SMARCC1
SMARCC1, also called BAF155, is a core SWI/SNF/BAF chromatin-remodeling complex subunit that helps ATP-dependent remodeling of nucleosomes and supports transcriptional regulation[1]. Mechanistically, BAF155-containing complexes regulate chromatin accessibility during stem-cell differentiation, embryonic stem-cell self-renewal exit, and hematopoietic lineage chromatin priming[2][3][4]. In developmental models, Baf155 loss disrupts myeloid and erythroid differentiation from erythromyeloid progenitors, while human SMARCC1 variants associate with congenital hydrocephalus, ventriculomegaly, aqueductal stenosis, developmental delay, and structural brain or cardiac defects[3][5][6]. Compared with the related isoform SMARCC2/BAF170, BAF155 predominates in stem cells, whereas BAF170 incorporation increases during differentiation; BAF170 can compete with BAF155 in BAF complexes to regulate cortical progenitor programs and cerebral cortical size[7][8]. For experimental applications, current evidence supports SMARCC1/BAF155 as a chromatin-remodeling, neurodevelopmental, hematopoietic, and cancer-biology research target, while structural work identifies conserved N-terminal pockets that may guide future small-molecule targeting rather than validated SMARCC1-specific agonists or inhibitors[9].
References:
- [1]. Phelan ML, et al. Reconstitution of a core chromatin remodeling complex from SWI/SNF subunits. Mol Cell. 1999 Feb;3(2):247-53. [Content Brief]
- [2]. Schaniel C, et al. Smarcc1/Baf155 couples self-renewal gene repression with changes in chromatin structure in mouse embryonic stem cells. Stem Cells. 2009 Dec;27(12):2979-91. [Content Brief]
- [3]. Wu J, et al. Requisite Chromatin Remodeling for Myeloid and Erythroid Lineage Differentiation from Erythromyeloid Progenitors. Cell Rep. 2020 Nov 17;33(7):108395. [Content Brief]
- [4]. Wu J, et al. Baf155 controls hematopoietic differentiation and regeneration through chromatin priming. Cell Rep. 2024 Aug 27;43(8):114558. [Content Brief]
- [5]. Al Mutairi F, et al. A mendelian form of neural tube defect caused by a de novo null variant in SMARCC1 in an identical twin. Ann Neurol. 2018 Feb;83(2):433-436. [Content Brief]
- [6]. Singh AK, et al. A novel SMARCC1 BAFopathy implicates neural progenitor epigenetic dysregulation in human hydrocephalus. Brain. 2024 Apr 4;147(4):1553-1570. [Content Brief]
- [7]. Tuoc TC, et al. Chromatin regulation by BAF170 controls cerebral cortical size and thickness. Dev Cell. 2013 May 13;25(3):256-69. [Content Brief]
- [8]. Allen MD, et al. SWI/SNF subunit BAF155 N-terminus structure informs the impact of cancer-associated mutations and reveals a potential drug binding site. Commun Biol. 2021 May 5;4(1):528. [Content Brief]
