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HIPK4 is essential for murine spermiogenesis

View ORCID ProfileJ. Aaron Crapster, Paul G. Rack, Zane J. Hellmann, Joshua E. Elias, John J. Perrino, Barry Behr, Yanfeng Li, Jennifer Lin, Hong Zeng, View ORCID ProfileJames K. Chen
doi: https://doi.org/10.1101/703637
J. Aaron Crapster
aDepartment of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, CA
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  • For correspondence: aaron.crapster@vibliome.com jameschen@stanford.edu
Paul G. Rack
aDepartment of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, CA
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Zane J. Hellmann
aDepartment of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, CA
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Joshua E. Elias
bChan Zuckerberg Biohub, Stanford University, Stanford, CA
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John J. Perrino
cCell Science Imaging Facility, Stanford University School of Medicine, Stanford, CA
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Barry Behr
dDepartment of Obstetrics and Gynecology, Reproductive Endocrinology and Infertility, Stanford University School of Medicine, Stanford, CA
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Yanfeng Li
eTransgenic, Knockout, and Tumor Model Center, Stanford University School of Medicine, Stanford, CA
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Jennifer Lin
eTransgenic, Knockout, and Tumor Model Center, Stanford University School of Medicine, Stanford, CA
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Hong Zeng
eTransgenic, Knockout, and Tumor Model Center, Stanford University School of Medicine, Stanford, CA
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James K. Chen
aDepartment of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, CA
fDepartment of Developmental Biology, Stanford University School of Medicine, Stanford, CA
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  • ORCID record for James K. Chen
  • For correspondence: aaron.crapster@vibliome.com jameschen@stanford.edu
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ABSTRACT

Mammalian spermiogenesis is a remarkable cellular transformation, during which round spermatids elongate into chromatin-condensed spermatozoa. The signaling pathways that coordinate this process are not well understood, and we demonstrate here that homeodomain-interacting protein kinase 4 (HIPK4) is essential for spermiogenesis and male fertility in mice. HIPK4 is predominantly expressed in round and early elongating spermatids, and Hipk4 knockout males are sterile, exhibiting phenotypes consistent with oligoasthenoteratozoospermia. Hipk4 mutant sperm have reduced oocyte binding and are incompetent for in vitro fertilization, but they can still produce viable offspring via intracytoplasmic sperm injection. Ultrastructural analyses of HIPK4-null male germ cells reveal defects in the filamentous actin (F-actin)-scaffolded acroplaxome during spermatid elongation and abnormal head morphologies in mature spermatozoa. We further observe that HIPK4 overexpression induces branched F-actin structures in cultured fibroblasts, supporting a role for this kinase in cytoskeleton remodeling. Our findings establish HIPK4 as an essential regulator of sperm head shaping and potential target for male contraception.

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Posted July 16, 2019.
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HIPK4 is essential for murine spermiogenesis
J. Aaron Crapster, Paul G. Rack, Zane J. Hellmann, Joshua E. Elias, John J. Perrino, Barry Behr, Yanfeng Li, Jennifer Lin, Hong Zeng, James K. Chen
bioRxiv 703637; doi: https://doi.org/10.1101/703637
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HIPK4 is essential for murine spermiogenesis
J. Aaron Crapster, Paul G. Rack, Zane J. Hellmann, Joshua E. Elias, John J. Perrino, Barry Behr, Yanfeng Li, Jennifer Lin, Hong Zeng, James K. Chen
bioRxiv 703637; doi: https://doi.org/10.1101/703637

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