Knockdown of ATPsyn-b caused larval growth defect and male infertility in Drosophila

Arch Insect Biochem Physiol. 2015 Feb;88(2):144-54. doi: 10.1002/arch.21209. Epub 2014 Oct 22.

Abstract

The ATPsyn-b encoding for subunit b of ATP synthase in Drosophila melanogaster is proposed to act in ATP synthesis and phagocytosis, and has been identified as one of the sperm proteins in both Drosophila and mammals. At present, its details of functions in animal growth and spermatogenesis have not been reported. In this study, we knocked down ATPsyn-b using Drosophila lines expressing inducible hairpin RNAi constructs and Gal4 drivers. Ubiquitous knockdown of ATPsyn-b resulted in growth defects in larval stage as the larvae did not grow bigger than the size of normal second-instar larvae. Knockdown in testes did not interrupt the developmental excursion to viable adult flies, however, these male adults were sterile. Analyses of testes revealed disrupted nuclear bundles during spermatogenesis and abnormal shaping in spermatid elongation. There were no mature sperm in the seminal vesicle of ATPsyn-b knockdown male testes. These findings suggest us that ATPsyn-b acts in growth and male fertility of Drosophila.

Keywords: ATPsyn-b; Drosophila melanogaster; larval growth; male fertility; spermatogenesis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Drosophila Proteins / genetics
  • Drosophila Proteins / metabolism
  • Drosophila melanogaster / genetics*
  • Drosophila melanogaster / growth & development*
  • Gene Expression Profiling
  • Infertility, Male / genetics
  • Larva / genetics
  • Larva / growth & development
  • Male
  • RNA Interference
  • Real-Time Polymerase Chain Reaction
  • Spermatogenesis*
  • Testis / growth & development

Substances

  • Drosophila Proteins