Combined Loss of JMJD1A and JMJD1B Reveals Critical Roles for H3K9 Demethylation in the Maintenance of Embryonic Stem Cells and Early Embryogenesis

Summary: Histone H3 lysine 9 (H3K9) methylation is unevenly distributed in mammalian chromosomes. However, the molecular mechanism controlling the uneven distribution and its biological significance remain to be elucidated. Here, we show that JMJD1A and JMJD1B preferentially target H3K9 demethylatio...
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Autor*in:	Shunsuke Kuroki [verfasserIn] Yuji Nakai [verfasserIn] Ryo Maeda [verfasserIn] Naoki Okashita [verfasserIn] Mika Akiyoshi [verfasserIn] Yutaro Yamaguchi [verfasserIn] Satsuki Kitano [verfasserIn] Hitoshi Miyachi [verfasserIn] Ryuichiro Nakato [verfasserIn] Kenji Ichiyanagi [verfasserIn] Katsuhiko Shirahige [verfasserIn] Hiroshi Kimura [verfasserIn] Yoichi Shinkai [verfasserIn] Makoto Tachibana [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2018

Übergeordnetes Werk:	In: Stem Cell Reports - Elsevier, 2015, 10(2018), 4, Seite 1340-1354
Übergeordnetes Werk:	volume:10 ; year:2018 ; number:4 ; pages:1340-1354

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1016/j.stemcr.2018.02.002

Katalog-ID:	DOAJ039429199

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520			\|a Summary: Histone H3 lysine 9 (H3K9) methylation is unevenly distributed in mammalian chromosomes. However, the molecular mechanism controlling the uneven distribution and its biological significance remain to be elucidated. Here, we show that JMJD1A and JMJD1B preferentially target H3K9 demethylation of gene-dense regions of chromosomes, thereby establishing an H3K9 hypomethylation state in euchromatin. JMJD1A/JMJD1B-deficient embryos died soon after implantation accompanying epiblast cell death. Furthermore, combined loss of JMJD1A and JMJD1B caused perturbed expression of metabolic genes and rapid cell death in embryonic stem cells (ESCs). These results indicate that JMJD1A/JMJD1B-meditated H3K9 demethylation has critical roles for early embryogenesis and ESC maintenance. Finally, genetic rescue experiments clarified that H3K9 overmethylation by G9A was the cause of the cell death and perturbed gene expression of JMJD1A/JMJD1B-depleted ESCs. We summarized that JMJD1A and JMJD1B, in combination, ensure early embryogenesis and ESC viability by establishing the correct H3K9 methylated epigenome. : Kuroki et al. showed that H3K9 demethylases JMJD1A and JMJD1B are redundantly but essentially required for ESC survival and early embryogenesis in mice. JMJD1A and JMJD1B ensure transcription accuracy by demethylating H3K9 at gene-dense euchromatin. Keywords: histone methylation, histone demethylation, transcription, embryonic stem cell
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700	0		\|a Ryo Maeda \|e verfasserin \|4 aut
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700	0		\|a Mika Akiyoshi \|e verfasserin \|4 aut
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700	0		\|a Hitoshi Miyachi \|e verfasserin \|4 aut
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700	0		\|a Kenji Ichiyanagi \|e verfasserin \|4 aut
700	0		\|a Katsuhiko Shirahige \|e verfasserin \|4 aut
700	0		\|a Hiroshi Kimura \|e verfasserin \|4 aut
700	0		\|a Yoichi Shinkai \|e verfasserin \|4 aut
700	0		\|a Makoto Tachibana \|e verfasserin \|4 aut
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Indexfelder

author_variant	s k sk y n yn r m rm n o no m a ma y y yy s k sk h m hm r n rn k i ki k s ks h k hk y s ys m t mt
matchkey_str	article:22136711:2018----::obndosfmdanjj1rvasrtcloefr39eehltoiteaneacoeby
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publishDate	2018
allfields	10.1016/j.stemcr.2018.02.002 doi (DE-627)DOAJ039429199 (DE-599)DOAJ873a67a4ed0542c7beb080526a64f47b DE-627 ger DE-627 rakwb eng R5-920 QH301-705.5 Shunsuke Kuroki verfasserin aut Combined Loss of JMJD1A and JMJD1B Reveals Critical Roles for H3K9 Demethylation in the Maintenance of Embryonic Stem Cells and Early Embryogenesis 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary: Histone H3 lysine 9 (H3K9) methylation is unevenly distributed in mammalian chromosomes. However, the molecular mechanism controlling the uneven distribution and its biological significance remain to be elucidated. Here, we show that JMJD1A and JMJD1B preferentially target H3K9 demethylation of gene-dense regions of chromosomes, thereby establishing an H3K9 hypomethylation state in euchromatin. JMJD1A/JMJD1B-deficient embryos died soon after implantation accompanying epiblast cell death. Furthermore, combined loss of JMJD1A and JMJD1B caused perturbed expression of metabolic genes and rapid cell death in embryonic stem cells (ESCs). These results indicate that JMJD1A/JMJD1B-meditated H3K9 demethylation has critical roles for early embryogenesis and ESC maintenance. Finally, genetic rescue experiments clarified that H3K9 overmethylation by G9A was the cause of the cell death and perturbed gene expression of JMJD1A/JMJD1B-depleted ESCs. We summarized that JMJD1A and JMJD1B, in combination, ensure early embryogenesis and ESC viability by establishing the correct H3K9 methylated epigenome. : Kuroki et al. showed that H3K9 demethylases JMJD1A and JMJD1B are redundantly but essentially required for ESC survival and early embryogenesis in mice. JMJD1A and JMJD1B ensure transcription accuracy by demethylating H3K9 at gene-dense euchromatin. Keywords: histone methylation, histone demethylation, transcription, embryonic stem cell Medicine (General) Biology (General) Yuji Nakai verfasserin aut Ryo Maeda verfasserin aut Naoki Okashita verfasserin aut Mika Akiyoshi verfasserin aut Yutaro Yamaguchi verfasserin aut Satsuki Kitano verfasserin aut Hitoshi Miyachi verfasserin aut Ryuichiro Nakato verfasserin aut Kenji Ichiyanagi verfasserin aut Katsuhiko Shirahige verfasserin aut Hiroshi Kimura verfasserin aut Yoichi Shinkai verfasserin aut Makoto Tachibana verfasserin aut In Stem Cell Reports Elsevier, 2015 10(2018), 4, Seite 1340-1354 (DE-627)749730862 (DE-600)2720528-9 22136711 nnns volume:10 year:2018 number:4 pages:1340-1354 https://doi.org/10.1016/j.stemcr.2018.02.002 kostenfrei https://doaj.org/article/873a67a4ed0542c7beb080526a64f47b kostenfrei http://www.sciencedirect.com/science/article/pii/S2213671118300936 kostenfrei https://doaj.org/toc/2213-6711 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 10 2018 4 1340-1354
spelling	10.1016/j.stemcr.2018.02.002 doi (DE-627)DOAJ039429199 (DE-599)DOAJ873a67a4ed0542c7beb080526a64f47b DE-627 ger DE-627 rakwb eng R5-920 QH301-705.5 Shunsuke Kuroki verfasserin aut Combined Loss of JMJD1A and JMJD1B Reveals Critical Roles for H3K9 Demethylation in the Maintenance of Embryonic Stem Cells and Early Embryogenesis 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary: Histone H3 lysine 9 (H3K9) methylation is unevenly distributed in mammalian chromosomes. However, the molecular mechanism controlling the uneven distribution and its biological significance remain to be elucidated. Here, we show that JMJD1A and JMJD1B preferentially target H3K9 demethylation of gene-dense regions of chromosomes, thereby establishing an H3K9 hypomethylation state in euchromatin. JMJD1A/JMJD1B-deficient embryos died soon after implantation accompanying epiblast cell death. Furthermore, combined loss of JMJD1A and JMJD1B caused perturbed expression of metabolic genes and rapid cell death in embryonic stem cells (ESCs). These results indicate that JMJD1A/JMJD1B-meditated H3K9 demethylation has critical roles for early embryogenesis and ESC maintenance. Finally, genetic rescue experiments clarified that H3K9 overmethylation by G9A was the cause of the cell death and perturbed gene expression of JMJD1A/JMJD1B-depleted ESCs. We summarized that JMJD1A and JMJD1B, in combination, ensure early embryogenesis and ESC viability by establishing the correct H3K9 methylated epigenome. : Kuroki et al. showed that H3K9 demethylases JMJD1A and JMJD1B are redundantly but essentially required for ESC survival and early embryogenesis in mice. JMJD1A and JMJD1B ensure transcription accuracy by demethylating H3K9 at gene-dense euchromatin. Keywords: histone methylation, histone demethylation, transcription, embryonic stem cell Medicine (General) Biology (General) Yuji Nakai verfasserin aut Ryo Maeda verfasserin aut Naoki Okashita verfasserin aut Mika Akiyoshi verfasserin aut Yutaro Yamaguchi verfasserin aut Satsuki Kitano verfasserin aut Hitoshi Miyachi verfasserin aut Ryuichiro Nakato verfasserin aut Kenji Ichiyanagi verfasserin aut Katsuhiko Shirahige verfasserin aut Hiroshi Kimura verfasserin aut Yoichi Shinkai verfasserin aut Makoto Tachibana verfasserin aut In Stem Cell Reports Elsevier, 2015 10(2018), 4, Seite 1340-1354 (DE-627)749730862 (DE-600)2720528-9 22136711 nnns volume:10 year:2018 number:4 pages:1340-1354 https://doi.org/10.1016/j.stemcr.2018.02.002 kostenfrei https://doaj.org/article/873a67a4ed0542c7beb080526a64f47b kostenfrei http://www.sciencedirect.com/science/article/pii/S2213671118300936 kostenfrei https://doaj.org/toc/2213-6711 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 10 2018 4 1340-1354
allfields_unstemmed	10.1016/j.stemcr.2018.02.002 doi (DE-627)DOAJ039429199 (DE-599)DOAJ873a67a4ed0542c7beb080526a64f47b DE-627 ger DE-627 rakwb eng R5-920 QH301-705.5 Shunsuke Kuroki verfasserin aut Combined Loss of JMJD1A and JMJD1B Reveals Critical Roles for H3K9 Demethylation in the Maintenance of Embryonic Stem Cells and Early Embryogenesis 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary: Histone H3 lysine 9 (H3K9) methylation is unevenly distributed in mammalian chromosomes. However, the molecular mechanism controlling the uneven distribution and its biological significance remain to be elucidated. Here, we show that JMJD1A and JMJD1B preferentially target H3K9 demethylation of gene-dense regions of chromosomes, thereby establishing an H3K9 hypomethylation state in euchromatin. JMJD1A/JMJD1B-deficient embryos died soon after implantation accompanying epiblast cell death. Furthermore, combined loss of JMJD1A and JMJD1B caused perturbed expression of metabolic genes and rapid cell death in embryonic stem cells (ESCs). These results indicate that JMJD1A/JMJD1B-meditated H3K9 demethylation has critical roles for early embryogenesis and ESC maintenance. Finally, genetic rescue experiments clarified that H3K9 overmethylation by G9A was the cause of the cell death and perturbed gene expression of JMJD1A/JMJD1B-depleted ESCs. We summarized that JMJD1A and JMJD1B, in combination, ensure early embryogenesis and ESC viability by establishing the correct H3K9 methylated epigenome. : Kuroki et al. showed that H3K9 demethylases JMJD1A and JMJD1B are redundantly but essentially required for ESC survival and early embryogenesis in mice. JMJD1A and JMJD1B ensure transcription accuracy by demethylating H3K9 at gene-dense euchromatin. Keywords: histone methylation, histone demethylation, transcription, embryonic stem cell Medicine (General) Biology (General) Yuji Nakai verfasserin aut Ryo Maeda verfasserin aut Naoki Okashita verfasserin aut Mika Akiyoshi verfasserin aut Yutaro Yamaguchi verfasserin aut Satsuki Kitano verfasserin aut Hitoshi Miyachi verfasserin aut Ryuichiro Nakato verfasserin aut Kenji Ichiyanagi verfasserin aut Katsuhiko Shirahige verfasserin aut Hiroshi Kimura verfasserin aut Yoichi Shinkai verfasserin aut Makoto Tachibana verfasserin aut In Stem Cell Reports Elsevier, 2015 10(2018), 4, Seite 1340-1354 (DE-627)749730862 (DE-600)2720528-9 22136711 nnns volume:10 year:2018 number:4 pages:1340-1354 https://doi.org/10.1016/j.stemcr.2018.02.002 kostenfrei https://doaj.org/article/873a67a4ed0542c7beb080526a64f47b kostenfrei http://www.sciencedirect.com/science/article/pii/S2213671118300936 kostenfrei https://doaj.org/toc/2213-6711 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 10 2018 4 1340-1354
allfieldsGer	10.1016/j.stemcr.2018.02.002 doi (DE-627)DOAJ039429199 (DE-599)DOAJ873a67a4ed0542c7beb080526a64f47b DE-627 ger DE-627 rakwb eng R5-920 QH301-705.5 Shunsuke Kuroki verfasserin aut Combined Loss of JMJD1A and JMJD1B Reveals Critical Roles for H3K9 Demethylation in the Maintenance of Embryonic Stem Cells and Early Embryogenesis 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary: Histone H3 lysine 9 (H3K9) methylation is unevenly distributed in mammalian chromosomes. However, the molecular mechanism controlling the uneven distribution and its biological significance remain to be elucidated. Here, we show that JMJD1A and JMJD1B preferentially target H3K9 demethylation of gene-dense regions of chromosomes, thereby establishing an H3K9 hypomethylation state in euchromatin. JMJD1A/JMJD1B-deficient embryos died soon after implantation accompanying epiblast cell death. Furthermore, combined loss of JMJD1A and JMJD1B caused perturbed expression of metabolic genes and rapid cell death in embryonic stem cells (ESCs). These results indicate that JMJD1A/JMJD1B-meditated H3K9 demethylation has critical roles for early embryogenesis and ESC maintenance. Finally, genetic rescue experiments clarified that H3K9 overmethylation by G9A was the cause of the cell death and perturbed gene expression of JMJD1A/JMJD1B-depleted ESCs. We summarized that JMJD1A and JMJD1B, in combination, ensure early embryogenesis and ESC viability by establishing the correct H3K9 methylated epigenome. : Kuroki et al. showed that H3K9 demethylases JMJD1A and JMJD1B are redundantly but essentially required for ESC survival and early embryogenesis in mice. JMJD1A and JMJD1B ensure transcription accuracy by demethylating H3K9 at gene-dense euchromatin. Keywords: histone methylation, histone demethylation, transcription, embryonic stem cell Medicine (General) Biology (General) Yuji Nakai verfasserin aut Ryo Maeda verfasserin aut Naoki Okashita verfasserin aut Mika Akiyoshi verfasserin aut Yutaro Yamaguchi verfasserin aut Satsuki Kitano verfasserin aut Hitoshi Miyachi verfasserin aut Ryuichiro Nakato verfasserin aut Kenji Ichiyanagi verfasserin aut Katsuhiko Shirahige verfasserin aut Hiroshi Kimura verfasserin aut Yoichi Shinkai verfasserin aut Makoto Tachibana verfasserin aut In Stem Cell Reports Elsevier, 2015 10(2018), 4, Seite 1340-1354 (DE-627)749730862 (DE-600)2720528-9 22136711 nnns volume:10 year:2018 number:4 pages:1340-1354 https://doi.org/10.1016/j.stemcr.2018.02.002 kostenfrei https://doaj.org/article/873a67a4ed0542c7beb080526a64f47b kostenfrei http://www.sciencedirect.com/science/article/pii/S2213671118300936 kostenfrei https://doaj.org/toc/2213-6711 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 10 2018 4 1340-1354
allfieldsSound	10.1016/j.stemcr.2018.02.002 doi (DE-627)DOAJ039429199 (DE-599)DOAJ873a67a4ed0542c7beb080526a64f47b DE-627 ger DE-627 rakwb eng R5-920 QH301-705.5 Shunsuke Kuroki verfasserin aut Combined Loss of JMJD1A and JMJD1B Reveals Critical Roles for H3K9 Demethylation in the Maintenance of Embryonic Stem Cells and Early Embryogenesis 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary: Histone H3 lysine 9 (H3K9) methylation is unevenly distributed in mammalian chromosomes. However, the molecular mechanism controlling the uneven distribution and its biological significance remain to be elucidated. Here, we show that JMJD1A and JMJD1B preferentially target H3K9 demethylation of gene-dense regions of chromosomes, thereby establishing an H3K9 hypomethylation state in euchromatin. JMJD1A/JMJD1B-deficient embryos died soon after implantation accompanying epiblast cell death. Furthermore, combined loss of JMJD1A and JMJD1B caused perturbed expression of metabolic genes and rapid cell death in embryonic stem cells (ESCs). These results indicate that JMJD1A/JMJD1B-meditated H3K9 demethylation has critical roles for early embryogenesis and ESC maintenance. Finally, genetic rescue experiments clarified that H3K9 overmethylation by G9A was the cause of the cell death and perturbed gene expression of JMJD1A/JMJD1B-depleted ESCs. We summarized that JMJD1A and JMJD1B, in combination, ensure early embryogenesis and ESC viability by establishing the correct H3K9 methylated epigenome. : Kuroki et al. showed that H3K9 demethylases JMJD1A and JMJD1B are redundantly but essentially required for ESC survival and early embryogenesis in mice. JMJD1A and JMJD1B ensure transcription accuracy by demethylating H3K9 at gene-dense euchromatin. Keywords: histone methylation, histone demethylation, transcription, embryonic stem cell Medicine (General) Biology (General) Yuji Nakai verfasserin aut Ryo Maeda verfasserin aut Naoki Okashita verfasserin aut Mika Akiyoshi verfasserin aut Yutaro Yamaguchi verfasserin aut Satsuki Kitano verfasserin aut Hitoshi Miyachi verfasserin aut Ryuichiro Nakato verfasserin aut Kenji Ichiyanagi verfasserin aut Katsuhiko Shirahige verfasserin aut Hiroshi Kimura verfasserin aut Yoichi Shinkai verfasserin aut Makoto Tachibana verfasserin aut In Stem Cell Reports Elsevier, 2015 10(2018), 4, Seite 1340-1354 (DE-627)749730862 (DE-600)2720528-9 22136711 nnns volume:10 year:2018 number:4 pages:1340-1354 https://doi.org/10.1016/j.stemcr.2018.02.002 kostenfrei https://doaj.org/article/873a67a4ed0542c7beb080526a64f47b kostenfrei http://www.sciencedirect.com/science/article/pii/S2213671118300936 kostenfrei https://doaj.org/toc/2213-6711 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 10 2018 4 1340-1354
language	English
source	In Stem Cell Reports 10(2018), 4, Seite 1340-1354 volume:10 year:2018 number:4 pages:1340-1354
sourceStr	In Stem Cell Reports 10(2018), 4, Seite 1340-1354 volume:10 year:2018 number:4 pages:1340-1354
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Medicine (General) Biology (General)
isfreeaccess_bool	true
container_title	Stem Cell Reports
authorswithroles_txt_mv	Shunsuke Kuroki @@aut@@ Yuji Nakai @@aut@@ Ryo Maeda @@aut@@ Naoki Okashita @@aut@@ Mika Akiyoshi @@aut@@ Yutaro Yamaguchi @@aut@@ Satsuki Kitano @@aut@@ Hitoshi Miyachi @@aut@@ Ryuichiro Nakato @@aut@@ Kenji Ichiyanagi @@aut@@ Katsuhiko Shirahige @@aut@@ Hiroshi Kimura @@aut@@ Yoichi Shinkai @@aut@@ Makoto Tachibana @@aut@@
publishDateDaySort_date	2018-01-01T00:00:00Z
hierarchy_top_id	749730862
id	DOAJ039429199
language_de	englisch
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However, the molecular mechanism controlling the uneven distribution and its biological significance remain to be elucidated. Here, we show that JMJD1A and JMJD1B preferentially target H3K9 demethylation of gene-dense regions of chromosomes, thereby establishing an H3K9 hypomethylation state in euchromatin. JMJD1A/JMJD1B-deficient embryos died soon after implantation accompanying epiblast cell death. Furthermore, combined loss of JMJD1A and JMJD1B caused perturbed expression of metabolic genes and rapid cell death in embryonic stem cells (ESCs). These results indicate that JMJD1A/JMJD1B-meditated H3K9 demethylation has critical roles for early embryogenesis and ESC maintenance. Finally, genetic rescue experiments clarified that H3K9 overmethylation by G9A was the cause of the cell death and perturbed gene expression of JMJD1A/JMJD1B-depleted ESCs. We summarized that JMJD1A and JMJD1B, in combination, ensure early embryogenesis and ESC viability by establishing the correct H3K9 methylated epigenome. : Kuroki et al. showed that H3K9 demethylases JMJD1A and JMJD1B are redundantly but essentially required for ESC survival and early embryogenesis in mice. JMJD1A and JMJD1B ensure transcription accuracy by demethylating H3K9 at gene-dense euchromatin. 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callnumber-first	R - Medicine
author	Shunsuke Kuroki
spellingShingle	Shunsuke Kuroki misc R5-920 misc QH301-705.5 misc Medicine (General) misc Biology (General) Combined Loss of JMJD1A and JMJD1B Reveals Critical Roles for H3K9 Demethylation in the Maintenance of Embryonic Stem Cells and Early Embryogenesis
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topic_title	R5-920 QH301-705.5 Combined Loss of JMJD1A and JMJD1B Reveals Critical Roles for H3K9 Demethylation in the Maintenance of Embryonic Stem Cells and Early Embryogenesis
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title	Combined Loss of JMJD1A and JMJD1B Reveals Critical Roles for H3K9 Demethylation in the Maintenance of Embryonic Stem Cells and Early Embryogenesis
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title_full	Combined Loss of JMJD1A and JMJD1B Reveals Critical Roles for H3K9 Demethylation in the Maintenance of Embryonic Stem Cells and Early Embryogenesis
author_sort	Shunsuke Kuroki
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author_browse	Shunsuke Kuroki Yuji Nakai Ryo Maeda Naoki Okashita Mika Akiyoshi Yutaro Yamaguchi Satsuki Kitano Hitoshi Miyachi Ryuichiro Nakato Kenji Ichiyanagi Katsuhiko Shirahige Hiroshi Kimura Yoichi Shinkai Makoto Tachibana
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title_sort	combined loss of jmjd1a and jmjd1b reveals critical roles for h3k9 demethylation in the maintenance of embryonic stem cells and early embryogenesis
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title_auth	Combined Loss of JMJD1A and JMJD1B Reveals Critical Roles for H3K9 Demethylation in the Maintenance of Embryonic Stem Cells and Early Embryogenesis
abstract	Summary: Histone H3 lysine 9 (H3K9) methylation is unevenly distributed in mammalian chromosomes. However, the molecular mechanism controlling the uneven distribution and its biological significance remain to be elucidated. Here, we show that JMJD1A and JMJD1B preferentially target H3K9 demethylation of gene-dense regions of chromosomes, thereby establishing an H3K9 hypomethylation state in euchromatin. JMJD1A/JMJD1B-deficient embryos died soon after implantation accompanying epiblast cell death. Furthermore, combined loss of JMJD1A and JMJD1B caused perturbed expression of metabolic genes and rapid cell death in embryonic stem cells (ESCs). These results indicate that JMJD1A/JMJD1B-meditated H3K9 demethylation has critical roles for early embryogenesis and ESC maintenance. Finally, genetic rescue experiments clarified that H3K9 overmethylation by G9A was the cause of the cell death and perturbed gene expression of JMJD1A/JMJD1B-depleted ESCs. We summarized that JMJD1A and JMJD1B, in combination, ensure early embryogenesis and ESC viability by establishing the correct H3K9 methylated epigenome. : Kuroki et al. showed that H3K9 demethylases JMJD1A and JMJD1B are redundantly but essentially required for ESC survival and early embryogenesis in mice. JMJD1A and JMJD1B ensure transcription accuracy by demethylating H3K9 at gene-dense euchromatin. Keywords: histone methylation, histone demethylation, transcription, embryonic stem cell
abstractGer	Summary: Histone H3 lysine 9 (H3K9) methylation is unevenly distributed in mammalian chromosomes. However, the molecular mechanism controlling the uneven distribution and its biological significance remain to be elucidated. Here, we show that JMJD1A and JMJD1B preferentially target H3K9 demethylation of gene-dense regions of chromosomes, thereby establishing an H3K9 hypomethylation state in euchromatin. JMJD1A/JMJD1B-deficient embryos died soon after implantation accompanying epiblast cell death. Furthermore, combined loss of JMJD1A and JMJD1B caused perturbed expression of metabolic genes and rapid cell death in embryonic stem cells (ESCs). These results indicate that JMJD1A/JMJD1B-meditated H3K9 demethylation has critical roles for early embryogenesis and ESC maintenance. Finally, genetic rescue experiments clarified that H3K9 overmethylation by G9A was the cause of the cell death and perturbed gene expression of JMJD1A/JMJD1B-depleted ESCs. We summarized that JMJD1A and JMJD1B, in combination, ensure early embryogenesis and ESC viability by establishing the correct H3K9 methylated epigenome. : Kuroki et al. showed that H3K9 demethylases JMJD1A and JMJD1B are redundantly but essentially required for ESC survival and early embryogenesis in mice. JMJD1A and JMJD1B ensure transcription accuracy by demethylating H3K9 at gene-dense euchromatin. Keywords: histone methylation, histone demethylation, transcription, embryonic stem cell
abstract_unstemmed	Summary: Histone H3 lysine 9 (H3K9) methylation is unevenly distributed in mammalian chromosomes. However, the molecular mechanism controlling the uneven distribution and its biological significance remain to be elucidated. Here, we show that JMJD1A and JMJD1B preferentially target H3K9 demethylation of gene-dense regions of chromosomes, thereby establishing an H3K9 hypomethylation state in euchromatin. JMJD1A/JMJD1B-deficient embryos died soon after implantation accompanying epiblast cell death. Furthermore, combined loss of JMJD1A and JMJD1B caused perturbed expression of metabolic genes and rapid cell death in embryonic stem cells (ESCs). These results indicate that JMJD1A/JMJD1B-meditated H3K9 demethylation has critical roles for early embryogenesis and ESC maintenance. Finally, genetic rescue experiments clarified that H3K9 overmethylation by G9A was the cause of the cell death and perturbed gene expression of JMJD1A/JMJD1B-depleted ESCs. We summarized that JMJD1A and JMJD1B, in combination, ensure early embryogenesis and ESC viability by establishing the correct H3K9 methylated epigenome. : Kuroki et al. showed that H3K9 demethylases JMJD1A and JMJD1B are redundantly but essentially required for ESC survival and early embryogenesis in mice. JMJD1A and JMJD1B ensure transcription accuracy by demethylating H3K9 at gene-dense euchromatin. Keywords: histone methylation, histone demethylation, transcription, embryonic stem cell
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title_short	Combined Loss of JMJD1A and JMJD1B Reveals Critical Roles for H3K9 Demethylation in the Maintenance of Embryonic Stem Cells and Early Embryogenesis
url	https://doi.org/10.1016/j.stemcr.2018.02.002 https://doaj.org/article/873a67a4ed0542c7beb080526a64f47b http://www.sciencedirect.com/science/article/pii/S2213671118300936 https://doaj.org/toc/2213-6711
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up_date	2024-07-03T23:18:28.530Z
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fullrecord_marcxml	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">DOAJ039429199</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230308031144.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230227s2018 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.stemcr.2018.02.002</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ039429199</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJ873a67a4ed0542c7beb080526a64f47b</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">R5-920</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">QH301-705.5</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Shunsuke Kuroki</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Combined Loss of JMJD1A and JMJD1B Reveals Critical Roles for H3K9 Demethylation in the Maintenance of Embryonic Stem Cells and Early Embryogenesis</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2018</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Summary: Histone H3 lysine 9 (H3K9) methylation is unevenly distributed in mammalian chromosomes. However, the molecular mechanism controlling the uneven distribution and its biological significance remain to be elucidated. Here, we show that JMJD1A and JMJD1B preferentially target H3K9 demethylation of gene-dense regions of chromosomes, thereby establishing an H3K9 hypomethylation state in euchromatin. JMJD1A/JMJD1B-deficient embryos died soon after implantation accompanying epiblast cell death. Furthermore, combined loss of JMJD1A and JMJD1B caused perturbed expression of metabolic genes and rapid cell death in embryonic stem cells (ESCs). These results indicate that JMJD1A/JMJD1B-meditated H3K9 demethylation has critical roles for early embryogenesis and ESC maintenance. Finally, genetic rescue experiments clarified that H3K9 overmethylation by G9A was the cause of the cell death and perturbed gene expression of JMJD1A/JMJD1B-depleted ESCs. We summarized that JMJD1A and JMJD1B, in combination, ensure early embryogenesis and ESC viability by establishing the correct H3K9 methylated epigenome. : Kuroki et al. showed that H3K9 demethylases JMJD1A and JMJD1B are redundantly but essentially required for ESC survival and early embryogenesis in mice. JMJD1A and JMJD1B ensure transcription accuracy by demethylating H3K9 at gene-dense euchromatin. 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Combined Loss of JMJD1A and JMJD1B Reveals Critical Roles for H3K9 Demethylation in the Maintenance of Embryonic Stem Cells and Early Embryogenesis

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