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Baf155 通过染色质引发控制造血分化和再生。

Baf155 controls hematopoietic differentiation and regeneration through chromatin priming.

机构信息

Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.

Department of Genetics, Washington University School of Medicine, St. Louis, MO 63110, USA; Edison Family Center for Genome Sciences and Systems Biology, Washington University School of Medicine, St. Louis, MO 63110, USA.

出版信息

Cell Rep. 2024 Aug 27;43(8):114558. doi: 10.1016/j.celrep.2024.114558. Epub 2024 Jul 30.

DOI:10.1016/j.celrep.2024.114558
PMID:39088321
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11465209/
Abstract

Chromatin priming promotes cell-type-specific gene expression, lineage differentiation, and development. The mechanism of chromatin priming has not been fully understood. Here, we report that mouse hematopoietic stem and progenitor cells (HSPCs) lacking the Baf155 subunit of the BAF (BRG1/BRM-associated factor) chromatin remodeling complex produce a significantly reduced number of mature blood cells, leading to a failure of hematopoietic regeneration upon transplantation and 5-fluorouracil (5-FU) injury. Baf155-deficient HSPCs generate particularly fewer neutrophils, B cells, and CD8 T cells at homeostasis, supporting a more immune-suppressive tumor microenvironment and enhanced tumor growth. Single-nucleus multiomics analysis reveals that Baf155-deficient HSPCs fail to establish accessible chromatin in selected regions that are enriched for putative enhancers and binding motifs of hematopoietic lineage transcription factors. Our study provides a fundamental mechanistic understanding of the role of Baf155 in hematopoietic lineage chromatin priming and the functional consequences of Baf155 deficiency in regeneration and tumor immunity.

摘要

染色质预激活促进细胞类型特异性基因表达、谱系分化和发育。染色质预激活的机制尚未完全理解。在这里，我们报告说，缺乏 BAF（BRG1/BRM 相关因子）染色质重塑复合物的 Baf155 亚基的小鼠造血干细胞和祖细胞 (HSPC) 产生的成熟血细胞数量显著减少，导致移植后造血再生失败和 5-氟尿嘧啶 (5-FU) 损伤。Baf155 缺陷的 HSPC 在稳态下产生的中性粒细胞、B 细胞和 CD8 T 细胞特别少，支持更具免疫抑制性的肿瘤微环境和增强的肿瘤生长。单细胞多组学分析表明，Baf155 缺陷的 HSPC 无法在富含造血谱系转录因子的假定增强子和结合基序的选定区域中建立可及染色质。我们的研究提供了对 Baf155 在造血谱系染色质预激活中的作用以及 Baf155 缺乏在再生和肿瘤免疫中的功能后果的基本机制理解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f476/11465209/6e828a7c160f/nihms-2019556-f0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f476/11465209/50d0b8af49da/nihms-2019556-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f476/11465209/5a4107fef1c4/nihms-2019556-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f476/11465209/dec7d9d87fc7/nihms-2019556-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f476/11465209/74ebda1ed430/nihms-2019556-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f476/11465209/54e8beab9b83/nihms-2019556-f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f476/11465209/a11aa612d6b5/nihms-2019556-f0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f476/11465209/6e828a7c160f/nihms-2019556-f0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f476/11465209/50d0b8af49da/nihms-2019556-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f476/11465209/5a4107fef1c4/nihms-2019556-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f476/11465209/dec7d9d87fc7/nihms-2019556-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f476/11465209/74ebda1ed430/nihms-2019556-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f476/11465209/54e8beab9b83/nihms-2019556-f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f476/11465209/a11aa612d6b5/nihms-2019556-f0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f476/11465209/6e828a7c160f/nihms-2019556-f0008.jpg

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