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. Author manuscript; available in PMC: 2022 Oct 11.
Published in final edited form as: Dev Cell. 2021 Sep 27;56(19):2765–2782.e10. doi: 10.1016/j.devcel.2021.09.001

Figure 8: H3K4me2/TET2 complex impairment leads to miR145 repression and loss of miR145-dependent cytoskeleton dynamics.

Figure 8:

A. miR145 expression in Myocd-LSD1 and PDGF-BB treated SMC (30 ng/ml, 24h). B. Expression of miR145 target genes associated with cell plasticity (yellow) and migration inhibition (orange) in Myocd-LSD1 SMC vs Myocd-LSD1NF SMC. C. Transcript levels of Srgap1, Ssh2, and Sema3a in Myocd-LSD1NF, Myocd-LSD1 SMC and SMC treated with PDGF-BB (normalized transcript counts). D. ChIPseq track showing H3K4me2 distribution on the miR143/miR145 gene cluster in human SMC. Source: ENCODE Project. E. CUT&Tag sequencing tracks for H3K4me2, HA-TET2 and Myocd-LSD1 occupancy at the miR143/miR145 gene in control and Myocd-LSD1 SMC. F. Enrichment of H3K4me2, TET2 and 5hmC level on miR145 CArG region Myocd-LSD1NF and Myocd-LSD1 SMC. G. Transwell assay using Myocd-LSD1 SMC transfected with miR-Control (10 nM) or miR-145 at different doses (1 nM, 3 nM, and 10 nM) for 24 hours. Scale bar = 0.5 mm. Data are represented as mean ± s.e.m of 3-4 independent biological replicates. Groups were compared by unpaired Student t-test or One-Way ANOVA. * p<0.05, ** p<0.001, *** p<0.0001.