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

Karla Gutierrez et al. (2004) West Coast Worm Meeting "A forward genetic screen for new genes that regulate asymmetric neuroblast divisions in C. elegans"

  • History

  • Referenced

  • Tree Display

  • My Favorites

  • My Library

  • Comments on Karla Gutierrez et al. (2004) West Coast Worm Meeting "A forward genetic screen for new genes that regulate asymmetric neuroblast divisions in C. elegans" (0)

  • Overview

    Status:
    Publication type:
    Meeting_abstract
    WormBase ID:
    WBPaper00023985

    Karla Gutierrez, Shaun Cordes, & Gian Garriga (2004). A forward genetic screen for new genes that regulate asymmetric neuroblast divisions in C. elegans presented in West Coast Worm Meeting. Unpublished information; cite only with author permission.

    We are interested in studying asymmetric cell division (ACD), the process by which a mother cell divides to produce daughter cells that adopt different fates. Our lab has shown that mutations in two genes, ham-1 and pig-1 , disrupt ACD in many neuroblast lineages including the HSN/PHB neuroblast lineage. In wild-type embryos, the HSN/PHB neuroblast division produces a smaller anterior cell that dies and a larger posterior cell that divides to produce the HSN and PHB neurons. In ham-1 and pig-1 mutants, the anterior daughter of the HSN/PHB neuroblast is frequently transformed into its sister, dividing to produce extra HSNs and PHBs. ham-1 and pig-1 mutations interact synergistically with mutations in ced-3 and ced-4 to control the penetrance of extra HSN and PHB neurons (Guenther and Garriga, 1996; Cordes, Frank and Garriga, in preparation). This observation suggests that both ham-1 and pig-1 act in parallel to the programmed cell death pathway and regulate both cell death and cell fate in the HSN/PHB lineage. The mechanism by which ham-1 and pig-1 control ACD in the HSN/PHB and other neuroblast lineages is not understood. To identify additional genes that work with ham-1 and pig-1 to regulate ACD in the nervous system, we are screening for mutants with extra neurons. Specifically, we are mutagenizing mec-4::gfp; ced-3(n2436) hermaphrodites with EMS and screening for mutants with extra AVMs, PVMs, and PLMs. ( ham-1 mutants have extra PLMs and pig-1 mutants have extra AVMs, PVMs, and PLMs). Since mutations in ham-1 and pig-1 interact synergistically with mutations in ced-3 to control the penetrance of extra neurons, we are using the ced-3 mutation in our screen to sensitize the genetic background. So far, we have identified eight mutant strains that produce extra PLMs, and four of these strains also produce extra AVMs and PVMs.


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