FB2025_01 , released February 20, 2025
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Citation
Minami, R., Wakabayashi, M., Sugimori, S., Taniguchi, K., Kokuryo, A., Imano, T., Adachi-Yamada, T., Watanabe, N., Nakagoshi, H. (2012). The homeodomain protein defective proventriculus is essential for male accessory gland development to enhance fecundity in Drosophila.  PLoS ONE 7(3): e32302.
FlyBase ID
FBrf0217789
Publication Type
Research paper
Abstract
The Drosophila male accessory gland has functions similar to those of the mammalian prostate gland and the seminal vesicle, and secretes accessory gland proteins into the seminal fluid. Each of the two lobes of the accessory gland is composed of two types of binucleate cell: about 1,000 main cells and 40 secondary cells. A well-known accessory gland protein, sex peptide, is secreted from the main cells and induces female postmating response to increase progeny production, whereas little is known about physiological significance of the secondary cells. The homeodomain transcriptional repressor Defective proventriculus (Dve) is strongly expressed in adult secondary cells, and its mutation resulted in loss of secondary cells, mononucleation of main cells, and reduced size of the accessory gland. dve mutant males had low fecundity despite the presence of sex peptide, and failed to induce the female postmating responses of increased egg laying and reduced sexual receptivity. RNAi-mediated dve knockdown males also had low fecundity with normally binucleate main cells. We provide the first evidence that secondary cells are crucial for male fecundity, and also that Dve activity is required for survival of the secondary cells. These findings provide new insights into a mechanism of fertility/fecundity.
PubMed ID
PubMed Central ID
PMC3299662 (PMC) (EuropePMC)
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Secondary IDs
    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    PLoS ONE
    Title
    PLoS ONE
    Publication Year
    2006-
    ISBN/ISSN
    1932-6203
    Data From Reference
    Aberrations (2)
    Alleles (11)
    Genes (6)
    Polypeptides (1)
    Natural transposons (1)
    Insertions (2)
    Experimental Tools (1)
    Transgenic Constructs (7)
    Transcripts (1)