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Reproduction (2007) 133 395-403
DOI: 10.1530/REP-06-0180
Copyright © 2007 Society for Reproduction and Fertility
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RESEARCH

Deficiency of co-chaperone immunophilin FKBP52 compromises sperm fertilizing capacity

Jiyoung Hong1, Sung Tae Kim1, Susanne Tranguch2, David F Smith4 and Sudhansu K Dey1,2,3

1 Departments of Pediatrics, 2 Cell and Developmental Biology, 3 Pharmacology, Vanderbilt University Medical Center, Nashville, Tennessee 37232, USA and 4 Department of Biochemistry and Molecular Biology, Mayo Clinic, Scottsdale, Arizona 85259, USA

Correspondence should be addressed to S K Dey, Division of Reproductive and Developmental Biology, Department of Pediatrics, Vanderbilt University Medical Center, MCN-D4100, Nashville, Tennessee 37232-2678, USA; Email: sk.dey{at}vanderbilt.edu

FKBP52 is a member of the FK506-binding family of immunophilins and serves as a co-chaperone for steroid hormone nuclear receptors to govern appropriate hormone action in target tissues. Male mice missing Fkbp52 are infertile, and this infertility has been ascribed to compromised sensitivity of the anterior prostate, external genitalia, and other accessory sex organs to androgen. Here, we show additional defects contributing to infertility. We found that epididymal Fkbp52–/– sperm are sparse often with aberrant morphology, and they have reduced fertilizing capacity. This phenotype, initially observed in null males on a C57BL/6/129 background, is also maintained on a CD1 background. Expression studies show that while FKBP52 and androgen receptor are co-expressed in similar cell types in the epididymis, FKBP52 is also present in epididymal sperm flagella. Collectively, our results suggest that reduced number and abnormal morphology contribute to compromised fertilizing capacity of Fkbp52–/– sperm. This study is clinically relevant because unraveling the role of immunophilin signaling in male fertility will help identify new targets for male contraceptives and/or alleviate male infertility.




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