Extended Data Fig. 2: cBAF is essential for SARS-CoV-2 viral entry in human cells.
From: Pharmacological disruption of mSWI/SNF complex activity restricts SARS-CoV-2 infection
(a) BAF complex subunit polyclonal KO pools of Huh7.5 cells were infected with SARS-CoV-2, HKU5-SARS-CoV-1-S and MERS-CoV at an MOI of 0.2. Cell viability relative to an uninfected control was measured 4 dpi using CellTiter Glo. (b) Bar graph depicting % mNeonGreen-expressing cells (control cells or those with polyclonal CRISPR-mediated KO of shared or unique mSWI/SNF subunits) following infection by icSARS-CoV-2-mNG at an MOI of 1. (c) Huh7.5 cells were infected with SARS-CoV-2 at an MOI of 0.1. Virus titer was measured by plaque assay. Dash line, limit of detection. (d) Cells were infected with VSV pseudovirus (VSVpp): VSVpp-VSV-G and VSVpp-SARS-CoV-2-S. Luciferase relative to a VSVpp-VSV-G control was measured 1 dpi. (e) CRISPR-mediated SMARCA4 knockout was confirmed by Western blot in Huh7.5 cells. (f) Calu-3 cells were infected with SARS-CoV-2 at an MOI of 0.2. Cell viability relative to an uninfected control was measured 3 dpi with CellTiter Glo. (g) Calu-3 cells were infected with VSV pseudovirus (VSVpp): VSVpp-VSV-G and VSVpp-SARS-CoV-2-S. Luciferase relative to a VSVpp-VSV-G control was measured 1 dpi. Data in (a-d, f-g) were analyzed by one-way ANOVA with Tukey’s multiple comparison test. Shown are mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. n = 3 biological replicates. Data in (e) is one representative one of three independent experiments.
