Klf4 glutamylation is required for cell reprogramming and early embryonic development in mice

Temporal and spatial-specific regulation of pluripotency networks is largely dependent on the precise modifications of core transcription factors. Misregulation of glutamylation is implicated in severe physiological abnormalities. However, how glutamylation regulates cell reprogramming and pluripote...

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Veröffentlicht in:Nature communications Jg. 9; H. 1; S. 1261 - 16
Hauptverfasser: Ye, Buqing, Liu, Benyu, Hao, Lu, Zhu, Xiaoxiao, Yang, Liuliu, Wang, Shuo, Xia, Pengyan, Du, Ying, Meng, Shu, Huang, Guanling, Qin, Xiwen, Wang, Yanying, Yan, Xinlong, Li, Chong, Hao, Junfeng, Zhu, Pingping, He, Luyun, Tian, Yong, Fan, Zusen
Format: Journal Article
Sprache:Englisch
Veröffentlicht: London Nature Publishing Group UK 28.03.2018
Nature Publishing Group
Nature Portfolio
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38/88
42/41
631/136/2444
631/136/532/2064/2158
631/136/532/2435
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Abnormalities
Animals
Carboxypeptidases - deficiency
Cell Differentiation
Cellular Reprogramming
Clonal deletion
Embryo cells
Embryogenesis
Embryonic growth stage
Embryonic Stem Cells - cytology
Female
Fibroblasts - cytology
Gene Deletion
Gene Expression Regulation, Developmental
Gene Knock-In Techniques
Glutamine - chemistry
HEK293 Cells
Humanities and Social Sciences
Humans
Induced Pluripotent Stem Cells - cytology
KLF4 protein
Kruppel-Like Transcription Factors - metabolism
Lethality
Lysine
Mice
multidisciplinary
Nerve Tissue Proteins - deficiency
Peptide Synthases - metabolism
Peptides - chemistry
Physiological effects
Pluripotency
Science
Science (multidisciplinary)
Stem cell transplantation
Stem cells
Transcription factors
Tubulin
Tyrosine
Ubiquitination
ISSN:2041-1723, 2041-1723
Online-Zugang:Volltext
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Abstract Temporal and spatial-specific regulation of pluripotency networks is largely dependent on the precise modifications of core transcription factors. Misregulation of glutamylation is implicated in severe physiological abnormalities. However, how glutamylation regulates cell reprogramming and pluripotency networks remains elusive. Here we show that cytosolic carboxypeptidases 1 (CCP1) or CCP6 deficiency substantially promotes induced pluripotent cell (iPSC) induction and pluripotency of embryonic stem cells (ESCs). Klf4 polyglutamylation at Glu381 by tubulin tyrosine ligase-like 4 (TTLL4) and TTLL1 during cell reprogramming impedes its lysine 48-linked ubiquitination and sustains Klf4 stability. Klf4-E381A knockin mice display impaired blastocyst development and embryonic lethality. Deletion of TTLL4 or TTLL1 abrogates cell reprogramming and early embryogenesis. Thus, Klf4 polyglutamylation plays a critical role in the regulation of cell reprogramming and pluripotency maintenance. Embryonic stem cell pluripotency depends upon precise regulation by a core transcription network. Here the authors show that polyglutamylation mediated stabilization of the transcription factor Klf4 by TTLL1 and TTLL4 promotes reprogramming, pluripotency and preimplantation embryonic development.
AbstractList Temporal and spatial-specific regulation of pluripotency networks is largely dependent on the precise modifications of core transcription factors. Misregulation of glutamylation is implicated in severe physiological abnormalities. However, how glutamylation regulates cell reprogramming and pluripotency networks remains elusive. Here we show that cytosolic carboxypeptidases 1 (CCP1) or CCP6 deficiency substantially promotes induced pluripotent cell (iPSC) induction and pluripotency of embryonic stem cells (ESCs). Klf4 polyglutamylation at Glu381 by tubulin tyrosine ligase-like 4 (TTLL4) and TTLL1 during cell reprogramming impedes its lysine 48-linked ubiquitination and sustains Klf4 stability. Klf4-E381A knockin mice display impaired blastocyst development and embryonic lethality. Deletion of TTLL4 or TTLL1 abrogates cell reprogramming and early embryogenesis. Thus, Klf4 polyglutamylation plays a critical role in the regulation of cell reprogramming and pluripotency maintenance. Embryonic stem cell pluripotency depends upon precise regulation by a core transcription network. Here the authors show that polyglutamylation mediated stabilization of the transcription factor Klf4 by TTLL1 and TTLL4 promotes reprogramming, pluripotency and preimplantation embryonic development.
Temporal and spatial-specific regulation of pluripotency networks is largely dependent on the precise modifications of core transcription factors. Misregulation of glutamylation is implicated in severe physiological abnormalities. However, how glutamylation regulates cell reprogramming and pluripotency networks remains elusive. Here we show that cytosolic carboxypeptidases 1 (CCP1) or CCP6 deficiency substantially promotes induced pluripotent cell (iPSC) induction and pluripotency of embryonic stem cells (ESCs). Klf4 polyglutamylation at Glu381 by tubulin tyrosine ligase-like 4 (TTLL4) and TTLL1 during cell reprogramming impedes its lysine 48-linked ubiquitination and sustains Klf4 stability. Klf4-E381A knockin mice display impaired blastocyst development and embryonic lethality. Deletion of TTLL4 or TTLL1 abrogates cell reprogramming and early embryogenesis. Thus, Klf4 polyglutamylation plays a critical role in the regulation of cell reprogramming and pluripotency maintenance.
Temporal and spatial-specific regulation of pluripotency networks is largely dependent on the precise modifications of core transcription factors. Misregulation of glutamylation is implicated in severe physiological abnormalities. However, how glutamylation regulates cell reprogramming and pluripotency networks remains elusive. Here we show that cytosolic carboxypeptidases 1 (CCP1) or CCP6 deficiency substantially promotes induced pluripotent cell (iPSC) induction and pluripotency of embryonic stem cells (ESCs). Klf4 polyglutamylation at Glu381 by tubulin tyrosine ligase-like 4 (TTLL4) and TTLL1 during cell reprogramming impedes its lysine 48-linked ubiquitination and sustains Klf4 stability. Klf4-E381A knockin mice display impaired blastocyst development and embryonic lethality. Deletion of TTLL4 or TTLL1 abrogates cell reprogramming and early embryogenesis. Thus, Klf4 polyglutamylation plays a critical role in the regulation of cell reprogramming and pluripotency maintenance.Temporal and spatial-specific regulation of pluripotency networks is largely dependent on the precise modifications of core transcription factors. Misregulation of glutamylation is implicated in severe physiological abnormalities. However, how glutamylation regulates cell reprogramming and pluripotency networks remains elusive. Here we show that cytosolic carboxypeptidases 1 (CCP1) or CCP6 deficiency substantially promotes induced pluripotent cell (iPSC) induction and pluripotency of embryonic stem cells (ESCs). Klf4 polyglutamylation at Glu381 by tubulin tyrosine ligase-like 4 (TTLL4) and TTLL1 during cell reprogramming impedes its lysine 48-linked ubiquitination and sustains Klf4 stability. Klf4-E381A knockin mice display impaired blastocyst development and embryonic lethality. Deletion of TTLL4 or TTLL1 abrogates cell reprogramming and early embryogenesis. Thus, Klf4 polyglutamylation plays a critical role in the regulation of cell reprogramming and pluripotency maintenance.
Temporal and spatial-specific regulation of pluripotency networks is largely dependent on the precise modifications of core transcription factors. Misregulation of glutamylation is implicated in severe physiological abnormalities. However, how glutamylation regulates cell reprogramming and pluripotency networks remains elusive. Here we show that cytosolic carboxypeptidases 1 (CCP1) or CCP6 deficiency substantially promotes induced pluripotent cell (iPSC) induction and pluripotency of embryonic stem cells (ESCs). Klf4 polyglutamylation at Glu381 by tubulin tyrosine ligase-like 4 (TTLL4) and TTLL1 during cell reprogramming impedes its lysine 48-linked ubiquitination and sustains Klf4 stability. Klf4-E381A knockin mice display impaired blastocyst development and embryonic lethality. Deletion of TTLL4 or TTLL1 abrogates cell reprogramming and early embryogenesis. Thus, Klf4 polyglutamylation plays a critical role in the regulation of cell reprogramming and pluripotency maintenance. Embryonic stem cell pluripotency depends upon precise regulation by a core transcription network. Here the authors show that polyglutamylation mediated stabilization of the transcription factor Klf4 by TTLL1 and TTLL4 promotes reprogramming, pluripotency and preimplantation embryonic development.
Embryonic stem cell pluripotency depends upon precise regulation by a core transcription network. Here the authors show that polyglutamylation mediated stabilization of the transcription factor Klf4 by TTLL1 and TTLL4 promotes reprogramming, pluripotency and preimplantation embryonic development.
ArticleNumber 1261
Author Wang, Shuo
Huang, Guanling
Hao, Junfeng
Meng, Shu
Qin, Xiwen
Hao, Lu
Du, Ying
Fan, Zusen
Zhu, Xiaoxiao
Li, Chong
Tian, Yong
Ye, Buqing
Yan, Xinlong
Wang, Yanying
Zhu, Pingping
Xia, Pengyan
He, Luyun
Liu, Benyu
Yang, Liuliu
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  givenname: Pengyan
  orcidid: 0000-0002-6210-4011
  surname: Xia
  fullname: Xia, Pengyan
  organization: Key Laboratory of Infection and Immunity of CAS, CAS Center for Excellence in Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences
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  givenname: Ying
  surname: Du
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  organization: Key Laboratory of Infection and Immunity of CAS, CAS Center for Excellence in Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences
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  organization: Laboratory Animal Center, Institute of Biophysics, Chinese Academy of Sciences, Key Laboratory of RNA Biology, Institute of Biophysics, Chinese Academy of Sciences
– sequence: 10
  givenname: Guanling
  surname: Huang
  fullname: Huang, Guanling
  organization: Key Laboratory of Infection and Immunity of CAS, CAS Center for Excellence in Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, University of Chinese Academy of Sciences
– sequence: 11
  givenname: Xiwen
  surname: Qin
  fullname: Qin, Xiwen
  organization: Key Laboratory of Infection and Immunity of CAS, CAS Center for Excellence in Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, University of Chinese Academy of Sciences
– sequence: 12
  givenname: Yanying
  surname: Wang
  fullname: Wang, Yanying
  organization: Key Laboratory of Infection and Immunity of CAS, CAS Center for Excellence in Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences
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  givenname: Xinlong
  surname: Yan
  fullname: Yan, Xinlong
  organization: Key Laboratory of Infection and Immunity of CAS, CAS Center for Excellence in Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences
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  givenname: Chong
  surname: Li
  fullname: Li, Chong
  organization: Key Laboratory of Infection and Immunity of CAS, CAS Center for Excellence in Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences
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  givenname: Junfeng
  surname: Hao
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  organization: Laboratory Animal Center, Institute of Biophysics, Chinese Academy of Sciences
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  givenname: Pingping
  surname: Zhu
  fullname: Zhu, Pingping
  organization: Key Laboratory of Infection and Immunity of CAS, CAS Center for Excellence in Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, University of Chinese Academy of Sciences
– sequence: 17
  givenname: Luyun
  surname: He
  fullname: He, Luyun
  organization: Key Laboratory of Infection and Immunity of CAS, CAS Center for Excellence in Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, University of Chinese Academy of Sciences
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  givenname: Yong
  orcidid: 0000-0002-8790-1148
  surname: Tian
  fullname: Tian, Yong
  email: ytian@ibp.ac.cn
  organization: Key Laboratory of RNA Biology, Institute of Biophysics, Chinese Academy of Sciences
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  givenname: Zusen
  orcidid: 0000-0002-7866-8217
  surname: Fan
  fullname: Fan, Zusen
  email: fanz@moon.ibp.ac.cn
  organization: Key Laboratory of Infection and Immunity of CAS, CAS Center for Excellence in Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, University of Chinese Academy of Sciences
BackLink https://www.ncbi.nlm.nih.gov/pubmed/29593216$$D View this record in MEDLINE/PubMed
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2018. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
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Snippet Temporal and spatial-specific regulation of pluripotency networks is largely dependent on the precise modifications of core transcription factors....
Embryonic stem cell pluripotency depends upon precise regulation by a core transcription network. Here the authors show that polyglutamylation mediated...
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StartPage 1261
SubjectTerms 13
13/100
14
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38
38/88
42/41
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631/136/532/2064/2158
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Abnormalities
Animals
Carboxypeptidases - deficiency
Cell Differentiation
Cellular Reprogramming
Clonal deletion
Embryo cells
Embryogenesis
Embryonic growth stage
Embryonic Stem Cells - cytology
Female
Fibroblasts - cytology
Gene Deletion
Gene Expression Regulation, Developmental
Gene Knock-In Techniques
Glutamine - chemistry
HEK293 Cells
Humanities and Social Sciences
Humans
Induced Pluripotent Stem Cells - cytology
KLF4 protein
Kruppel-Like Transcription Factors - metabolism
Lethality
Lysine
Mice
multidisciplinary
Nerve Tissue Proteins - deficiency
Peptide Synthases - metabolism
Peptides - chemistry
Physiological effects
Pluripotency
Science
Science (multidisciplinary)
Stem cell transplantation
Stem cells
Transcription factors
Tubulin
Tyrosine
Ubiquitination
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Title Klf4 glutamylation is required for cell reprogramming and early embryonic development in mice
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