Disruption of ectoplasmic specializations between Sertoli cells and maturing spermatids by anti-nectin-2 and anti-nectin-3 antibodies

Aim: To understand the biological functions of the ectoplasmic specializations between Sertoli cells and maturing spermatids in seminiferous epithelia. Methods: In order to disrupt the function of the ectoplasmic specializations, nectin-2, which is expressed at the specialization, was neutralized wi...

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Published in:Asian journal of andrology Vol. 10; no. 4; pp. 577 - 584
Main Authors: Toyama, Yoshiro, Suzuki‐Toyota, Fumie, Maekawa, Mamiko, Ito, Chizuru, Toshimori, Kiyotaka
Format: Journal Article
Language:English
Published: Oxford, UK Blackwell Publishing Ltd 01-07-2008
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Summary:Aim: To understand the biological functions of the ectoplasmic specializations between Sertoli cells and maturing spermatids in seminiferous epithelia. Methods: In order to disrupt the function of the ectoplasmic specializations, nectin-2, which is expressed at the specialization, was neutralized with anti-nectin-2 antibody micro-injected into the lumen of the mouse seminiferous tubule. Anti-nectin-3 antibody was also micro-injected into the lumen in order to neutralize nectin-3, which is expressed at the specialization. Results: The actin filaments at the specialization disappeared, and exfoliation of maturing spermatids was observed by electron microscopy. Conclusion: Nectin-2 was neutralized by anti-nectin-2 antibody and nectin-3 was neutralized by anti-nectin-3 antibody, respectively. Inactivated nectin-2 and nectin-3 disrupted the nectin-afadin-actin system, and finally the actin filaments disappeared. As a result, the specialization lost the holding function and detachment of spermatids was observed. One of the functions of the specialization seems to be to hold maturing spermatids until spermiation.
Bibliography:Sertoli cell
ectoplasmic specialization
actin
spermatogenic cell
31-1795/R
R339.21
testis
mice
ectoplasmic specialization; Sertoli cell; spermatogenic cell; testis; actin; nectin; mice
nectin
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:1008-682X
1745-7262
DOI:10.1111/j.1745-7262.2008.00357.x