Compensatory upregulation of myelin protein zero-like 2 expression in spermatogenic cells in cell adhesion molecule-1-deficient mice
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概要
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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.
著者
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Iseki Shoichi
Department Of Anatomy Kanazawa University School Of Medicine
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TAKAI YOSHIMI
The Departments of Biochemistry, Kobe University School of Medicine
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Murakami Yoshinori
Division Of Molecular Pathology Department Of Cancer Biology Institute Of Medical Science The Univer
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若山 友彦
Department of Anatomy, School of Medicine, Kanazawa Univeristy
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Iseki Shoichi
Department of Histology and Embryology, Graduate School of Medical Science, Kanazawa University
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Nishiuchi Takumi
Division of Functional Genomics, Advanced Science Research Center, Kanazawa University
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Nakata Hiroki
Department of Histology and Embryology, Graduate School of Medical Science, Kanazawa University
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仲田 浩規
Department of Histology and Embryology, Graduate School of Medical Science, Kanazawa University
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西内 巧
Department of Histology and Embryology, Graduate School of Medical Science, Kanazawa University
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井関 尚一
Division of Functional Genomics, Advanced Science Research Center, Kanazawa University
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