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A type I DnaJ homolog, DjA1, regulates androgen receptor signaling and spermatogenesis
Author(s) -
Terada Kazutoyo,
Yomogida Kentaro,
Imai Tomoaki,
Kiyonari Hiroshi,
Takeda Naoki,
Kadomatsu Tsuyoshi,
Yano Masato,
Aizawa Shinichi,
Mori Masataka
Publication year - 2005
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1038/sj.emboj.7600549
Subject(s) - biology , androgen receptor , spermatogenesis , signal transduction , receptor , microbiology and biotechnology , androgen , genetics , endocrinology , prostate cancer , cancer , hormone
Two type I DnaJ homologs DjA1 (DNAJA1; dj2, HSDJ/hdj‐2, rdj1) and DjA2 (DNAJA2; dj3, rdj2) work similarly as a cochaperone of Hsp70s in protein folding and mitochondrial protein import in vitro . To study the in vivo role of DjA1, we generated DjA1 ‐mutant mice. Surprisingly, loss of DjA1 in mice led to severe defects in spermatogenesis that involve aberrant androgen signaling. Transplantation experiments with green fluorescent protein‐labeled spermatogonia into DjA1 −/− mice revealed a primary defect of Sertoli cells in maintaining spermiogenesis at steps 8 and 9. In Sertoli cells of DjA1 −/− mice, the androgen receptor markedly accumulated with enhanced transcription of several androgen‐responsive genes, including Pem and testin. Disruption of Sertoli–germ cell adherens junctions was also evident in DjA1 −/− mice. Experiments with DjA1 −/− fibroblasts and primary Sertoli cells indicated aberrant androgen receptor signaling. These results revealed a critical role of DjA1 in spermiogenesis and suggest that DjA1 and DjA2 are not functionally equivalent in vivo .