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Citation
Greig, S., Akam, M. (1995). The role of homeotic genes in the specification of the Drosophila gonad.  Curr. Biol. 5(9): 1057--1062.
FlyBase ID
FBrf0083977
Publication Type
Research paper
Abstract
In Drosophila, the gonads are composed of two cell populations: the germ line, derived from the pole cells, and a somatic component, derived from the mesoderm of abdominal segments 5-8. Formation of the gonad requires the function of a specific homeotic gene, abdominal-A (abd-A). Other genes of the bithorax complex, Ultrabithorax (Ubx) or Abdominal-B (Abd-B), cannot substitute for this requirement when abd-A is removed.We show here that, in embryos lacking the entire bithorax complex, experimentally induced expression of either ABD-A or UBX protein in the mesoderm will rescue the expression of a gonad-specific marker, 412 RNA. Ubiquitous expression of these homeotic proteins within the mesoderm results in the formation of ectopic gonad tissue anterior to the normal location of the gonads. In the absence of any endogenous bithorax-complex gene expression, however, mesoderm expressing gonad markers still condenses preferentially in the posterior segments of the abdomen, even in the absence of pole cells.The specific requirement for abd-A and not Ubx in gonad development does not reflect differences in the properties of the proteins that these genes encode, but presumably reflects differences in their regulation. In normal development, the restriction of gonad formation to the posterior abdomen does not depend on the overlap of abd-A and Abd-B expression, but must depend on the regulation of abd-A and Ubx in the sub-population of the mesoderm that forms the gonad. Factors other than homeotic gene expression provide some cues that direct gonadal mesoderm to condense in the correct location.
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    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Curr. Biol.
    Title
    Current Biology
    Publication Year
    1991-
    ISBN/ISSN
    0960-9822
    Data From Reference
    Aberrations (2)
    Alleles (4)
    Genes (5)
    Natural transposons (1)
    Transgenic Constructs (4)