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. 2018 Aug 1;115(34):E7997–E8006. doi: 10.1073/pnas.1805882115

Fig. 6.

Fig. 6.

A model for novel site recognition by Tec1-independent Ste12 variants. Wild-type Ste12 protein (blue) is compared with the K150A mutant (tan) for binding at a mating gene with two perfect recognition sites (tail-to-tail with a 3-bp spacing, shown in blue) and an invasion gene with a single perfect site along with a degenerate site. Due to its altered dimer interface, the “kinked” mutant K150A is less capable of binding symmetrically at two perfect sites, consistent with its phenotype of reduced mating efficiency. However, the conformation of K150A allows the variant protein to occupy novel sites within invasion genes that contain one perfect or nearly perfect site paired with a degenerate site; wild-type Ste12 is unable to occupy these sites.