Figure 3.

Mechanisms of different self-incompatibility systems.

(A) Papaveraceae GSI. The interaction between PrpS and PrsS activates Ca²⁺-dependent signaling events, including an increase in cytosolic free Ca²⁺ and ROS, a reduction in ATP depletion and acidification of the cytosol, the inhibition of soluble inorganic pyrophosphatase P26.1, and the initiation of two key regulators of SI-PCD, MAPK9 and caspase-3-like/DEVDase, thereby resulting in programmed cell death of self-pollen.

(B)Brassica SSI. Phosphorylated SRK/MLPK activates ARC1, which targets three compatibility factors, EXO70A1, GLO1, and PLDα1, for degradation. A second signaling pathway is mediated by the FER–Rac/Rop–Rboh module, which triggers a rapid increase in NADPH oxidase–produced ROS, leading to self-pollen rejection.

(C)Arabidopsis SSI. The SRK/SCR interaction triggers a rapid increase in cytosolic free Ca²⁺ and the activation of autophagy, eventually resulting in inhibition of compatibility factors for pollen acceptance.

(D)Primula HSI. SI occurs in short (S)-style morphs with stigmas positioned above the anther or long (L)-style morphs with stigmas situated below the anther. In the S-morph, the cytochrome P450 CYP734A50 inhibits cell elongation by repressing brassinosteroid.