Sex-Specific Apoptosis Regulates Sexual Dimorphism in the Drosophila Embryonic Gonad

Sexually dimorphic development of the gonad is essential for germ cell development and sexual reproduction. We have found that the Drosophila embryonic gonad is already sexually dimorphic at the time of initial gonad formation. Male-specific somatic gonadal precursors (msSGPs) contribute only to the...

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Bibliographic Details
Published in:Developmental cell 2003-08, Vol.5 (2), p.205-216
Main Authors: DeFalco, Tony J, Verney, Geraldine, Jenkins, Allison B, McCaffery, J.Michael, Russell, Steven, Van Doren, Mark
Format: Article
Language:English
Subjects:
Animals
Apoptosis - physiology
DNA-Binding Proteins - metabolism
Drosophila melanogaster - anatomy & histology
Drosophila melanogaster - embryology
Drosophila Proteins - metabolism
Female
Genes, Homeobox
Gonads - cytology
Gonads - embryology
Gonads - physiology
High Mobility Group Proteins - metabolism
Homeodomain Proteins - genetics
Homeodomain Proteins - metabolism
Humans
Male
Nuclear Proteins - metabolism
Recombinant Fusion Proteins - metabolism
Sex Characteristics
Sex Chromosomes - metabolism
Sex Differentiation - physiology
SOX9 Transcription Factor
Transcription Factors - metabolism
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Summary:Sexually dimorphic development of the gonad is essential for germ cell development and sexual reproduction. We have found that the Drosophila embryonic gonad is already sexually dimorphic at the time of initial gonad formation. Male-specific somatic gonadal precursors (msSGPs) contribute only to the testis and express a Drosophila homolog of Sox9 (Sox100B), a gene essential for testis formation in humans. The msSGPs are specified in both males and females, but are only recruited into the developing testis. In females, these cells are eliminated via programmed cell death dependent on the sex determination regulatory gene doublesex. Our work furthers the hypotheses that a conserved pathway controls gonad sexual dimorphism in diverse species and that sex-specific cell recruitment and programmed cell death are common mechanisms for creating sexual dimorphism.
ISSN:1534-5807
1878-1551
DOI:10.1016/S1534-5807(03)00204-1