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Spermatogenesis of mice lacking CK2α′: Failure of germ cell survival and characteristic modifications of the spermatid nucleus
Author(s) -
Escalier Denise,
Silvius Derek,
Xu Xin
Publication year - 2003
Publication title -
molecular reproduction and development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.745
H-Index - 105
eISSN - 1098-2795
pISSN - 1040-452X
DOI - 10.1002/mrd.10346
Subject(s) - spermatid , biology , microbiology and biotechnology , chromatin , germ cell , spermatogenesis , spermiogenesis , nucleus , nuclear membrane , cell nucleus , inner membrane , genetics , dna , endocrinology , gene , mitochondrion
Csnk2a2 encodes the CK2α′catalytic subunit of CK2 that is predominantly expressed in testis. Male mice in which Csnk2a2 has been disrupted were infertile and displayed oligozoospermia with an abnormal shape of the spermatid nucleus. In this study, Csnk2a2 null testes revealed extensive germ cell degenerative processes at all stages of spermatogenesis, including the first spermatogenesis wave. Nuclear envelope (NE) protrusions with loss of nuclear pores, swelling of the outer membrane, and disruption of the inner membrane were observed in cells ranging from spermatogonia to early spermatids. Most early round spermatids were depleted, and DNA‐specific fluorescent dyes showed a large chromatin‐free nuclear domain near the chromocenter. Spermatids that were not eliminated retained NE defects that could explain the acrosomal and nuclear abnormalities of Csnk2a2 null spermatozoa. Data suggest that CK2α′ deficiency could impair the phosphorylation of nuclear proteins of male germ cells leading to a particular cell‐death pathway characterized by NE protrusions and an unusual pattern of chromatin modifications in spermatids. Mol. Reprod. Dev. 66: 190–201, 2003. © 2003 Wiley‐Liss, Inc.