染色质重塑因子 Chd7 在神经嵴中受组织特异性转录因子的发育调控。

IF 9.8 1区 生物学 Q1 Agricultural and Biological Sciences PLoS Biology Pub Date : 2024-10-17 eCollection Date: 2024-10-01 DOI:10.1371/journal.pbio.3002786
Ruth M Williams, Guneş Taylor, Irving T C Ling, Ivan Candido-Ferreira, Daniel M Fountain, Sarah Mayes, Perihan Seda Ateş-Kalkan, Julianna O Haug, Andrew J Price, Sean A McKinney, Yavor K Bozhilovh, Richard C V Tyser, Shankar Srinivas, Jim R Hughes, Tatjana Sauka-Spengler
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引用次数: 0

摘要

神经嵴发育异常会导致神经嵴病,如 CHARGE 综合征。很大一部分 CHARGE 病例是由于编码 CHD7(染色质域螺旋酶 DNA 结合蛋白 7)的基因中的致病变体造成的,该基因可重塑染色质。虽然CHD7在神经嵴发育过程中的作用已得到充分证实,但该因子是如何在神经嵴细胞中特异性上调的还不清楚。在这里,我们利用雏鸡和人类神经嵴的表观基因组图谱鉴定了一组调控神经嵴细胞和其他组织中 Chd7 表达的增强子。我们从功能上验证了上游转录因子与候选增强子的结合,揭示了神经嵴主调控因子与 Chd7 之间新的表观关系,显示了全球作用的染色质重塑因子对组织的特异性调控。此外,我们还发现了人类胚胎表观基因组数据中保守的增强子特征,并验证了人类等效的 CHD7 增强子在小鸡胚胎中的活性。我们的研究结果将 Chd7 嵌入了神经嵴基因调控网络,并为解释无因果关系分配的 CHARGE 综合征病例提供了潜在的临床相关因素。
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Chromatin remodeller Chd7 is developmentally regulated in the neural crest by tissue-specific transcription factors.

Neurocristopathies such as CHARGE syndrome result from aberrant neural crest development. A large proportion of CHARGE cases are attributed to pathogenic variants in the gene encoding CHD7, chromodomain helicase DNA binding protein 7, which remodels chromatin. While the role for CHD7 in neural crest development is well documented, how this factor is specifically up-regulated in neural crest cells is not understood. Here, we use epigenomic profiling of chick and human neural crest to identify a cohort of enhancers regulating Chd7 expression in neural crest cells and other tissues. We functionally validate upstream transcription factor binding at candidate enhancers, revealing novel epistatic relationships between neural crest master regulators and Chd7, showing tissue-specific regulation of a globally acting chromatin remodeller. Furthermore, we find conserved enhancer features in human embryonic epigenomic data and validate the activity of the human equivalent CHD7 enhancers in the chick embryo. Our findings embed Chd7 in the neural crest gene regulatory network and offer potentially clinically relevant elements for interpreting CHARGE syndrome cases without causative allocation.

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来源期刊
PLoS Biology
PLoS Biology BIOCHEMISTRY & MOLECULAR BIOLOGY-BIOLOGY
CiteScore
15.40
自引率
2.00%
发文量
359
审稿时长
3-8 weeks
期刊介绍: PLOS Biology is the flagship journal of the Public Library of Science (PLOS) and focuses on publishing groundbreaking and relevant research in all areas of biological science. The journal features works at various scales, ranging from molecules to ecosystems, and also encourages interdisciplinary studies. PLOS Biology publishes articles that demonstrate exceptional significance, originality, and relevance, with a high standard of scientific rigor in methodology, reporting, and conclusions. The journal aims to advance science and serve the research community by transforming research communication to align with the research process. It offers evolving article types and policies that empower authors to share the complete story behind their scientific findings with a diverse global audience of researchers, educators, policymakers, patient advocacy groups, and the general public. PLOS Biology, along with other PLOS journals, is widely indexed by major services such as Crossref, Dimensions, DOAJ, Google Scholar, PubMed, PubMed Central, Scopus, and Web of Science. Additionally, PLOS Biology is indexed by various other services including AGRICOLA, Biological Abstracts, BIOSYS Previews, CABI CAB Abstracts, CABI Global Health, CAPES, CAS, CNKI, Embase, Journal Guide, MEDLINE, and Zoological Record, ensuring that the research content is easily accessible and discoverable by a wide range of audiences.
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