KIF2C Deletion Causes Meiotic Abnormalities and Nonobstructive Azoospermia in Mice

Kitakaze, Hiroaki; Miyata, Haruhiko; Oyama, Yuki; Pan, Chen; Kujime, Yuma; Tsujimura, Go; Imanaka, Takahiro; Kuribayashi, Sohei; Ueda, Norichika; Takezawa, Kentaro; Fukuhara, Shinichiro; Nonomura, Norio; Ikawa, Masahito

doi:https://doi.org/10.1002/rmb2.12659

KIF2C Deletion Causes Meiotic Abnormalities and Nonobstructive Azoospermia in Mice

Kitakaze, Hiroaki; Miyata, Haruhiko; Oyama, Yuki et al.

Reproductive Medicine and Biology, 2025, 24(1), e12659

Number of Access:36（2025-08-22 01:04 Counts）

Identifier to cite or link to this item: https://hdl.handle.net/11094/102237

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Title	KIF2C Deletion Causes Meiotic Abnormalities and Nonobstructive Azoospermia in Mice
Creator	NRID 1000050981958 1000050981958 researchmap permalink hiroakikitakaze hiroakikitakaze CreatorName Kitakaze, Hiroaki
	NRID 1000050604732 1000050604732 ORCID 0000-0003-4758-5803 0000-0003-4758-5803 researchmap permalink hmiyata hmiyata Scopus Author ID 37161837000 37161837000 CreatorName Miyata, Haruhiko
	CreatorName Oyama, Yuki
	CreatorName Pan, Chen
	CreatorName Kujime, Yuma
	CreatorName Tsujimura, Go
	CreatorName Imanaka, Takahiro
	CreatorName Kuribayashi, Sohei
	NRID 1000040759528 1000040759528 researchmap permalink 090 090 CreatorName Ueda, Norichika
	NRID 1000090648015 1000090648015 ORCID 0000-0003-1137-1846 0000-0003-1137-1846 researchmap permalink urouro urouro Scopus Author ID 35171791000 35171791000 CreatorName Takezawa, Kentaro
	NRID 1000020609870 1000020609870 researchmap permalink sf55 sf55 Scopus Author ID 8635237400 8635237400 CreatorName Fukuhara, Shinichiro
	NRID 1000030263263 1000030263263 researchmap permalink read0185096 read0185096 Scopus Author ID 7005880662 7005880662 CreatorName Nonomura, Norio
	NRID 1000020304066 1000020304066 ORCID 0000-0001-9859-6217 0000-0001-9859-6217 researchmap permalink read0054910 read0054910 Scopus Author ID 16689054500 16689054500 CreatorName Ikawa, Masahito
Subject	KIF2C
	knockout mice
	male infertility
	nonobstructive azoospermia
Description	Kitakaze H., Miyata H., Oyama Y., et al. KIF2C Deletion Causes Meiotic Abnormalities and Nonobstructive Azoospermia in Mice. Reproductive Medicine and Biology 24(1), e12659 (2025); https://doi.org/10.1002/rmb2.12659.
Abstract	Purpose: Kinesin Family Member 2C (KIF2C) is a key regulator of microtubule dynamics and chromosome segregation in mitosis. However, its role in spermatogenesis remains unclear. Recent transcriptomic analyses suggest a potential link between KIF2C and male infertility. This study aimed to clarify KIF2C's roles in spermatogenesis using Kif2c knockout (KO) mice. Methods: To overcome the preweaning lethality associated with Kif2c deletion, we generated Kif2c KO mice with a mixed genetic background of 129X1/SvJ and B6D2. We assessed male fertility, epididymal sperm counts, and testicular sections of Kif2c KO mice. Results: Global Kif2c KO mice were obtained and showed male infertility. Histological analyses and epididymal sperm count revealed that Kif2c KO mice exhibited severely impaired spermatogenesis and absence of mature spermatozoa. These findings are consistent with those observed in patients with nonobstructive azoospermia (NOA). Our classification of Kif2c KO seminiferous tubules indicated that most spermatogenic cells were arrested at the early stages, particularly during meiosis. Conclusions: This study provides in vivo evidence that KIF2C is essential for spermatogenesis and male fertility in mice. The successful generation of global Kif2c KO mice establishes an animal model for NOA, supporting research on germ cell development and reproductive health.
Publisher	John Wiley and Sons Ltd
Source Title	Reproductive Medicine and Biology
Volume (Issue)	24(1)
Page	e12659
Date of Issued	2025-05-27
Language	English
Handle URL	https://hdl.handle.net/11094/102237
PISSN	14455781
eISSN	14470578
Relation.isIdenticalTo	DOI (Publisher Version) https://doi.org/10.1002/rmb2.12659
Access Rights	open access
CopyRight	This article is licensed under a Creative Commons Attribution 4.0 International License.
oaire:version	Version of Record
Category	学術雑誌論文 Journal Article

Resource Type	journal article
Local Type	Journal Article
DCMI Type	Text
DCTERMS.bibliographicCitation	Reproductive Medicine and Biology. 2025, 24(1), p. e12659
DC.title	KIF2C Deletion Causes Meiotic Abnormalities and Nonobstructive Azoospermia in Mice
DC.creator	Kitakaze, Hiroaki
	Miyata, Haruhiko
	Oyama, Yuki
	Pan, Chen
	Kujime, Yuma
	Tsujimura, Go
	Imanaka, Takahiro
	Kuribayashi, Sohei
	Ueda, Norichika
	Takezawa, Kentaro
	Fukuhara, Shinichiro
	Nonomura, Norio
	Ikawa, Masahito
DC.publisher	John Wiley and Sons Ltd
DC.language' scheme='DCTERMS.RFC1766	English
DC.type' scheme='DCTERMS.DCMIType	Text
DCTERMS.issued' scheme='DCTERMS.W3CDTF	2025-05-27
DC.identifier	https://doi.org/10.1002/rmb2.12659
DC.subject	KIF2C
	knockout mice
	male infertility
	nonobstructive azoospermia
DC.description	Kitakaze H., Miyata H., Oyama Y., et al. KIF2C Deletion Causes Meiotic Abnormalities and Nonobstructive Azoospermia in Mice. Reproductive Medicine and Biology 24(1), e12659 (2025); https://doi.org/10.1002/rmb2.12659.
DCTERMS.abstract	Purpose: Kinesin Family Member 2C (KIF2C) is a key regulator of microtubule dynamics and chromosome segregation in mitosis. However, its role in spermatogenesis remains unclear. Recent transcriptomic analyses suggest a potential link between KIF2C and male infertility. This study aimed to clarify KIF2C's roles in spermatogenesis using Kif2c knockout (KO) mice. Methods: To overcome the preweaning lethality associated with Kif2c deletion, we generated Kif2c KO mice with a mixed genetic background of 129X1/SvJ and B6D2. We assessed male fertility, epididymal sperm counts, and testicular sections of Kif2c KO mice. Results: Global Kif2c KO mice were obtained and showed male infertility. Histological analyses and epididymal sperm count revealed that Kif2c KO mice exhibited severely impaired spermatogenesis and absence of mature spermatozoa. These findings are consistent with those observed in patients with nonobstructive azoospermia (NOA). Our classification of Kif2c KO seminiferous tubules indicated that most spermatogenic cells were arrested at the early stages, particularly during meiosis. Conclusions: This study provides in vivo evidence that KIF2C is essential for spermatogenesis and male fertility in mice. The successful generation of global Kif2c KO mice establishes an animal model for NOA, supporting research on germ cell development and reproductive health.
DC.rights	This article is licensed under a Creative Commons Attribution 4.0 International License.
DC.format	102237
citation_title	KIF2C Deletion Causes Meiotic Abnormalities and Nonobstructive Azoospermia in Mice
citation_author	Kitakaze, Hiroaki
	Miyata, Haruhiko
	Oyama, Yuki
	Pan, Chen
	Kujime, Yuma
	Tsujimura, Go
	Imanaka, Takahiro
	Kuribayashi, Sohei
	Ueda, Norichika
	Takezawa, Kentaro
	Fukuhara, Shinichiro
	Nonomura, Norio
	Ikawa, Masahito
citation_publisher	John Wiley and Sons Ltd
citation_language	English
citation_date	2025-05-27
citation_journal_title	Reproductive Medicine and Biology
citation_volume	24
citation_issue	1
citation_firstpage	e12659
citation_doi	https://doi.org/10.1002/rmb2.12659
citation_public_url	https://hdl.handle.net/11094/102237

KIF2C Deletion Causes Meiotic Abnormalities and Nonobstructive Azoospermia in Mice

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