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GhPYL-11A-PP2C interactions are partially mediated by proline (P84) and histidine (H111) in the gate-latch region of GhPYL9-11A. Replacement of P84 by serine (GhPYL9-11AP84S) (A) and H111 by alanine (GhPYL9-11AH111A) (B) abolished binding to AtABI1 both in the absence and presence of 10 μM ABA. However, these mutations partially affected binding to AtABI2, GhPP2C1, and GhPP2C2 both in the presence and absence of 10 μM ABA.
