start-ver=1.4 cd-journal=joma no-vol=42 cd-vols= no-issue=19 article-no= start-page=11903 end-page=11911 dt-received= dt-revised= dt-accepted= dt-pub-year=2014 dt-pub=20140927 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=HSP90α plays an important role in piRNA biogenesis and retrotransposon repression in mouse en-subtitle= kn-subtitle= en-abstract= kn-abstract=HSP90, found in all kingdoms of life, is a major chaperone protein regulating many client proteins. We demonstrated that HSP90α, one of two paralogs duplicated in vertebrates, plays an important role in the biogenesis of fetal PIWI-interacting RNAs (piRNA), which act against the transposon activities, in mouse male germ cells. The knockout mutation of Hsp90α resulted in a large reduction in the expression of primary and secondary piRNAs and mislocalization of MIWI2, a PIWI homolog. Whereas the mutation in Fkbp6 encoding a co-chaperone reduced piRNAs of 28–32 nucleotides in length, the Hsp90α mutation reduced piRNAs of 24–32 nucleotides, suggesting the presence of both FKBP6-dependent and -independent actions of HSP90α. Although DNA methylation and mRNA levels of L1 retrotransposon were largely unchanged in the Hsp90α mutant testes, the L1-encoded protein was increased, suggesting the presence of post-transcriptional regulation. This study revealed the specialized function of the HSP90α isofom in the piRNA biogenesis and repression of retrotransposons during the development of male germ cells in mammals. en-copyright= kn-copyright= en-aut-name=IchiyanagiTomoko en-aut-sei=Ichiyanagi en-aut-mei=Tomoko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=IchiyanagiKenji en-aut-sei=Ichiyanagi en-aut-mei=Kenji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=OgawaAyako en-aut-sei=Ogawa en-aut-mei=Ayako kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=Kuramochi-MiyagawaSatomi en-aut-sei=Kuramochi-Miyagawa en-aut-mei=Satomi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=NakanoToru en-aut-sei=Nakano en-aut-mei=Toru kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=ChumaShinichiro en-aut-sei=Chuma en-aut-mei=Shinichiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=SasakiHiroyuki en-aut-sei=Sasaki en-aut-mei=Hiroyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=UdonoHeiichiro en-aut-sei=Udono en-aut-mei=Heiichiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= affil-num=1 en-affil= kn-affil=Department of Immunology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Division of Epigenomics and Development, Medical Institute of Bioregulation, Kyushu University affil-num=3 en-affil= kn-affil=Division of Epigenomics and Development, Medical Institute of Bioregulation, Kyushu University affil-num=4 en-affil= kn-affil=Department of Pathology, Medical School and Graduate School of Frontier Biosciences, Osaka University affil-num=5 en-affil= kn-affil=Department of Pathology, Medical School and Graduate School of Frontier Biosciences, Osaka University affil-num=6 en-affil= kn-affil=Department of Development and Differentiation, Institute for Frontier Medical Sciences, Kyoto University affil-num=7 en-affil= kn-affil=Division of Epigenomics and Development, Medical Institute of Bioregulation, Kyushu University affil-num=8 en-affil= kn-affil=Department of Immunology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences END