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

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    Author
    Dominado, N; La Marca, JE; Siddall, NA; Heaney, J; Tran, M; Cai, Y; Yu, F; Wang, H; Somers, WG; Quinn, LM; ...
    Date
    2016-12-13
    Source Title
    Stem Cell Reports
    Publisher
    CELL PRESS
    University of Melbourne Author/s
    Heaney, James; Hime, Gary; Quinn, Leonie; Siddall, Nicole; Dominado, Nicole; Tran, Mai
    Affiliation
    Anatomy and Neuroscience
    Metadata
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    Document Type
    Journal Article
    Citations
    Dominado, N., La Marca, J. E., Siddall, N. A., Heaney, J., Tran, M., Cai, Y., Yu, F., Wang, H., Somers, W. G., Quinn, L. M. & Hime, G. R. (2016). Rbf Regulates Drosophila Spermatogenesis via Control of Somatic Stem and Progenitor Cell Fate in the Larval Testis. STEM CELL REPORTS, 7 (6), pp.1152-1163. https://doi.org/10.1016/j.stemcr.2016.11.007.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/257364
    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.

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