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Citation
Mantrova, E.Y., Schulz, R.A., Hsu, T. (1999). Oogenic function of the myogenic factor D-MEF2: negative regulation of the decapentaplegic receptor gene thick veins.  Proc. Natl. Acad. Sci. U.S.A. 96(21): 11889--11894.
FlyBase ID
FBrf0111962
Publication Type
Research paper
Abstract

The myogenic factor D-MEF2 is required for the proper differentiation of muscle cells during Drosophila embryogenesis and the correct patterning of indirect flight muscles assembled during later metamorphosis. In addition to these essential myogenic functions, mutant D-mef2 adult females are weakly fertile and produce defective eggs. D-MEF2 is expressed in nurse and follicle cells of the wild-type egg chamber. We have analyzed the D-mef2 oogenic phenotype and show that the gene is required for the normal patterning and differentiation of the centripetally migrating follicle cells that are crucial for development of the anterior chorionic structures. D-mef2 alleles exhibit a genetic interaction with a dominant-negative allele of thick veins (tkv), which encodes a type I receptor of the Decapentaplegic-signaling pathway. tkv RNA is overexpressed in D-mef2 mutant egg chambers, and, conversely, forced expression of D-mef2 represses tkv expression. These results indicate a role for D-MEF2 in the regulation of tkv gene expression and Decapentaplegic signal transduction that are essential for proper determination and/or differentiation of the anterior follicle cells. Additionally, they demonstrate a vital function for the D-MEF2 transcription factor in multiple genetic pathways during Drosophila development.

PubMed ID
PubMed Central ID
PMC18382 (PMC) (EuropePMC)
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Secondary IDs
    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Proc. Natl. Acad. Sci. U.S.A.
    Title
    Proceedings of the National Academy of Sciences of the United States of America
    Publication Year
    1915-
    ISBN/ISSN
    0027-8424
    Data From Reference
    Alleles (9)
    Genes (7)
    Insertions (2)
    Transgenic Constructs (2)