Display Settings:

Format

Send to:

Choose Destination
See comment in PubMed Commons below
PLoS One. 2007 May 16;2(5):e453.

Screen for genetic modifiers of stbm reveals that photoreceptor fate and rotation can be genetically uncoupled in the Drosophila eye.

Author information

  • 1Department of Genetics, Washington University School of Medicine, St. Louis, Missouri, United States of America. twolff@genetics.wustl.edu

Abstract

BACKGROUND:

Polarity of the Drosophila compound eye arises primarily as a consequence of two events that are tightly linked in time and space: fate specification of two photoreceptor cells, R3 and R4, and the subsequent directional movement of the unit eyes of the compound eye, or ommatidia. While it is thought that these fates dictate the direction of ommatidial rotation, the phenotype of mutants in the genes that set up this polarity led to the hypothesis that these two events could be uncoupled.

METHODOLOGY/PRINCIPAL FINDINGS:

To definitively demonstrate these events are genetically separable, we conducted a dominant modifier screen to determine if genes, when misexpressed, could selectively enhance subclasses of mutant ommatidia in which the direction of rotation does not follow the R3/R4 cell fates, yet not affect the number of ommatidia in which rotation follows the R3/R4 cell fates. We identified a subset of P element lines that exhibit this selective enhancement. We also identified lines that behave in the opposite manner: They enhance the number of ommatidia that rotate in the right direction, but do not alter the number of ommatidia that rotate incorrectly with respect to the R3/R4 fates.

CONCLUSIONS/SIGNIFICANCE:

These results indicate that fate and direction of rotation can be genetically separated, and that there are genes that act between R3/R4 fate specification and direction of ommatidial rotation. These data affirm what has been a long-standing assumption about the genetic control of ommatidial polarity.

PMID:
17505545
[PubMed - indexed for MEDLINE]
PMCID:
PMC1866179
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Public Library of Science Icon for PubMed Central
    Loading ...
    Write to the Help Desk