The mechanistic target of rapamycin (mTOR) and its complex 1 associated protein RPTOR are germ cell-autonomously required for spermatogonial development & chapter IV : investigating changes in the testicular transcriptome during the prospermatogonial transition / by Nicholas Serra.

Author/creator Serra, Nicholas author.
Other author Geyer, Christopher B., degree supervisor.
Other author East Carolina University. Department of Anatomy and Cell Biology.
Format Theses and dissertations
Publication[Greenville, N.C.] : [East Carolina University], 2019.
Description211 pages : illustrations (chiefly color).
Supplemental ContentAccess via ScholarShip
Subjects

SeriesECU Brody School of Medicine dissertation
ECU Brody School of Medicine dissertation. UNAUTHORIZED
Summary Stem, progenitor, and differentiating spermatogonia are formed in the neonatal mouse testis, and they provide the foundation for spermatogenesis and life-long fertility. Currently, the factors that regulate these varying spermatogonial fates, in particular the molecular mediators that regulate spermatogonial differentiation, are poorly understood. Our lab previously reported that retinoic acid (RA) activates kinase signaling pathways to stimulate synthesis of proteins required for spermatogonial differentiation. The work presented here extends those findings, and is organized into chapters. In chapters 1-2, I present published studies describing key roles for 'mechanistic target of rapamycin kinase' (MTOR) and 'regulatory associated protein of MTOR, complex 1' (RPTOR) in normal spermatogonial development in vivo. In chapter 3, I present the results from an unbiased RNA-seq analysis of testicular gene expression in the fetal and neonatal mouse testis prior to establishment of the spermatogonial pool.
General notePresented to the faculty of the Department of Anatomy and Cell Biology
General noteAdvisor: Christopher B. Geyer
General noteTitle from PDF t.p. (viewed February 10, 2020).
Dissertation notePh.D. East Carolina University 2019.
Bibliography noteIncludes bibliographical references.
Technical detailsSystem requirements: Adobe Reader.
Technical detailsMode of access: World Wide Web.

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