Extended Data Fig. 1: Canonical BAF (cBAF) is essential for SARS-CoV-2 infection at viral entry in Vero E6 cells.
From: Pharmacological disruption of mSWI/SNF complex activity restricts SARS-CoV-2 infection
(a) Schematic of CRISPR/Cas9-based screen to identify SARS-CoV-2 anti- and pro-viral determinants. (b) Heatmap of z-scores of mSWI/SNF complex subunits (cBAF, PBAF, ncBAF) in SARS-CoV-2, rcVSV-SARS-CoV-2-S, HKU5-SARS-CoV-1-S, and MERS-CoV CRISPR resistance screens. (c) Polyclonal KO of BAF complex subunits and ACE2 KO 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. (d) Vero E6 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) Left, CRISPR-mediated SMARCA4 knockout was confirmed by Western blot in Vero E6 cells; Right, densitometry analysis of ACE2 levels normalized to LMNB1. Data in (c-d) 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.
