BAF chromatin complexes do not mediate GLI transcriptional repression of Hedgehog target genes

The Hedgehog (HH) signaling pathway is primarily modulated by GLI transcriptional repression in the mouse limb. Previous studies have suggested a role for the BAF chromatin remodeling complex in mediating GLI repression. Consistent with this possibility, the core BAF complex protein SMARCC1 is present at most active limb enhancers including the majority of GLI enhancers. Despite this, we find that SMARCC1 maintains chromatin accessibility at GLI enhancers suggesting that it contributes to enhancer activation rather than helping to mediate GLI repression. Furthermore, SMARCC1 binds GLI-regulated enhancers independently of GLI3 and does not facilitate transcriptional repression of most GLI target genes. Finally, Smarcc1- and Shh- double knockout phenotypes suggest that SMARCC1 is not required to mediate constitutive GLI repression in HH mutants. We conclude that the BAF complex does not mediate GLI3 repression, which we propose instead utilizes alternative chromatin remodeling complexes. ### Competing Interest Statement The authors have declared no competing interest.