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Open Access Highly Accessed Research article

The endocytic recycling regulator EHD1 is essential for spermatogenesis and male fertility in mice

Mark A Rainey1, Manju George1, GuoGuang Ying2, Reiko Akakura3, Daniel J Burgess4, Ed Siefker4, Tom Bargar5, Lynn Doglio6, Susan E Crawford7, Gordon L Todd5, Venkatesh Govindarajan4, Rex A Hess8, Vimla Band15, Mayumi Naramura1* and Hamid Band159*

Author Affiliations

1 Eppley Institute for Research in Cancer and Allied Diseases, UNMC-Eppley Cancer Center, University of Nebraska Medical Center, Omaha, Nebraska, USA

2 Laboratory of Molecular Oncology, Tianjin Medical University Cancer Institute and Hospital, Tianjin, PR China

3 Department of Biochemistry and Molecular Biology, UNDNJ-New Jersey Medical School, Newark, New Jersey, USA

4 Department of Surgery, Creighton University, Omaha, Nebraska, USA

5 Department of Genetics, Cell Biology and Anatomy, College of Medicine, University of Nebraska Medical Center, Omaha, Nebraska, USA

6 Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA

7 Department of Pathology, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA

8 Department of Veterinary Bioscience, University of Illinois at Urbana-Champaign, Urbana, Illinois, USA

9 Department of Biochemistry and Molecular Biology, College of Medicine, University of Nebraska Medical Center, Omaha, Nebraska, USA

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BMC Developmental Biology 2010, 10:37  doi:10.1186/1471-213X-10-37

Published: 2 April 2010

Abstract

Background

The C-terminal Eps15 homology domain-containing protein 1 (EHD1) is ubiquitously expressed and regulates the endocytic trafficking and recycling of membrane components and several transmembrane receptors. To elucidate the function of EHD1 in mammalian development, we generated Ehd1-/- mice using a Cre/loxP system.

Results

Both male and female Ehd1-/- mice survived at sub-Mendelian ratios. A proportion of Ehd1-/- mice were viable and showed smaller size at birth, which continued into adulthood. Ehd1-/- adult males were infertile and displayed decreased testis size, whereas Ehd1-/- females were fertile. In situ hybridization and immunohistochemistry of developing wildtype mouse testes revealed EHD1 expression in most cells of the seminiferous epithelia. Histopathology revealed abnormal spermatogenesis in the seminiferous tubules and the absence of mature spermatozoa in the epididymides of Ehd1-/- males. Seminiferous tubules showed disruption of the normal spermatogenic cycle with abnormal acrosomal development on round spermatids, clumping of acrosomes, misaligned spermatids and the absence of normal elongated spermatids in Ehd1-/- males. Light and electron microscopy analyses indicated that elongated spermatids were abnormally phagocytosed by Sertoli cells in Ehd1-/- mice.

Conclusions

Contrary to a previous report, these results demonstrate an important role for EHD1 in pre- and post-natal development with a specific role in spermatogenesis.