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Submitted on September 27, 2004
Accepted on December 1, 2004
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
* To whom correspondence should be addressed. E-mail: Y-Cheng{at}popcbr.rockefeller.edu.
Apical ectoplasmic specialization (ES) is a unique cell-cell actin-based adherens junction (AJ) 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 (FA) site in other epithelia. For instance, the protein levels of 
1-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 1-integrin, was stimulated during T suppression-induced germ cell loss. Extracellular signal-regulated kinase (ERK), a MAPK known to regulate FA 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 AJ 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.
1-integrin •
c-Src •
ectoplasmic specialization •
focal adhesion kinase
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