4.4 Article

Regulation of male fertility and accessory gland gene expression by the Drosophila HR39 nuclear receptor

Journal

DEVELOPMENTAL BIOLOGY
Volume 479, Issue -, Pages 51-60

Publisher

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ydbio.2021.07.011

Keywords

Gene regulation; Fertility; Nuclear receptors; Accessory gland

Funding

  1. Transgenic RNAi Project (TRiP) [NIH R01GM084947]
  2. NCI [P30CA042014]
  3. NIH [T32 DK091317]
  4. NIH grant from the NIDDK [R01 DK075607]

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The Drosophila HR39 nuclear receptor is essential for the proper expression of genes encoding male accessory gland proteins, resulting in infertility in HR39 mutant males. This demonstrates the crucial role of HR39 in regulating gene expression and male fertility within the accessory glands. These findings provide insights into mammalian orthologs SF-1 and LRH-1 nuclear receptors, which are also involved in glandular secretions and reproduction.
Successful reproduction is dependent on the transfer of male seminal proteins to females upon mating. These proteins arise from secretory tissues in the male reproductive tract, including the prostate and seminal vesicles in mammals and the accessory gland in insects. Although detailed functional studies have provided important insights into the mechanisms by which accessory gland proteins support reproduction, much less is known about the molecular mechanisms that regulate their expression within this tissue. Here we show that the Drosophila HR39 nuclear receptor is required for the proper expression of most genes that encode male accessory gland proteins. Consistent with this role, HR39 mutant males are infertile. In addition, tissue-specific RNAi and genetic rescue experiments indicate that HR39 acts within the accessory glands to regulate gene expression and male fertility. These results provide new directions for characterizing the mammalian orthologs of HR39, the SF-1 and LRH-1 nuclear receptors, both of which are required for glandular secretions and reproduction. In addition, our studies provide a molecular mechanism to explain how the accessory glands can maintain the abundant levels of seminal fluid production required to support fertility.

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