Fig. 2: SMARCA4 regulates ALDH16A1’s chromatin accessibility and expression. | Nature Communications

Fig. 2: SMARCA4 regulates ALDH16A1’s chromatin accessibility and expression.

From: Targeting ALDH16A1 mediated thioredoxin lysosomal degradation to enhance ferroptosis susceptibility in SMARCA4-deficient NSCLC

Fig. 2

a Schematic outline of the identification of SMARCA4’s downstream targets using ATAC-Seq, CUT&TAG and RNA-Seq in Cas9-NC and SMARCA4-KO PC9 cells. Created in BioRender. Bi, G. (2025) https://BioRender.com/fjloxzm. b Volcano plots showing the differentially expressed genes between Cas9-NC and SMARCA4-KO PC9 cells. c Heatmap for SMARCA4, H3K27ac, H3K4me1 (CUT&TAG) levels and ATAC-Seq chromatin accessibility in Cas9-NC and SMARCA4-KO PC9 cells across merged SMARCA4 sites. d Venn diagram showing the intersection of potential SMARCA4 targets identified by ATAC-Seq, CUT&TAG and RNA-Seq. e Representative browser track of ATAC-Seq and SMARCA4 (CUT&TAG) on the ALDH16A1 locus in indicated PC9 cells. f, g mRNA (f) and protein (g) levels of ALDH16A1 in PC9, H1975, HCC827, A549 and H23 cells with indicated genotypes, determined by qPCR and western blotting. Data are presented as the mean ± SD, n = 3 independent experiments. Consistent results were observed across three biological replicates in (g). Unpaired two-tailed Student’s t tests are used. Source data are provided as a Source Data file.

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