دورية أكاديمية
أعرض في EDS

CHD4 and SMYD1 repress common transcriptional programs in the developing heart.

التفاصيل البيبلوغرافية
العنوان: CHD4 and SMYD1 repress common transcriptional programs in the developing heart.
المؤلفون: Shi W; Department of Biology and Genetics, McAllister Heart Institute, UNC-Chapel Hill, Chapel Hill, NC 27599, USA., Wasson LK; Department of Genetics, Harvard Medical School, Boston, MA 02115, USA.; Department of Medicine and Howard Hughes Medical Institute, Chevy Chase, MD 20815, USA., Dorr KM; Department of Biology and Genetics, McAllister Heart Institute, UNC-Chapel Hill, Chapel Hill, NC 27599, USA., Robbe ZL; Department of Biology and Genetics, McAllister Heart Institute, UNC-Chapel Hill, Chapel Hill, NC 27599, USA., Wilczewski CM; Department of Biology and Genetics, McAllister Heart Institute, UNC-Chapel Hill, Chapel Hill, NC 27599, USA., Hepperla AJ; Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA., Davis IJ; Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA., Seidman CE; Department of Genetics, Harvard Medical School, Boston, MA 02115, USA.; Department of Medicine and Howard Hughes Medical Institute, Chevy Chase, MD 20815, USA.; Division of Cardiovascular Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA., Seidman JG; Department of Genetics, Harvard Medical School, Boston, MA 02115, USA., Conlon FL; Department of Biology and Genetics, McAllister Heart Institute, UNC-Chapel Hill, Chapel Hill, NC 27599, USA.; Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
المصدر: Development (Cambridge, England) [Development] 2024 Apr 15; Vol. 151 (8). Date of Electronic Publication: 2024 May 03.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Company Of Biologists Limited Country of Publication: England NLM ID: 8701744 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1477-9129 (Electronic) Linking ISSN: 09501991 NLM ISO Abbreviation: Development Subsets: MEDLINE
أسماء مطبوعة: Publication: Cambridge Eng : Company Of Biologists Limited
Original Publication: [Cambridge] : Company of Biologists, [c1987-
مواضيع طبية MeSH: DNA Helicases* , DNA-Binding Proteins* , Gene Expression Regulation, Developmental* , Heart*/embryology , Mi-2 Nucleosome Remodeling and Deacetylase Complex*/metabolism , Mi-2 Nucleosome Remodeling and Deacetylase Complex*/genetics , Myocytes, Cardiac*/metabolism , Transcription Factors*, Animals ; Humans ; Mice ; Cell Differentiation/genetics ; Chromatin/metabolism ; Glycolysis/genetics ; Histone-Lysine N-Methyltransferase/metabolism ; Histone-Lysine N-Methyltransferase/genetics ; Mice, Knockout ; Muscle Proteins/metabolism ; Muscle Proteins/genetics ; Proteomics ; Transcription, Genetic
مستخلص: Regulation of chromatin states is essential for proper temporal and spatial gene expression. Chromatin states are modulated by remodeling complexes composed of components that have enzymatic activities. CHD4 is the catalytic core of the nucleosome remodeling and deacetylase (NuRD) complex, which represses gene transcription. However, it remains to be determined how CHD4, a ubiquitous enzyme that remodels chromatin structure, functions in cardiomyocytes to maintain heart development. In particular, whether other proteins besides the NuRD components interact with CHD4 in the heart is controversial. Using quantitative proteomics, we identified that CHD4 interacts with SMYD1, a striated muscle-restricted histone methyltransferase that is essential for cardiomyocyte differentiation and cardiac morphogenesis. Comprehensive transcriptomic and chromatin accessibility studies of Smyd1 and Chd4 null embryonic mouse hearts revealed that SMYD1 and CHD4 repress a group of common genes and pathways involved in glycolysis, response to hypoxia, and angiogenesis. Our study reveals a mechanism by which CHD4 functions during heart development, and a previously uncharacterized mechanism regarding how SMYD1 represses cardiac transcription in the developing heart.
Competing Interests: Competing interests The authors declare no competing or financial interests.
(© 2024. Published by The Company of Biologists Ltd.)
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معلومات مُعتمدة: R01 HL126509 United States HL NHLBI NIH HHS; R01 R01HL126509 United States NH NIH HHS; P30 CA016086 United States CA NCI NIH HHS; United States HHMI Howard Hughes Medical Institute; UM1 HL098166 United States HL NHLBI NIH HHS; R01HL126509 United States NH NIH HHS; UM1 HL098147 United States HL NHLBI NIH HHS; R01 HD089275 United States HD NICHD NIH HHS
فهرسة مساهمة: Keywords: CHD4; Chromatin accessibility; Mouse; SMYD1; Transcription
المشرفين على المادة: 0 (Chromatin)
EC 3.6.4.- (DNA Helicases)
0 (DNA-Binding Proteins)
EC 2.1.1.43 (Histone-Lysine N-Methyltransferase)
EC 3.5.1.98 (Mi-2 Nucleosome Remodeling and Deacetylase Complex)
EC 3.6.1.3 (Mi-2beta protein, mouse)
0 (Muscle Proteins)
0 (Smyd1 protein, mouse)
0 (Transcription Factors)
0 (CHD4 protein, human)
تواريخ الأحداث: Date Created: 20240415 Date Completed: 20240503 Latest Revision: 20240525
رمز التحديث: 20240525
مُعرف محوري في PubMed: PMC11112163
DOI: 10.1242/dev.202505
PMID: 38619323
قاعدة البيانات: MEDLINE
الوصف
تدمد:1477-9129
DOI:10.1242/dev.202505