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Compensatory upregulation of myelin protein zero-like 2 expression in spermatogenic cells in cell adhesion molecule-1-deficient mice

フォーマット:
論文
責任表示:
仲田, 浩規 ; 若山, 友彦 ; 西内, 巧 ; 井関, 尚一
言語:
英語
出版情報:
Japan Society of Histochemistry and Cytochemistry = 日本組織細胞化学会, 2012-01-01
著者名:
掲載情報:
Acta Histochemica et Cytochemica
ISSN:
0044-5991  CiNii Articles  Webcat Plus  JAIRO
巻:
45
通号:
1
開始ページ:
47
終了ページ:
56
バージョン:
publisher
概要:
The cell adhesion molecule-1 (Cadm1) is a member of the immunoglobulin superfamily. In the mouse testis, Cadm1 is expressed in the earlier spermatogenic cells up to early pachytene spermatocytes and also in elongated spermatids, but not in Sertoli cells. Cadm1-deficient mice have male infertility due to defective spermatogenesis, in which detachment of spermatids is prominent while spermatocytes appear intact. To elucidate the molecular mechanisms of the impaired spermatogenesis caused by Cadm1 deficiency, we performed DNA microarray analysis of global gene expression in the testis compared between Cadm1-deficient and wild-type mice. Out of the 25 genes upregulated in Cadm1-deficient mice, we took a special interest in myelin protein zero-like 2 (Mpzl2), another cell adhesion molecule of the immunoglobulin superfamily. The levels of Mpzl2 mRNA increased by 20-fold and those of Mpzl2 protein increased by 2-fold in the testis of Cadm1-deficient mice, as analyzed with quantitative PCR and western blotting, respectively. In situ hybridization and immunohistochemistry demonstrated that Mpzl2 mRNA and protein are localized in the earlier spermatogenic cells but not in elongated spermatids or Sertoli cells, in both wild-type and Cadm1-deficient mice. These results suggested that Mpzl2 can compensate for the deficiency of Cadm1 in the earlier spermatogenic cells. © 2012 The Japan Society of Histochemistry and Cytochemistry.<br />金沢大学大学院医学系研究科 仲田 浩規 学位論文 / Thesis of Hiroki Nakata 続きを見る
URL:
http://hdl.handle.net/2297/30293

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