“…This involves a complex genetic mechanism, and the display of the complete trait of self-incompatibility not only depends on the S-site genes (pistil S gene and pollen S gene) but, also, several modifier genes associated with complex mechanisms that have been gradually explored [ 29 ]. These modifier genes are involved in multiple signal transduction systems [ 29 ], for example, calcium ion signaling [ 29 , 30 , 31 ], reactive oxygen signaling [ 32 ], hormone signaling [ 33 ], inositol phosphate signaling [ 34 , 35 ], biochemical metabolism processes [ 36 ], programmed cell death (PCD) [ 32 , 37 ], and cell wall and cytoskeletal construction [ 28 , 38 , 39 , 40 , 41 ]. These modifiers, distributed in a determined location of the chromosome, will affect the intensity of self-incompatibility to varying degrees, and be directly reflected in the fruit-set rate.…”