This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Wong, C.-H. Articles by Cheng, C. Y. Search for Related Content PubMed PubMed Citation Articles by Wong, C.-H. Articles by Cheng, C. Y.

Regulation of Ectoplasmic Specialization Dynamics in the Seminiferous Epithelium by Focal Adhesion-Associated Proteins in Testosterone-Suppressed Rat Testes

Population Council (C.-H.W., W.X., N.P.Y.L., D.D.M., C.Y.C.), Center for Biomedical Research, New York, New York 10021; and Department of Zoology (W.M.L.), University of Hong Kong, Hong Kong, China

Address all correspondence and requests for reprints to: C. Yan Cheng, Ph.D., Population Council, 1230 York Avenue, New York, New York 10021. E-mail: y-cheng{at}popcbr.rockefeller.edu.

Apical ectoplasmic specialization (ES) is a unique testis-specific cell-cell actin-based adherens junction type restricted to the Sertoli-round/elongating/elongate spermatid interface in the seminiferous epithelium. An endogenous testosterone (T) suppression model was used to study the regulation of apical ES dynamics in the testis. By providing sustained releases of T and estradiol using subdermal implants in rats, this treatment reduced endogenous testicular T level. This in turn led to sloughing of spermatids (step 8 and beyond) from the seminiferous epithelium, which can be reversed by removing the implants, or replacing them with a higher dose of T implants. This model thus allows us to study the restructuring events at the apical ES. It was shown that apical ES restructuring involved proteins that were usually restricted to the cell-matrix focal adhesion site in other epithelia. For instance, the protein levels of ß1-integrin, Tyr-phosphorylated focal adhesion kinase (p-FAK), and c-Src were induced during the T suppression-induced germ cell loss and recovery, implicating that these proteins are putative regulators of ES dynamics. Indeed, the formation of p-FAK/c-Src protein complex, but not their association with ß1-integrin, was stimulated during T suppression-induced germ cell loss. ERK, a MAPK known to regulate focal adhesion turnover, was also activated during the androgen suppression-induced spermatid loss and the early phase of the recovery when germ cells began to repopulate the epithelium. Collectively, these data suggest that the apical ES is a cell-cell adherens junction type with the characteristics of cell-matrix focal contacts. In addition to its role in conferring cell adhesion formation, the p-FAK/c-Src protein complex apparently also regulates apical ES disruption via the ERK signaling pathway.

This article has been cited by other articles:

				S. Sun, E. W P Wong, M. W M Li, W. M Lee, and C Y. Cheng 14-3-3 and its binding partners are regulators of protein-protein interactions during spermatogenesis J. Endocrinol., September 1, 2009; 202(3): 327 - 336. [Abstract] [Full Text] [PDF]

				W.-Y. Lui and W. M Lee Molecular mechanisms by which hormones and cytokines regulate cell junction dynamics in the testis J. Mol. Endocrinol., August 1, 2009; 43(2): 43 - 51. [Abstract] [Full Text] [PDF]

				D. D. Mruk, B. Silvestrini, and C. Y. Cheng Anchoring Junctions As Drug Targets: Role in Contraceptive Development Pharmacol. Rev., June 1, 2008; 60(2): 146 - 180. [Abstract] [Full Text] [PDF]

				J. Cheng, S. C. Watkins, and W. H. Walker Testosterone Activates Mitogen-Activated Protein Kinase via Src Kinase and the Epidermal Growth Factor Receptor in Sertoli Cells Endocrinology, May 1, 2007; 148(5): 2066 - 2074. [Abstract] [Full Text] [PDF]

				E. Aivatiadou, E. Mattei, M. Ceriani, L. Tilia, and G. Berruti Impaired Fertility and Spermiogenetic Disorders with Loss of Cell Adhesion in Male Mice Expressing an Interfering Rap1 Mutant Mol. Biol. Cell, April 1, 2007; 18(4): 1530 - 1542. [Abstract] [Full Text] [PDF]

				W. Xia, D. D Mruk, W. M Lee, and C Y. Cheng Unraveling the molecular targets pertinent to junction restructuring events during spermatogenesis using the Adjudin-induced germ cell depletion model J. Endocrinol., March 1, 2007; 192(3): 563 - 583. [Abstract] [Full Text] [PDF]

				N. P Y Lee, D. D Mruk, W. Xia, and C Y. Cheng Cellular localization of sphingomyelin synthase 2 in the seminiferous epithelium of adult rat testes J. Endocrinol., January 1, 2007; 192(1): 17 - 32. [Abstract] [Full Text] [PDF]

				P. P Y Lie, W. Xia, C. Q F Wang, D. D Mruk, H. H N Yan, C.-h. Wong, W. M Lee, and C Y. Cheng Dynamin II interacts with the cadherin- and occludin-based protein complexes at the blood-testis barrier in adult rat testes J. Endocrinol., December 1, 2006; 191(3): 571 - 586. [Abstract] [Full Text] [PDF]

				H. H. N. Yan and C. Y. Cheng Laminin {alpha} 3 Forms a Complex with beta3 and {gamma}3 Chains That Serves as the Ligand for {alpha} 6beta1-Integrin at the Apical Ectoplasmic Specialization in Adult Rat Testes J. Biol. Chem., June 23, 2006; 281(25): 17286 - 17303. [Abstract] [Full Text] [PDF]

				N. P.Y. Lee, D. D. Mruk, C.-h. Wong, and C. Y. Cheng Regulation of Sertoli-Germ Cell Adherens Junction Dynamics in the Testis Via the Nitric Oxide Synthase (NOS)/cGMP/Protein Kinase G (PRKG)/{beta}-Catenin (CATNB) Signaling Pathway: An In Vitro and In Vivo Study Biol Reprod, September 1, 2005; 73(3): 458 - 471. [Abstract] [Full Text] [PDF]

				H. H. N. Yan and C. Y. Cheng Blood-testis barrier dynamics are regulated by an engagement/disengagement mechanism between tight and adherens junctions via peripheral adaptors PNAS, August 16, 2005; 102(33): 11722 - 11727. [Abstract] [Full Text] [PDF]