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Mol. Cells 2011; 31(1): 39-48

Published online January 31, 2011

https://doi.org/10.1007/s10059-011-0002-1

© The Korean Society for Molecular and Cellular Biology

Abnormal Sperm Development in pcd3J-/- Mice: the Importance of Agtpbp1 in Spermatogenesis

Nameun Kim1, Rui Xiao1, Hojun Choi, Haiin Jo, Jin-Hoi Kim, Sang-Jun Uhm, and Chankyu Park*

Department of Animal Biotechnology, Konkuk University, Seoul 143-701, Korea, 1These authors contributed equally to this work.

Correspondence to : *Correspondence: chankyu@konkuk.ac.kr

Received: August 9, 2010; Revised: October 7, 2010; Accepted: October 11, 2010

Abstract

Homozygous Purkinje cell degeneration (pcd) mutant males exhibit abnormal sperm development. Microscopic examination of the testes from pcd3J-/- mice at postnatal days 12, 15, 18 and 60 revealed histological differences, in comparison to wild-type mice, which were evident by day 18. Greatly reduced numbers of spermatocytes and spermatids were found in the adult testes, and apoptotic cells were identified among the differentiating germ cells after day 15. Our immunohistological analysis using an anti-human AGTPBP1 antibody showed that AGTPBP1 was expressed in spermatogenic cells between late stage primary spermatocytes and round spermatids. A global gene expression analysis from the testes of pcd3J-/- mice showed that expression of cyclin B3 and de-ubiquitinating enzymes USP2 and USP9y was altered by > 1.5-fold compared to the expression levels in the wild-type. Our results suggest that the pcd mutant mice have defects in spermatogenesis that begin with the pachytene spermatocyte stage and continue through subsequent stages. Thus, Agtpbp1, the gene responsible for the pcd phenotype, plays an important role in spermatogenesis and is important for survival of germ cells at spermatocytes stage onward.

Keywords Agtpbp1, apoptosis, cyclin B3, meiosis, microarray, Nna1, pcd, spermatogenesis, testis, TUNEL

Article

Research Article

Mol. Cells 2011; 31(1): 39-48

Published online January 31, 2011 https://doi.org/10.1007/s10059-011-0002-1

Copyright © The Korean Society for Molecular and Cellular Biology.

Abnormal Sperm Development in pcd3J-/- Mice: the Importance of Agtpbp1 in Spermatogenesis

Nameun Kim1, Rui Xiao1, Hojun Choi, Haiin Jo, Jin-Hoi Kim, Sang-Jun Uhm, and Chankyu Park*

Department of Animal Biotechnology, Konkuk University, Seoul 143-701, Korea, 1These authors contributed equally to this work.

Correspondence to:*Correspondence: chankyu@konkuk.ac.kr

Received: August 9, 2010; Revised: October 7, 2010; Accepted: October 11, 2010

Abstract

Homozygous Purkinje cell degeneration (pcd) mutant males exhibit abnormal sperm development. Microscopic examination of the testes from pcd3J-/- mice at postnatal days 12, 15, 18 and 60 revealed histological differences, in comparison to wild-type mice, which were evident by day 18. Greatly reduced numbers of spermatocytes and spermatids were found in the adult testes, and apoptotic cells were identified among the differentiating germ cells after day 15. Our immunohistological analysis using an anti-human AGTPBP1 antibody showed that AGTPBP1 was expressed in spermatogenic cells between late stage primary spermatocytes and round spermatids. A global gene expression analysis from the testes of pcd3J-/- mice showed that expression of cyclin B3 and de-ubiquitinating enzymes USP2 and USP9y was altered by > 1.5-fold compared to the expression levels in the wild-type. Our results suggest that the pcd mutant mice have defects in spermatogenesis that begin with the pachytene spermatocyte stage and continue through subsequent stages. Thus, Agtpbp1, the gene responsible for the pcd phenotype, plays an important role in spermatogenesis and is important for survival of germ cells at spermatocytes stage onward.

Keywords: Agtpbp1, apoptosis, cyclin B3, meiosis, microarray, Nna1, pcd, spermatogenesis, testis, TUNEL

Mol. Cells
Jun 30, 2022 Vol.45 No.6, pp. 353~434
COVER PICTURE
ERα is modified by UFM1 and this modification (ufmylation) plays a crucial role in promoting the stability of ERα and breast cancer development. However, when ERα is deufmylated and then ubiquitinated, it disappears by proteasome-mediated degradation (Yoo et al., pp. 425-434).

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