HDAC1 and HDAC2 regulate oligodendrocyte differentiation by disrupting the β-catenin–TCF interaction

Feng, Yongzeng; Chen, Ying; Hoang, ThaoNguyen; Montgomery, Rusty L.; Xian, Zhao; Bu, Hong; Hu, Tom C.‐C.; Taketo, Makoto Mark; Es, Johan H. van; Clevers, Hans; Hsieh, Jenny; Bassel‐Duby, Rhonda; Olson, Eric N.; Lü, Qing

doi:10.1038/nn.2333

Cited by 514 publications

(625 citation statements)

References 51 publications

(83 reference statements)

Supporting

Mentioning

598

Contrasting

Unclassified

Order By: Relevance

“…Indeed, loss-of-function studies in mice provide important insights regarding the compensatory functions of HDAC1 and HDAC2 in regulating cell proliferation, apoptosis, and differentiation in different cell types and tissues. 8,28 Tissue-specific conditional knockout of Hdac1 or Hdac2 alone does not evoke an obvious phenotype in cardiomyocytes, 29 neuron precursors, 30 oligodendrocyte, 31 B cells, 32 embryonic epidermis, 33 and T cells, 34 whereas deletion of both genes results in severe phenotypes in all tissues examined. In contrast, results of other studies support the notion that HDAC1 and HDAC2 have distinct functions.…”

Section: Structure and Complexes Of Mammalian Hdac1 And Hdac2mentioning

confidence: 99%

HDAC1 and HDAC2 in mouse oocytes and preimplantation embryos: Specificity versus compensation

Schultz

2016

Cell Death Differ

View full text Add to dashboard Cite

Oocyte and preimplantation embryo development entail dynamic changes in chromatin structure and gene expression, which are regulated by a number of maternal and zygotic epigenetic factors. Histone deacetylases (HDACs), which tighten chromatin structure, repress transcription and gene expression by removing acetyl groups from histone or non-histone proteins. HDAC1 and HDAC2 are two highly homologous Class I HDACs and display compensatory or specific roles in different cell types or in response to different stimuli and signaling pathways. We summarize here the current knowledge about the functions of HDAC1 and HDAC2 in regulating histone modifications, transcription, DNA methylation, chromosome segregation, and cell cycle during oocyte and preimplantation embryo development. What emerges from these studies is that although HDAC1 and HDAC2 are highly homologous, HDAC2 is more critical than HDAC1 for oocyte development and reciprocally, HDAC1 is more critical than HDAC2 for preimplantation development. In eukaryotes, DNA is organized into a highly ordered nucleoprotein assembly called chromatin, whose fundamental unit is the nucleosome. The nucleosome consists of 146 bp of DNA wrapped around a histone core comprised of two molecules each of histones H2A, H2B, H3 and H4. Histone H1 is bound to linker DNA between nucleosomes. 1,2 Histones are subject to multiple post-translational modifications (PTMs), including acetylation, methylation, ubiquitylation, phosphorylation, and sumoylation. These PTMs determine open and closed chromatin conformations, which, in turn, regulate the differential access and recruitment of transcription factors and other regulatory chromatin-binding proteins to DNA. 3-5 Among these histone modifications, histone acetylation is the most well-studied modification, which occurs at the ε-amino groups of evolutionarily conserved lysine residues located at the N termini. Although all core histones are acetylated in vivo, modifications of histones H3 and H4 are more extensively characterized than those of H2A and H2B. Abbreviations: HDAC, histone deacetylase; HAT, histone acetyl transferase; PTM, post-translational modification; KDAC, lysine deacetylase; TSA, trichostatin A; NAD + , nicotinamide adenine dinucleotide; HAD, HDAC association domain ; GVBD, germinal vesicle breakdown; ChIP-seq, chromatin immunoprecipitation sequencing; TFIID, transcription factor II D; YY1, yin yang 1; Pol II CTD S2, serine 2 within the RNApolymerase II C-terminal domain; H3K4, lysine 4 of histone 3; H3K9, lysine 9 of histone 3; H4K16, lysine 16 of histone 4; SIRT, NAD-dependent deacetylase sirtuin; TBP2, TATA-binding protein 2; DNMT, DNA methyltransferases; RBAP46, retinoblastoma binding protein P46; RNAi, RNA interference; aa, amino acidic; BrUTP, 5-Bromouridine 5′-triphosphate; qRT-PCR, quantitative reverse transcription polymerase chain reaction;

show abstract

Section: Structure and Complexes Of Mammalian Hdac1 And Hdac2mentioning

confidence: 99%

HDAC1 and HDAC2 in mouse oocytes and preimplantation embryos: Specificity versus compensation

Schultz

2016

Cell Death Differ

View full text Add to dashboard Cite

show abstract

“…Enforced expression of constitutive β-catenin leads to delayed differentiation of oPCs in development. Dissociation of Tcf4/ β-catenin through developmental down-regulation of Tcf4 itself, upregulation of the β-catenin antagonist adenomatous polyposis coli or competition for β-catenin binding by histone deacetylases or Groucho/Tle1, drives oligodendrocytes to differentiate and myelinate [39] . All these data suggest that promoting the degradation of β-catenin and thus blocking the Wnt pathway in oPCs may be an effective approach to facilitating oPC differentiation and myelination.…”

Section: Wnt Signalingmentioning

confidence: 99%

Promoting remyelination for the treatment of multiple sclerosis: opportunities and challenges

Zhang

Guo

2013

Neurosci. Bull.

View full text Add to dashboard Cite

Multiple sclerosis (MS) is a chronic and devastating autoimmune demyelinating disease of the central nervous system. With the increased understanding of the pathophysiology of this disease in the past two decades, many disease-modifying therapies that primarily target adaptive immunity have been shown to prevent exacerbations and new lesions in patients with relapsing-remitting MS. However, these therapies only have limited efficacy on the progression of disability. Increasing evidence has pointed to innate immunity, axonal damage and neuronal loss as important contributors to disease progression. Remyelination of denuded axons is considered an effective way to protect neurons from damage and to restore neuronal function. The identification of several key molecules and pathways controlling the differentiation of oligodendrocyte progenitor cells and myelination has yielded clues for the development of drug candidates that directly target remyelination and neuroprotection. The long-term efficacy of this strategy remains to be evaluated in clinical trials. Here, we provide an overview of current and emerging therapeutic concepts, with a focus on the opportunities and challenges for the remyelination approach to the treatment of MS.

show abstract

“…Tcf4 is expressed in the mouse white matter immediately after birth, but it is barely detectable in the adult [55][56][57]. However, following CNS injury, Tcf4 is reexpressed and upregulated in OPCs that are recruited to the lesion [56].…”

Section: Wnt Signalingmentioning

confidence: 99%

Myelin Regeneration in Multiple Sclerosis: Targeting Endogenous Stem Cells

et al. 2011

View full text Add to dashboard Cite

Regeneration of myelin sheaths (remyelination) after central nervous system demyelination is important to restore saltatory conduction and to prevent axonal loss. In multiple sclerosis, the insufficiency of remyelination leads to the irreversible degeneration of axons and correlated clinical decline. Therefore, a regenerative strategy to encourage remyelination may protect axons and improve symptoms in multiple sclerosis. We highlight recent studies on factors that influence endogenous remyelination and potential promising pharmacological targets that may be considered for enhancing central nervous system remyelination.

show abstract

HDAC1 and HDAC2 regulate oligodendrocyte differentiation by disrupting the β-catenin–TCF interaction

Cited by 514 publications

References 51 publications

HDAC1 and HDAC2 in mouse oocytes and preimplantation embryos: Specificity versus compensation

HDAC1 and HDAC2 in mouse oocytes and preimplantation embryos: Specificity versus compensation

Promoting remyelination for the treatment of multiple sclerosis: opportunities and challenges

Myelin Regeneration in Multiple Sclerosis: Targeting Endogenous Stem Cells

Contact Info

Product

Resources

About