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Dev Biol. 2018 Jan 1;433(1):84-93. doi: 10.1016/j.ydbio.2017.11.007. Epub 2017 Nov 16.

Stk33 is required for spermatid differentiation and male fertility in mice.

Author information

1
Division of Applied Functional Genomics, German Cancer Research Center (DKFZ) and National Center for Tumor Diseases (NCT) Heidelberg, 69120 Heidelberg, Germany.
2
Division of Molecular Embryology, DKFZ-ZMBH Alliance, 69120 Heidelberg, Germany.
3
Core Facility Electron Microscopy, DKFZ, 69120 Heidelberg, Germany.
4
Molecular Biology of Centrosomes and Cilia Unit, DKFZ-ZMBH Alliance, 69120 Heidelberg, Germany.
5
Division of Molecular Embryology, DKFZ-ZMBH Alliance, 69120 Heidelberg, Germany; Institute of Molecular Biology (IMB), 55128 Mainz, Germany.
6
Department of Internal Medicine III, Ulm University, 89081 Ulm, Germany.
7
Department of Developmental Biology, Centre for Organismal Studies (COS), 69120 Heidelberg, Germany.
8
Division of Translational Oncology, National Center for Tumor Diseases (NCT) Heidelberg and German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany; Section for Personalized Oncology, Heidelberg University Hospital, 69120 Heidelberg, Germany; German Cancer Consortium (DKTK), 69120 Heidelberg, Germany.
9
Division of Translational Oncology, National Center for Tumor Diseases (NCT) Heidelberg and German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany; German Cancer Consortium (DKTK), 69120 Heidelberg, Germany.
10
Division of Applied Functional Genomics, German Cancer Research Center (DKFZ) and National Center for Tumor Diseases (NCT) Heidelberg, 69120 Heidelberg, Germany; German Cancer Consortium (DKTK), 69120 Heidelberg, Germany. Electronic address: claudia.scholl@nct-heidelberg.de.

Abstract

Spermiogenesis is the final phase during sperm cell development in which round spermatids undergo dramatic morphological changes to generate spermatozoa. Here we report that the serine/threonine kinase Stk33 is essential for the differentiation of round spermatids into functional sperm cells and male fertility. Constitutive Stk33 deletion in mice results in severely malformed and immotile spermatozoa that are particularly characterized by disordered structural tail elements. Stk33 expression first appears in primary spermatocytes, and targeted deletion of Stk33 in these cells recapitulates the defects observed in constitutive knockout mice, confirming a germ cell-intrinsic function. Stk33 protein resides in the cytoplasm and partially co-localizes with the caudal end of the manchette, a transient structure that guides tail elongation, in elongating spermatids, and loss of Stk33 leads to the appearance of a tight, straight and elongated manchette. Together, these results identify Stk33 as an essential regulator of spermatid differentiation and male fertility.

KEYWORDS:

Infertility; Kinase; Manchette; Spermatogenesis; Spermiogenesis; Stk33

PMID:
29155043
DOI:
10.1016/j.ydbio.2017.11.007
[Indexed for MEDLINE]

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