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Fig. 2 | BMC Biology

Fig. 2

From: Switching of OAS1 splicing isoforms overcomes SNP-derived vulnerability to SARS-CoV-2 infection

Fig. 2

CLK inhibitor CaNDY induces splice-switching in the OAS1 rs10774671 A allele. a Allele-dependent OAS1 alternative splicing. Pre-mRNA of OAS1, with the rs10774671 G allele at -1 position of exon 6 splice acceptor (SA), dominantly produces the p46 variant; the A allele leads to alternative splicing to produce the p42, p48, p44a, and p44b variants with differences in the last exon (yellow boxes). b SRSF6-binding motif (red letters) near the U1-binding site of the OAS1 donor site for p44a/p44b/p48 splicing. Blue dots: U1snRNA pairing. c Western blotting of U1-70 k and phosphorylated SRSF6 (p-SRSF6) for RNA pull-down products of the OAS1 exon 5 splice donor (SD) sequence in si-non-specific targets (NS) and si-SRSF6 Calu-3 cells. Input, input samples; bait (-), negative control products without the bait RNA oligo. ACTB served as a loading control. d Western blotting of U1-70 k and p-SRSF6 for the RNA pull-down products of the OAS1 exon 5 SD sequence in Calu-3 cells treated with 0.1% DMSO or 10 µM CaNDY. Captions are the same as in Fig. 2c

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