Quality control in oocytes by p63 is based on a spring-loaded activation mechanism on the molecular and cellular level

Mammalian oocytes are arrested in the dictyate stage of meiotic prophase I for long periods of time, during which the high concentration of the p53 family member TAp63α sensitizes them to DNA damage-induced apoptosis. TAp63α is kept in an inactive and exclusively dimeric state but undergoes rapid ph...
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Autor*in:	Daniel Coutandin [verfasserIn] Christian Osterburg [verfasserIn] Ratnesh Kumar Srivastav [verfasserIn] Manuela Sumyk [verfasserIn] Sebastian Kehrloesser [verfasserIn] Jakob Gebel [verfasserIn] Marcel Tuppi [verfasserIn] Jens Hannewald [verfasserIn] Birgit Schäfer [verfasserIn] Eidarus Salah [verfasserIn] Sebastian Mathea [verfasserIn] Uta Müller-Kuller [verfasserIn] James Doutch [verfasserIn] Manuel Grez [verfasserIn] Stefan Knapp [verfasserIn] Volker Dötsch [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2016

Schlagwörter:	DNA damage kinetically trapped state p63 quality control oocytes spring-loaded activation

Übergeordnetes Werk:	In: eLife - eLife Sciences Publications Ltd, 2013, 5(2016)
Übergeordnetes Werk:	volume:5 ; year:2016

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.7554/eLife.13909

Katalog-ID:	DOAJ084226765

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allfields	10.7554/eLife.13909 doi (DE-627)DOAJ084226765 (DE-599)DOAJdbeb5b0472134bb4993b7f21d2d2f81c DE-627 ger DE-627 rakwb eng QH301-705.5 Daniel Coutandin verfasserin aut Quality control in oocytes by p63 is based on a spring-loaded activation mechanism on the molecular and cellular level 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Mammalian oocytes are arrested in the dictyate stage of meiotic prophase I for long periods of time, during which the high concentration of the p53 family member TAp63α sensitizes them to DNA damage-induced apoptosis. TAp63α is kept in an inactive and exclusively dimeric state but undergoes rapid phosphorylation-induced tetramerization and concomitant activation upon detection of DNA damage. Here we show that the TAp63α dimer is a kinetically trapped state. Activation follows a spring-loaded mechanism not requiring further translation of other cellular factors in oocytes and is associated with unfolding of the inhibitory structure that blocks the tetramerization interface. Using a combination of biophysical methods as well as cell and ovary culture experiments we explain how TAp63α is kept inactive in the absence of DNA damage but causes rapid oocyte elimination in response to a few DNA double strand breaks thereby acting as the key quality control factor in maternal reproduction. DNA damage kinetically trapped state p63 quality control oocytes spring-loaded activation Medicine R Science Q Biology (General) Christian Osterburg verfasserin aut Ratnesh Kumar Srivastav verfasserin aut Manuela Sumyk verfasserin aut Sebastian Kehrloesser verfasserin aut Jakob Gebel verfasserin aut Marcel Tuppi verfasserin aut Jens Hannewald verfasserin aut Birgit Schäfer verfasserin aut Eidarus Salah verfasserin aut Sebastian Mathea verfasserin aut Uta Müller-Kuller verfasserin aut James Doutch verfasserin aut Manuel Grez verfasserin aut Stefan Knapp verfasserin aut Volker Dötsch verfasserin aut In eLife eLife Sciences Publications Ltd, 2013 5(2016) (DE-627)728518384 (DE-600)2687154-3 2050084X nnns volume:5 year:2016 https://doi.org/10.7554/eLife.13909 kostenfrei https://doaj.org/article/dbeb5b0472134bb4993b7f21d2d2f81c kostenfrei https://elifesciences.org/articles/13909 kostenfrei https://doaj.org/toc/2050-084X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 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_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2016
spelling	10.7554/eLife.13909 doi (DE-627)DOAJ084226765 (DE-599)DOAJdbeb5b0472134bb4993b7f21d2d2f81c DE-627 ger DE-627 rakwb eng QH301-705.5 Daniel Coutandin verfasserin aut Quality control in oocytes by p63 is based on a spring-loaded activation mechanism on the molecular and cellular level 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Mammalian oocytes are arrested in the dictyate stage of meiotic prophase I for long periods of time, during which the high concentration of the p53 family member TAp63α sensitizes them to DNA damage-induced apoptosis. TAp63α is kept in an inactive and exclusively dimeric state but undergoes rapid phosphorylation-induced tetramerization and concomitant activation upon detection of DNA damage. Here we show that the TAp63α dimer is a kinetically trapped state. Activation follows a spring-loaded mechanism not requiring further translation of other cellular factors in oocytes and is associated with unfolding of the inhibitory structure that blocks the tetramerization interface. Using a combination of biophysical methods as well as cell and ovary culture experiments we explain how TAp63α is kept inactive in the absence of DNA damage but causes rapid oocyte elimination in response to a few DNA double strand breaks thereby acting as the key quality control factor in maternal reproduction. DNA damage kinetically trapped state p63 quality control oocytes spring-loaded activation Medicine R Science Q Biology (General) Christian Osterburg verfasserin aut Ratnesh Kumar Srivastav verfasserin aut Manuela Sumyk verfasserin aut Sebastian Kehrloesser verfasserin aut Jakob Gebel verfasserin aut Marcel Tuppi verfasserin aut Jens Hannewald verfasserin aut Birgit Schäfer verfasserin aut Eidarus Salah verfasserin aut Sebastian Mathea verfasserin aut Uta Müller-Kuller verfasserin aut James Doutch verfasserin aut Manuel Grez verfasserin aut Stefan Knapp verfasserin aut Volker Dötsch verfasserin aut In eLife eLife Sciences Publications Ltd, 2013 5(2016) (DE-627)728518384 (DE-600)2687154-3 2050084X nnns volume:5 year:2016 https://doi.org/10.7554/eLife.13909 kostenfrei https://doaj.org/article/dbeb5b0472134bb4993b7f21d2d2f81c kostenfrei https://elifesciences.org/articles/13909 kostenfrei https://doaj.org/toc/2050-084X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 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_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2016
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allfieldsSound	10.7554/eLife.13909 doi (DE-627)DOAJ084226765 (DE-599)DOAJdbeb5b0472134bb4993b7f21d2d2f81c DE-627 ger DE-627 rakwb eng QH301-705.5 Daniel Coutandin verfasserin aut Quality control in oocytes by p63 is based on a spring-loaded activation mechanism on the molecular and cellular level 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Mammalian oocytes are arrested in the dictyate stage of meiotic prophase I for long periods of time, during which the high concentration of the p53 family member TAp63α sensitizes them to DNA damage-induced apoptosis. TAp63α is kept in an inactive and exclusively dimeric state but undergoes rapid phosphorylation-induced tetramerization and concomitant activation upon detection of DNA damage. Here we show that the TAp63α dimer is a kinetically trapped state. Activation follows a spring-loaded mechanism not requiring further translation of other cellular factors in oocytes and is associated with unfolding of the inhibitory structure that blocks the tetramerization interface. Using a combination of biophysical methods as well as cell and ovary culture experiments we explain how TAp63α is kept inactive in the absence of DNA damage but causes rapid oocyte elimination in response to a few DNA double strand breaks thereby acting as the key quality control factor in maternal reproduction. DNA damage kinetically trapped state p63 quality control oocytes spring-loaded activation Medicine R Science Q Biology (General) Christian Osterburg verfasserin aut Ratnesh Kumar Srivastav verfasserin aut Manuela Sumyk verfasserin aut Sebastian Kehrloesser verfasserin aut Jakob Gebel verfasserin aut Marcel Tuppi verfasserin aut Jens Hannewald verfasserin aut Birgit Schäfer verfasserin aut Eidarus Salah verfasserin aut Sebastian Mathea verfasserin aut Uta Müller-Kuller verfasserin aut James Doutch verfasserin aut Manuel Grez verfasserin aut Stefan Knapp verfasserin aut Volker Dötsch verfasserin aut In eLife eLife Sciences Publications Ltd, 2013 5(2016) (DE-627)728518384 (DE-600)2687154-3 2050084X nnns volume:5 year:2016 https://doi.org/10.7554/eLife.13909 kostenfrei https://doaj.org/article/dbeb5b0472134bb4993b7f21d2d2f81c kostenfrei https://elifesciences.org/articles/13909 kostenfrei https://doaj.org/toc/2050-084X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 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_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2016
language	English
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authorswithroles_txt_mv	Daniel Coutandin @@aut@@ Christian Osterburg @@aut@@ Ratnesh Kumar Srivastav @@aut@@ Manuela Sumyk @@aut@@ Sebastian Kehrloesser @@aut@@ Jakob Gebel @@aut@@ Marcel Tuppi @@aut@@ Jens Hannewald @@aut@@ Birgit Schäfer @@aut@@ Eidarus Salah @@aut@@ Sebastian Mathea @@aut@@ Uta Müller-Kuller @@aut@@ James Doutch @@aut@@ Manuel Grez @@aut@@ Stefan Knapp @@aut@@ Volker Dötsch @@aut@@
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callnumber-first	Q - Science
author	Daniel Coutandin
spellingShingle	Daniel Coutandin misc QH301-705.5 misc DNA damage misc kinetically trapped state misc p63 misc quality control misc oocytes misc spring-loaded activation misc Medicine misc R misc Science misc Q misc Biology (General) Quality control in oocytes by p63 is based on a spring-loaded activation mechanism on the molecular and cellular level
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topic_title	QH301-705.5 Quality control in oocytes by p63 is based on a spring-loaded activation mechanism on the molecular and cellular level DNA damage kinetically trapped state p63 quality control oocytes spring-loaded activation
topic	misc QH301-705.5 misc DNA damage misc kinetically trapped state misc p63 misc quality control misc oocytes misc spring-loaded activation misc Medicine misc R misc Science misc Q misc Biology (General)
topic_unstemmed	misc QH301-705.5 misc DNA damage misc kinetically trapped state misc p63 misc quality control misc oocytes misc spring-loaded activation misc Medicine misc R misc Science misc Q misc Biology (General)
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title	Quality control in oocytes by p63 is based on a spring-loaded activation mechanism on the molecular and cellular level
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title_full	Quality control in oocytes by p63 is based on a spring-loaded activation mechanism on the molecular and cellular level
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author_browse	Daniel Coutandin Christian Osterburg Ratnesh Kumar Srivastav Manuela Sumyk Sebastian Kehrloesser Jakob Gebel Marcel Tuppi Jens Hannewald Birgit Schäfer Eidarus Salah Sebastian Mathea Uta Müller-Kuller James Doutch Manuel Grez Stefan Knapp Volker Dötsch
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title_sort	quality control in oocytes by p63 is based on a spring-loaded activation mechanism on the molecular and cellular level
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title_auth	Quality control in oocytes by p63 is based on a spring-loaded activation mechanism on the molecular and cellular level
abstract	Mammalian oocytes are arrested in the dictyate stage of meiotic prophase I for long periods of time, during which the high concentration of the p53 family member TAp63α sensitizes them to DNA damage-induced apoptosis. TAp63α is kept in an inactive and exclusively dimeric state but undergoes rapid phosphorylation-induced tetramerization and concomitant activation upon detection of DNA damage. Here we show that the TAp63α dimer is a kinetically trapped state. Activation follows a spring-loaded mechanism not requiring further translation of other cellular factors in oocytes and is associated with unfolding of the inhibitory structure that blocks the tetramerization interface. Using a combination of biophysical methods as well as cell and ovary culture experiments we explain how TAp63α is kept inactive in the absence of DNA damage but causes rapid oocyte elimination in response to a few DNA double strand breaks thereby acting as the key quality control factor in maternal reproduction.
abstractGer	Mammalian oocytes are arrested in the dictyate stage of meiotic prophase I for long periods of time, during which the high concentration of the p53 family member TAp63α sensitizes them to DNA damage-induced apoptosis. TAp63α is kept in an inactive and exclusively dimeric state but undergoes rapid phosphorylation-induced tetramerization and concomitant activation upon detection of DNA damage. Here we show that the TAp63α dimer is a kinetically trapped state. Activation follows a spring-loaded mechanism not requiring further translation of other cellular factors in oocytes and is associated with unfolding of the inhibitory structure that blocks the tetramerization interface. Using a combination of biophysical methods as well as cell and ovary culture experiments we explain how TAp63α is kept inactive in the absence of DNA damage but causes rapid oocyte elimination in response to a few DNA double strand breaks thereby acting as the key quality control factor in maternal reproduction.
abstract_unstemmed	Mammalian oocytes are arrested in the dictyate stage of meiotic prophase I for long periods of time, during which the high concentration of the p53 family member TAp63α sensitizes them to DNA damage-induced apoptosis. TAp63α is kept in an inactive and exclusively dimeric state but undergoes rapid phosphorylation-induced tetramerization and concomitant activation upon detection of DNA damage. Here we show that the TAp63α dimer is a kinetically trapped state. Activation follows a spring-loaded mechanism not requiring further translation of other cellular factors in oocytes and is associated with unfolding of the inhibitory structure that blocks the tetramerization interface. Using a combination of biophysical methods as well as cell and ovary culture experiments we explain how TAp63α is kept inactive in the absence of DNA damage but causes rapid oocyte elimination in response to a few DNA double strand breaks thereby acting as the key quality control factor in maternal reproduction.
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title_short	Quality control in oocytes by p63 is based on a spring-loaded activation mechanism on the molecular and cellular level
url	https://doi.org/10.7554/eLife.13909 https://doaj.org/article/dbeb5b0472134bb4993b7f21d2d2f81c https://elifesciences.org/articles/13909 https://doaj.org/toc/2050-084X
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author2	Christian Osterburg Ratnesh Kumar Srivastav Manuela Sumyk Sebastian Kehrloesser Jakob Gebel Marcel Tuppi Jens Hannewald Birgit Schäfer Eidarus Salah Sebastian Mathea Uta Müller-Kuller James Doutch Manuel Grez Stefan Knapp Volker Dötsch
author2Str	Christian Osterburg Ratnesh Kumar Srivastav Manuela Sumyk Sebastian Kehrloesser Jakob Gebel Marcel Tuppi Jens Hannewald Birgit Schäfer Eidarus Salah Sebastian Mathea Uta Müller-Kuller James Doutch Manuel Grez Stefan Knapp Volker Dötsch
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up_date	2024-07-03T21:52:31.462Z
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Quality control in oocytes by p63 is based on a spring-loaded activation mechanism on the molecular and cellular level

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