Histone deacetylation promotes mouse neural induction by restricting Nodal-dependent mesendoderm fate

Liu, Pingyu; Dou, Xiaoyang; Liu, Chang; Wang, Lingbo; Xing, Can; Peng, Guangdun; Chen, Jun; Yu, Fang; Qiao, Yong; Song, Lu; Wu, Yuxuan; Yue, Chunmei; Li, Jinsong; Han, Jing–Dong Jackie; Tang, Ke; Jing, Naihe

doi:10.1038/ncomms7830

Cited by 25 publications

(18 citation statements)

References 70 publications

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“…For example, Sin3a was shown to interact with HDACs, particularly HDAC1, to repress gene transcription ( 25 , 26 ). Interestingly, HDAC1 is a known transcriptional repressor of Lefty1 in ESCs ( 51 ). However, our results revealed that Sin3a mainly functions as a transcriptional coactivator for Lefty1 , suggesting that the regulation of Sin3a on Lefty1 expression might be independent of HDAC1.…”

Section: Discussionmentioning

confidence: 99%

Sin3a–Tet1 interaction activates gene transcription and is required for embryonic stem cell pluripotency

Zhu

et al. 2018

Nucleic Acids Research

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Sin3a is a core component of histone-deacetylation-activity-associated transcriptional repressor complex, playing important roles in early embryo development. Here, we reported that down-regulation of Sin3a led to the loss of embryonic stem cell (ESC) self-renewal and skewed differentiation into mesendoderm lineage. We found that Sin3a functioned as a transcriptional coactivator of the critical Nodal antagonist Lefty1 through interacting with Tet1 to de-methylate the Lefty1 promoter. Further studies showed that two amino acid residues (Phe147, Phe182) in the PAH1 domain of Sin3a are essential for Sin3a–Tet1 interaction and its activity in regulating pluripotency. Furthermore, genome-wide analyses of Sin3a, Tet1 and Pol II ChIP-seq and of 5mC MeDIP-seq revealed that Sin3a acted with Tet1 to facilitate the transcription of a set of their co-target genes. These results link Sin3a to epigenetic DNA modifications in transcriptional activation and have implications for understanding mechanisms underlying versatile functions of Sin3a in mouse ESCs.

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Section: Discussionmentioning

confidence: 99%

Sin3a–Tet1 interaction activates gene transcription and is required for embryonic stem cell pluripotency

Zhu

et al. 2018

Nucleic Acids Research

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“…Moreover, the reported effects of HDAC inhibition in cultured ESCs appear to vary significantly dependent on the inhibitor utilized, the concentration and duration of treatment and the source of the stem cells (murine versus human). Studies in cultured mouse and human ESCs revealed that levels of histone acetylation (H3K9/14Ac) increase and decrease dynamically when the cells are induced to differentiate (Hezroni et al, 2011;Liu et al, 2015;Markowetz et al, 2010;Melcer et al, 2012;Moussaieff et al, 2015;Qiao et al, 2015). Moreover, HDAC inhibition during differentiation of mouse epiblast stem cells (mEpiSCs) prevents neural differentiation, whereas, in hESCs, the effects are time dependent; early inhibition leads to maintenance of pluripotency, whereas later inhibition promotes neural fate commitment (Liu et al, 2015;Qiao et al, 2015;Yang et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

“…Studies in cultured mouse and human ESCs revealed that levels of histone acetylation (H3K9/14Ac) increase and decrease dynamically when the cells are induced to differentiate (Hezroni et al, 2011;Liu et al, 2015;Markowetz et al, 2010;Melcer et al, 2012;Moussaieff et al, 2015;Qiao et al, 2015). Moreover, HDAC inhibition during differentiation of mouse epiblast stem cells (mEpiSCs) prevents neural differentiation, whereas, in hESCs, the effects are time dependent; early inhibition leads to maintenance of pluripotency, whereas later inhibition promotes neural fate commitment (Liu et al, 2015;Qiao et al, 2015;Yang et al, 2014). It has been suggested that HDAC inhibition promotes the progression of naïve murine (m)ESCs towards a primed mEpiSC state, and hESCs to an earlier state, but in both cases, it promotes self-renewal of these cells (Ware et al, 2009).…”

Section: Discussionmentioning

confidence: 99%

Histone deacetylase activity has an essential role in establishing and maintaining the vertebrate neural crest

Rao

LaBonne

2018

Development

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The neural crest, a progenitor population that drove vertebrate evolution, retains the broad developmental potential of the blastula cells it is derived from, even as neighboring cells undergo lineage restriction. The mechanisms that enable these cells to preserve their developmental potential remain poorly understood. Here, we explore the role of histone deacetylase (HDAC) activity in this process in We show that HDAC activity is essential for the formation of neural crest, as well as for proper patterning of the early ectoderm. The requirement for HDAC activity initiates in naïve blastula cells; HDAC inhibition causes loss of pluripotency gene expression and blocks the ability of blastula stem cells to contribute to lineages of the three embryonic germ layers. We find that pluripotent naïve blastula cells and neural crest cells are both characterized by low levels of histone acetylation, and show that increasing HDAC1 levels enhance the ability of blastula cells to be reprogrammed to a neural crest state. Together, these findings elucidate a previously uncharacterized role for HDAC activity in establishing the neural crest stem cell state.

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“…Upon withdrawal of 2i, ES cells embark on a path to lineage commitment either in vitro or in vivo when injected into a pre-implantation embryo (Ying et al, 2008; Dunn et al, 2014; Marks et al, 2012). Recent studies have begun to explore the dissolution of naïve pluripotency and the route towards multi-lineage differentiation in vitro (Buecker et al, 2014; Leeb et al, 2014; Kurimoto et al, 2015; Thomson et al, 2011; Respuela et al, 2016; Yang et al, 2014; Betschinger et al, 2013; Davies et al, 2013; Liu et al, 2015; Acampora et al, 2013). However, differentiating cultures become heterogeneous (Marks et al, 2012; Kalkan and Smith, 2014; Buecker et al, 2014; Hayashi et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Tracking the embryonic stem cell transition from ground state pluripotency

et al. 2017

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Mouse embryonic stem (ES) cells are locked into self-renewal by shielding from inductive cues. Release from this ground state in minimal conditions offers a system for delineating developmental progression from naïve pluripotency. Here, we examine the initial transition process. The ES cell population behaves asynchronously. We therefore exploited a short-half-life Rex1::GFP reporter to isolate cells either side of exit from naïve status. Extinction of ES cell identity in single cells is acute. It occurs only after near-complete elimination of naïve pluripotency factors, but precedes appearance of lineage specification markers. Cells newly departed from the ES cell state display features of early post-implantation epiblast and are distinct from primed epiblast. They also exhibit a genome-wide increase in DNA methylation, intermediate between early and late epiblast. These findings are consistent with the proposition that naïve cells transition to a distinct formative phase of pluripotency preparatory to lineage priming.

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Histone deacetylation promotes mouse neural induction by restricting Nodal-dependent mesendoderm fate

Cited by 25 publications

References 70 publications

Sin3a–Tet1 interaction activates gene transcription and is required for embryonic stem cell pluripotency

Sin3a–Tet1 interaction activates gene transcription and is required for embryonic stem cell pluripotency

Histone deacetylase activity has an essential role in establishing and maintaining the vertebrate neural crest

Tracking the embryonic stem cell transition from ground state pluripotency

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