Compensatory upregulation of myelin protein zero-like 2 expression in spermatogenic cells in cell adhesion molecule-1-deficient mice.
Compensatory upregulation of myelin protein zero-like 2 expression in spermatogenic cells in cell adhesion molecule-1-deficient mice.
复制标题
DOI:
10.1267/ahc.11057
复制
发表时间:
2012-02-29
影响因子:
2.4
通讯作者:
Iseki S
中科院分区:
文献类型:
--
作者:
Nakata H;Wakayama T;Adthapanyawanich K;Nishiuchi T;Murakami Y;Takai Y;Iseki S
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.
登录
查看更多内容
影响因子:
5.3
作者:
Yamada, D;Yoshida, M;Murakami, Y
通讯作者:
Murakami, Y
影响因子:
2.1
作者:
Inagaki, Maiko;Irie, Kenji;Takai, Yoshimi
通讯作者:
Takai, Yoshimi
影响因子:
2.4
作者:
Wakayama, Tomohiko;Kato, Yukio;Iseki, Shoichi
通讯作者:
Iseki, Shoichi
影响因子:
3.7
作者:
Mirza, M;Hreinsson, J;Sollerbrant, K
通讯作者:
Sollerbrant, K
影响因子:
4.8
作者:
Shingai, T;Ikeda, W;Takai, Y
通讯作者:
Takai, Y