Advances in Chromodomain Helicase DNA-Binding (CHD) Proteins Regulating Stem Cell Differentiation and Human Diseases

Liu, Caojie; Kang, Ning; Guo, Yuchen; Gong, Ping

doi:10.3389/fcell.2021.710203

Cited by 9 publications

(14 citation statements)

References 95 publications

(181 reference statements)

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“…As reported previously, in mammals, CHD7 could be recruited at the promoters or superenhancers of the transcriptionally active region of specific genes to increase or decrease transcription 20 , 45 . Existing studies of CHD7 preferentially shed light on nervous system development and the differentiation of neural stem cells and neural crest stem cells, and CHD7 has been proven to be crucial for neurogenesis and adult neural stem cell maintenance 9 , 10 , 13 , 46 , 47 . Widely observed in clinical work, the alteration of CHD7 expression levels in specific cell lineages leads to severe malfunction or diseases, e.g., CHARGE syndrome, Kallmann syndrome, autism spectrum disorder, developmental disorders of multiple organ systems, and tumorigenesis 13 , 15 , 45 – 49 .…”

Section: Discussionmentioning

confidence: 99%

CHD7 regulates bone-fat balance by suppressing PPAR-γ signaling

Liu

Xiong

et al. 2022

Nat Commun

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Chromodomain helicase DNA-binding protein 7 (CHD7), an ATP-dependent eukaryotic chromatin remodeling enzyme, is essential for the development of organs. The mutation of CHD7 is the main cause of CHARGE syndrome, but its function and mechanism in skeletal system remain unclear. Here, we show conditional knockout of Chd7 in bone marrow mesenchymal stem cells (MSCs) and preosteoblasts leads to a pathological phenotype manifested as low bone mass and severely high marrow adiposity. Mechanistically, we identify enhancement of the peroxisome proliferator-activated receptor (PPAR) signaling in Chd7-deficient MSCs. Loss of Chd7 reduces the restriction of PPAR-γ and then PPAR-γ associates with trimethylated histone H3 at lysine 4 (H3K4me3), which subsequently activates the transcription of downstream adipogenic genes and disrupts the balance between osteogenic and adipogenic differentiation. Our data illustrate the pathological manifestations of Chd7 mutation in MSCs and reveal an epigenetic mechanism in skeletal health and diseases.

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Section: Discussionmentioning

confidence: 99%

CHD7 regulates bone-fat balance by suppressing PPAR-γ signaling

Liu

Xiong

et al. 2022

Nat Commun

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“…There is considerable interest in understanding the respective contributions of these remodelers to chromatin-associated processes due to the critical roles played by these factors in development and disease ( Alendar and Berns 2021 ). For example, CHD2 mutations are associated with chronic lymphocytic leukemia in H. sapiens and M. musculus ( Marfella et al 2006 ; Nagarajan et al 2009 ; Rodríguez et al 2015 ), CHD4 and CHD5 proteins in H. sapiens and M. musculus play an important role in neurogenesis and tumor suppression ( Kolla et al 2014 ; Liu et al 2021 ), and mutation of CHD7 and CHD8 genes in H. sapiens and M. musculus results in the congenital disease known as CHARGE syndrome and autism, respectively ( Zentner et al 2010 ; Liu et al 2021 ). It is thus medically relevant to understand how and when data derived from studying CHD remodelers in various other organisms can be used to provide substantive insight into the function of their human homologs.…”

Section: Introductionmentioning

confidence: 99%

CHD Chromatin Remodeling Protein Diversification Yields Novel Clades and Domains Absent in Classic Model Organisms

Trujillo

Long

Aboelnour

et al. 2022

Genome Biology and Evolution

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Chromatin remodelers play a fundamental role in the assembly of chromatin, regulation of transcription, and DNA repair. Biochemical and functional characterization of the CHD family of chromatin remodelers from a variety of model organisms have shown that these remodelers participate in a wide range of activities. However, because the evolutionary history of CHD homologs is unclear, it is difficult to predict which of these activities are broadly conserved and which have evolved more recently in individual eukaryotic lineages. Here, we performed a comprehensive phylogenetic analysis of 8,042 CHD homologs from 1,894 species to create a model for the evolution of this family across eukaryotes with a particular focus on the timing of duplications that gave rise to the diverse copies observed in plants, animals, and fungi. Our analysis confirms that the three major subfamilies of CHD remodelers originated in the eukaryotic last common ancestor, and subsequent losses occurred independently in different lineages. Improved taxon sampling identified several subfamilies of CHD remodelers in plants that were absent or highly divergent in the model plant Arabidopsis thaliana. Whereas the timing of CHD subfamily expansions in vertebrates correspond to whole genome duplication events, the mechanisms underlying CHD diversification in land plants appears more complicated. Analysis of protein domains reveals that CHD remodeler diversification has been accompanied by distinct transitions in domain architecture, contributing to the functional differences observed between these remodelers. This study demonstrates the importance of proper taxon sampling when studying ancient evolutionary events to prevent misinterpretation of subsequent lineage-specific changes and provides an evolutionary framework for functional and comparative analysis of this critical chromatin remodeler family across eukaryotes.

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“…Compared to other ATP-dependent chromatin remodelers, the CHD family proteins are represented by tandem chromatin organization modifier domains (chromodomain) in addition to the sucrose nonfermentable2 (SNF2)-like ATP-dependent helicase domains [12,13]. The chromodomain is capable of directly binding to methylated lysine at histone H3 tail to establish an association with chromatin, serving as a nucleosome recognition surface for the ATPase of CHD proteins [12,14].…”

Section: Chromodomain Helicase Dna-binding Family Proteinsmentioning

confidence: 99%

“…In general, most CHD proteins are important for chromatin access and gene expression in cell-type specific manner. Although the role of CHDs in neural stem cells and neurodevelopmental process has been well documented [8,13,[15][16][17][18], their regulatory functions in HSPC maintenance and differentiation have only been appreciated recently.…”

Section: Chromodomain Helicase Dna-binding Family Proteinsmentioning

confidence: 99%

Role of ATP-dependent chromatin remodelers in hematopoietic stem and progenitor cell maintenance

Zheng

2022

Current Opinion in Hematology

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Purpose of review ATP-dependent chromatin remodeling factors utilize energy from ATP hydrolysis to modulate DNA-histone structures and regulate gene transcription. They are essential during hematopoiesis and for hematopoietic stem and progenitor cell (HSPC) function. This review discusses the recently unveiled roles of these chromatin remodelers in HSPC regulation, with an emphasis on the mechanism of chromodomain helicase DNA-binding (CHD) family members. Recent findingsRecent studies of ATP-dependent chromatin remodelers have revealed that individual CHD family members engage in distinct mechanisms in regulating HSPC cell fate. For example, CHD8 is required for HSPC survival by restricting both P53 transcriptional activity and protein stability in steady state hematopoiesis while the related CHD7 physically interacts with RUNX family transcription factor 1 (RUNX1) and suppresses RUNX1-induced expansion of HSPCs during blood development. Moreover, other CHD subfamily members such as CHD1/CHD2 and CHD3/CHD4, as well as the switch/sucrose nonfermentable, imitation SWI, and SWI2/SNF2 related (SWR) families of chromatin modulators, have also been found important for HSPC maintenance by distinct mechanisms.

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Advances in Chromodomain Helicase DNA-Binding (CHD) Proteins Regulating Stem Cell Differentiation and Human Diseases

Cited by 9 publications

References 95 publications

CHD7 regulates bone-fat balance by suppressing PPAR-γ signaling

CHD7 regulates bone-fat balance by suppressing PPAR-γ signaling

CHD Chromatin Remodeling Protein Diversification Yields Novel Clades and Domains Absent in Classic Model Organisms

Role of ATP-dependent chromatin remodelers in hematopoietic stem and progenitor cell maintenance

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