and Molecular Biology, University of Wisconsin, Madison, WI 53706 Department of MCD Biology, University of California, Santa Barbara, CA 93106


    Tip: Seeing your name marked red? Please help us identify you.