Rbf Regulates Drosophila Spermatogenesis via Control of Somatic Stem and Progenitor Cell Fate in the Larval Testis

Stem Cell Reports. 2016 Dec 13;7(6):1152-1163. doi: 10.1016/j.stemcr.2016.11.007.

Abstract

The Drosophila testis has been fundamental to understanding how stem cells interact with their endogenous microenvironment, or niche, to control organ growth in vivo. Here, we report the identification of two independent alleles for the highly conserved tumor suppressor gene, Retinoblastoma-family protein (Rbf), in a screen for testis phenotypes in X chromosome third-instar lethal alleles. Rbf mutant alleles exhibit overproliferation of spermatogonial cells, which is phenocopied by the molecularly characterized Rbf11 null allele. We demonstrate that Rbf promotes cell-cycle exit and differentiation of the somatic and germline stem cells of the testes. Intriguingly, depletion of Rbf specifically in the germline does not disrupt stem cell differentiation, rather Rbf loss of function in the somatic lineage drives overproliferation and differentiation defects in both lineages. Together our observations suggest that Rbf in the somatic lineage controls germline stem cell renewal and differentiation non-autonomously via essential roles in the microenvironment of the germline lineage.

Keywords: Drosophila; germline; proliferation; retinoblastoma protein; self-renewal; stem cell; stem cell niche; testis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Differentiation
  • Cell Lineage*
  • Cell Proliferation
  • Drosophila Proteins / metabolism*
  • Drosophila melanogaster / cytology*
  • Drosophila melanogaster / metabolism*
  • Germ Cells / cytology
  • Germ Cells / metabolism
  • Larva
  • Male
  • Mutation / genetics
  • Retinoblastoma Protein / metabolism*
  • Spermatogenesis*
  • Stem Cell Niche
  • Stem Cells / cytology*
  • Stem Cells / metabolism
  • Testis / cytology*
  • Transcription Factors / metabolism*

Substances

  • Drosophila Proteins
  • Rbf protein, Drosophila
  • Retinoblastoma Protein
  • Transcription Factors