Sertoli cells synthesize and secrete glycoproteins which interact with developing germinal cells in the male. It is the long-term goal of our research to ascertain the structure and function of these glycoproteins and thereby better define the role of Sertoli cells in spermatogenesis. Previous studies have concerned the role of testicular transferrin and sulfated glycoproteins 1 and 2. It was also shown that seminiferous tubules could be synchronized to contain only a few of the stages of the cycle of the seminiferous epithelium. The experiments in this proposal are designed to achieve 5 specific goals. First, the lipid binding properties of SGP-1 and SGP-2 will be investigated and the cloning of cDNA for SGP-1 will be completed. Second, cDNA probes will be constructed for previously uncharacterized secreted proteins from Sertoli cells. Third, the new cDNA probes will be used in studies designed to quantify the mRNA in cultured cells, hypophysectomized rats and vitamin A deficient rats. The mRNA's present at each stage of the cycle of the seminiferous epithelium will be quantified by in situ hybridization. Fourth, aspects of the model we have developed for transferrin action in the testis will be examined in detail. Specifically we will examine iron transport into germinal cells and the ontogeny of transferrin receptor mRNA and ferritin mRNA in germinal cells. Finally, the synchronized testis model system will be further defined and utilized to study stage- specific synthesis and secretion in Sertoli cells.

Agency
National Institute of Health (NIH)
Institute
Eunice Kennedy Shriver National Institute of Child Health & Human Development (NICHD)
Type
Research Project (R01)
Project #
5R01HD010808-14
Application #
3311413
Study Section
Reproductive Endocrinology Study Section (REN)
Project Start
1977-08-01
Project End
1992-11-30
Budget Start
1990-12-01
Budget End
1991-11-30
Support Year
14
Fiscal Year
1991
Total Cost
Indirect Cost
Name
Washington State University
Department
Type
Schools of Arts and Sciences
DUNS #
041485301
City
Pullman
State
WA
Country
United States
Zip Code
99164
Jauregui, Estela J; Mitchell, Debra; Topping, Traci et al. (2018) Retinoic acid receptor signaling is necessary in steroidogenic cells for normal spermatogenesis and epididymal function. Development 145:
Griswold, Michael D; Hogarth, Cathryn (2018) Beyond stem cells: Commitment of progenitor cells to meiosis. Stem Cell Res 27:169-171
Agrimson, Kellie S; Oatley, Melissa J; Mitchell, Debra et al. (2017) Retinoic acid deficiency leads to an increase in spermatogonial stem number in the neonatal mouse testis, but excess retinoic acid results in no change. Dev Biol 432:229-236
Griswold, Michael D (2016) Spermatogenesis: The Commitment to Meiosis. Physiol Rev 96:1-17
Agrimson, Kellie S; Onken, Jennifer; Mitchell, Debra et al. (2016) Characterizing the Spermatogonial Response to Retinoic Acid During the Onset of Spermatogenesis and Following Synchronization in the Neonatal Mouse Testis. Biol Reprod 95:81
Chen, Yao; Ma, Li; Hogarth, Cathryn et al. (2016) Retinoid signaling controls spermatogonial differentiation by regulating expression of replication-dependent core histone genes. Development 143:1502-11
Kent, Travis; Arnold, Samuel L; Fasnacht, Rachael et al. (2016) ALDH Enzyme Expression Is Independent of the Spermatogenic Cycle, and Their Inhibition Causes Misregulation of Murine Spermatogenic Processes. Biol Reprod 94:12
Arnold, Samuel L M; Kent, Travis; Hogarth, Cathryn A et al. (2015) Pharmacological inhibition of ALDH1A in mice decreases all-trans retinoic acid concentrations in a tissue specific manner. Biochem Pharmacol 95:177-92
Hogarth, Cathryn A; Evans, Elizabeth; Onken, Jennifer et al. (2015) CYP26 Enzymes Are Necessary Within the Postnatal Seminiferous Epithelium for Normal Murine Spermatogenesis. Biol Reprod 93:19
Arnold, Samuel L; Kent, Travis; Hogarth, Cathryn A et al. (2015) Importance of ALDH1A enzymes in determining human testicular retinoic acid concentrations. J Lipid Res 56:342-57

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