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Lookup NU author(s): Professor David Elliott
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The Yd1 deletion in mice removes most of the multi-copy Rbmy gene cluster that is located adjacent to the centromere on the Y short arm (Yp). XYd1 mice develop as females because Sry is inactivated, probably because it is now juxtaposed to centromeric heterochromatin. We have previously produced XYd1 Sry transgenic males and found that they have a substantially increased frequency of abnormal sperm. Staining of testis sections with a polyclonal anti-RBMY antibody appeared to show a marked decrease of RBMY protein in the spermatids of XYd1 Sry males compared to control males, which led us to suggest that this may be responsible for the increase in sperm anomalies. In the current study we sought to determine whether augmenting Rbmy expression specifically in the spermatids of XYd1 Sry males would ameliorate the sperm defects. An expressing Rbmy transgene driven by the spermatid-specific mouse protamine 1 promotor (mP1Rbmy) was therefore introduced into XYd1 Sry males. This failed to reduce the frequency of abnormal sperm. In the course of this study, a new RBMY antibody was generated that, in contrast to the original antibody, failed to detect RBMY in spermatid stages by immunostaining. The lack of RBMY was confirmed by western blotting of lysates from purified round spermatids and elongating spermatids. The implications of these results for the proposed role for RBMY in sperm development are discussed. Copyright © 2003 S. Karger AG, Basel.
Author(s): Szot M, Grigoriev V, Mahadevaiah SK, Ojarikre OA, Tour A, Von Glasenapp E, Rattigan A, Turner JMA, Elliott DJ, Burgoyne PS
Publication type: Article
Publication status: Published
Journal: Cytogenetic and Genome Research
Print publication date: 01/01/2003
ISSN (print): 1424-8581
ISSN (electronic): 1424-859X
Publisher: S. Karger AG
PubMed id: 15051956
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