An azoospermic factor gene, Ddx3y and its paralog, Ddx3x are dispensable in germ cells for male fertility

Matsumura, Takafumi; Endo, Tsutomu; Isotani, Ayako; Ogawa, Masaki; Ikawa, Masahito

doi:https://doi.org/10.1262/jrd.2018-145

アクセス数:139件（2024-06-02 18:44 集計）

固定URL: https://hdl.handle.net/11094/78562

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タイトル	An azoospermic factor gene, Ddx3y and its paralog, Ddx3x are dispensable in germ cells for male fertility
著者	著者名 Matsumura, Takafumi
	NRID 1000040813936 1000040813936 著者名 Endo, Tsutomu
	NRID 1000020444523 1000020444523 著者名 Isotani, Ayako
	著者名 Ogawa, Masaki
	NRID 1000020304066 1000020304066 ORCID 0000-0001-9859-6217 0000-0001-9859-6217 researchmap permalink read0054910 read0054910 Scopus Author ID 16689054500 16689054500 著者名 Ikawa, Masahito
キーワード等	Azoospermia factor region
	Chimeric analysis
	CRISPR/Cas9
	Male infertility
	Y chromosome
内容	Takafumi MATSUMURA, Tsutomu ENDO, Ayako ISOTANI, Masaki OGAWA, Masahito IKAWA, An azoospermic factor gene, Ddx3y and its paralog, Ddx3x are dispensable in germ cells for male fertility, Journal of Reproduction and Development, 2019, Volume 65, Issue 2, Pages 121-128, Released April 12, 2019, [Advance publication] Released January 07, 2019, Online ISSN 1348-4400, Print ISSN 0916-8818, https://doi.org/10.1262/jrd.2018-145, https://www.jstage.jst.go.jp/article/jrd/65/2/65_2018-145/_article/-char/en
抄録	About 10% of male infertile patients show abnormalities in spermatogenesis. The microdeletion of azoospermia factor a (AZFa) region of the Y chromosome is thought to be a cause of spermatogenic failure. However, candidate gene responsible for the spermatogenic failure in AZFa deleted patients has not been elucidated yet. Using mice, we explored the function of Ddx3y, a strong candidate gene in the Azfa region, and Ddx3x, a Ddx3y paralog on the X chromosome, in spermatogenesis. We first generated Ddx3y KO male mice using CRISPR/Cas9 and found that the Ddx3y KO male mice show normal spermatogenesis, produce morphologically normal spermatozoa, and sire healthy offspring. Because Ddx3x KO males were embryonic lethal, we next generated chimeric mice, which contain Ddx3x and Ddx3y double KO (dKO) germ cells, and found that the dKO germ cells can differentiate into spermatozoa and transmit their mutant alleles to offspring by normal mating. We conclude that Ddx3x and Ddx3y are dispensable for spermatogenesis at least in mice. Unlike human, mice have an additional Ddx3y paralog D1pas1, that has been reported to be essential for spermatogenesis. These findings suggest that human and mouse DDX3 related proteins have distinct differences in their functions.
出版者	The Japanese Society of Animal Reproduction (JSAR)
収録物名	Journal of Reproduction and Development
巻(号)	65(2)
ページ	121-128
刊行年月	2019
言語	英語
ハンドルURL	https://hdl.handle.net/11094/78562
PISSN	09168818
eISSN	13484400
NCID	AA12018734
関連情報 (isIdenticalTo)	DOI (出版社版) https://doi.org/10.1262/jrd.2018-145
関連情報 (isIdenticalTo)	PMID 30613052
アクセス権	open access
権利情報	© 2019 the Society for Reproduction and Development. This article is licensed under a Creative Commons Attribution 4.0 International License.
出版タイプ	Version of Record
カテゴリ	学術雑誌論文 Journal Article

資源タイプ	学術雑誌論文
ローカル資源タイプ	学術雑誌論文
DCTERMS.bibliographicCitation	Journal of Reproduction and Development. 2019, 65(2), p. 121-128
DC.title	An azoospermic factor gene, Ddx3y and its paralog, Ddx3x are dispensable in germ cells for male fertility
DC.creator	Matsumura, Takafumi
	Endo, Tsutomu
	Isotani, Ayako
	Ogawa, Masaki
	Ikawa, Masahito
DC.publisher	The Japanese Society of Animal Reproduction (JSAR)
DC.language' scheme='DCTERMS.RFC1766	英語
DCTERMS.issued' scheme='DCTERMS.W3CDTF	2019
DC.identifier	https://doi.org/10.1262/jrd.2018-145
DC.subject	Azoospermia factor region
	Chimeric analysis
	CRISPR/Cas9
	Male infertility
	Y chromosome
DC.description	Takafumi MATSUMURA, Tsutomu ENDO, Ayako ISOTANI, Masaki OGAWA, Masahito IKAWA, An azoospermic factor gene, Ddx3y and its paralog, Ddx3x are dispensable in germ cells for male fertility, Journal of Reproduction and Development, 2019, Volume 65, Issue 2, Pages 121-128, Released April 12, 2019, [Advance publication] Released January 07, 2019, Online ISSN 1348-4400, Print ISSN 0916-8818, https://doi.org/10.1262/jrd.2018-145, https://www.jstage.jst.go.jp/article/jrd/65/2/65_2018-145/_article/-char/en
DCTERMS.abstract	About 10% of male infertile patients show abnormalities in spermatogenesis. The microdeletion of azoospermia factor a (AZFa) region of the Y chromosome is thought to be a cause of spermatogenic failure. However, candidate gene responsible for the spermatogenic failure in AZFa deleted patients has not been elucidated yet. Using mice, we explored the function of Ddx3y, a strong candidate gene in the Azfa region, and Ddx3x, a Ddx3y paralog on the X chromosome, in spermatogenesis. We first generated Ddx3y KO male mice using CRISPR/Cas9 and found that the Ddx3y KO male mice show normal spermatogenesis, produce morphologically normal spermatozoa, and sire healthy offspring. Because Ddx3x KO males were embryonic lethal, we next generated chimeric mice, which contain Ddx3x and Ddx3y double KO (dKO) germ cells, and found that the dKO germ cells can differentiate into spermatozoa and transmit their mutant alleles to offspring by normal mating. We conclude that Ddx3x and Ddx3y are dispensable for spermatogenesis at least in mice. Unlike human, mice have an additional Ddx3y paralog D1pas1, that has been reported to be essential for spermatogenesis. These findings suggest that human and mouse DDX3 related proteins have distinct differences in their functions.
DC.rights	© 2019 the Society for Reproduction and Development. This article is licensed under a Creative Commons Attribution 4.0 International License.
DC.format	78562
citation_title	An azoospermic factor gene, Ddx3y and its paralog, Ddx3x are dispensable in germ cells for male fertility
citation_author	Matsumura, Takafumi
	Endo, Tsutomu
	Isotani, Ayako
	Ogawa, Masaki
	Ikawa, Masahito
citation_publisher	The Japanese Society of Animal Reproduction (JSAR)
citation_language	英語
citation_date	2019
citation_journal_title	Journal of Reproduction and Development
citation_volume	65
citation_issue	2
citation_firstpage	121
citation_lastpage	128
citation_doi	https://doi.org/10.1262/jrd.2018-145
citation_pmid	30613052
citation_public_url	https://hdl.handle.net/11094/78562

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