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Aberrant distribution of junctional complex components in retinoic acid receptor alpha‐deficient mice
Author(s) -
Chung Sanny S.W.,
Choi Cindy,
Wang Xiangyuan,
Hallock Loretta,
Wolgemuth Debra J.
Publication year - 2010
Publication title -
microscopy research and technique
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.536
H-Index - 118
eISSN - 1097-0029
pISSN - 1059-910X
DOI - 10.1002/jemt.20797
Subject(s) - retinoic acid , tight junction , connexin , biology , microbiology and biotechnology , cell junction , sertoli cell , retinoic acid receptor alpha , vimentin , spermiogenesis , gap junction , retinoic acid receptor , in situ hybridization , ectopic expression , blood–testis barrier , spermatogenesis , cell , endocrinology , gene expression , cell culture , genetics , immunology , nucleus , gene , immunohistochemistry , intracellular
Retinoic acid receptor alpha (RARα)‐deficient mice are sterile, with abnormalities in the progression of spermatogenesis and spermiogenesis. In this study, we investigated whether defective retinoid signaling involved at least in part, disrupted cell–cell interactions. Hypertonic fixation approaches revealed defects in the integrity of the Sertoli‐cell barrier in the tubules of RARα‐deficient testes. Dye transfer experiments further revealed that coupling between cells from the basal to adluminal compartments was aberrant. There were also differences in the expression of several known retinoic acid (RA)‐responsive genes encoding structural components of tight junctions and gap junctions. Immunostaining demonstrated a delay in the incorporation of zonula occludens (ZO‐1), a peripheral component protein of tight junctions, into the Sertoli cell tight junctions. Markedly reduced expression of connexin‐40 in mutant pachytene spermatocytes and round spermatids was found by in situ hybridization. An ectopic distribution of vimentin and disrupted cyclic expression of vimentin, which is usually tightly regulated during spermiogenesis, was found in RARα‐deficient testes at all ages examined. Thus, the specific defects in spermiogenesis in RARα‐deficient testes may correlate with a disrupted cyclic expression of RA‐responsive structural components, including vimentin, a downregulation of connexin‐40 in spermatogenic cells, and delayed assembly of ZO‐1 into Sertoli cell tight junctions. Interestingly, bioinformatic analysis revealed that many genes that are components of tight junctions and gap junctions contained potential retinoic acid response element binding sites. Microsc. Res. Tech., 2010. © 2009 Wiley‐Liss, Inc.