染色质
染色质重塑
细胞生物学
生物
组蛋白脱乙酰基酶
转录组
组蛋白
染色质免疫沉淀
遗传学
基因表达
基因
发起人
作者
Jin Yong Kim,Minji Park,Jungyoon Ohn,Rho Hyun Seong,Jin Ho Chung,Kyu Han Kim,Seong Jin Jo,Oh Sang Kwon
出处
期刊:Cell Reports
[Elsevier]
日期:2022-05-01
卷期号:39 (7): 110821-110821
被引量:13
标识
DOI:10.1016/j.celrep.2022.110821
摘要
Summary
Dermal fibroblasts lose stem cell potency after birth, which prevents regenerative healing. However, the underlying intracellular mechanisms are largely unknown. We uncover the postnatal maturation of papillary fibroblasts (PFs) driven by the extensive Twist2-mediated remodeling of chromatin accessibility. A loss of the regenerative ability of postnatal PFs occurs with decreased H3K27ac levels. Single-cell transcriptomics, assay for transposase-accessible chromatin sequencing (ATAC-seq), and chromatin immunoprecipitation sequencing (ChIP-seq) reveal the postnatal maturation trajectory associated with the loss of the regenerative trajectory in PFs, which is characterized by a marked decrease in chromatin accessibility and H3K27ac modifications. Histone deacetylase inhibition delays spontaneous chromatin remodeling, thus maintaining the regenerative ability of postnatal PFs. Genomic analysis identifies Twist2 as a major regulator within chromatin regions with decreased accessibility during the postnatal period. When Twist2 is genetically deleted in dermal fibroblasts, the intracellular cascade of postnatal maturation is significantly delayed. Our findings reveal the comprehensive intracellular mechanisms underlying intrinsic postnatal changes in dermal fibroblasts.
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