前期研究发现，苹果的自交不亲和性是自花授粉的花柱S-RNase在进入花粉管后会引起焦磷酸大量积累，阻碍tRNA氨酰化，阻止花粉管生长；同时，自花与异花授粉后蛋白质高通量测序比较分析寻找到一个花粉特异表达且受自我S-RNase诱导的MAPK家族蛋白；但MAPK蛋白是如何在自我S-RNase作用下参与焦磷酸积累并引起花粉管停止生长的机制尚不清楚。鉴于此，本研究首先明确S-RNase进入花粉管所激活的MAPK信号转导路径；其次，反义寡核苷链转染沉默培养中花粉的MAPK基因再添加S-RNase蛋白，明确S-RNase是否通过MAPK调控焦磷酸积累抑制花粉管生长；再次，寻找受MAPK磷酸化的互作蛋白，明确S-RNase是否通过MAPK磷酸化其下游蛋白而引起了花粉管焦磷酸的积累；最后验证MAPK其是否参与了自交不亲和反应。最终明确苹果花粉特异MAPK在花柱S-RNase作用下参与自交不亲和反应的机制。

Based on the previous study, apple self-incompatibility is apple style S-RNase leads to accumulation of pyrophosphoric acid, and eventually causes pollen tube inhibition in self-pollinated reaction. Meanwhile, we used protein high-throughput sequencing to find the differential expression proteins between the style of self and cross pollination, and obtained a pollen specific MAPK protein. However, the mechanism of self S-RNase contribute to pollen tube inhibition is still unclear. In our study, we firstly explore the MAPK signal transduction pathways activated by S-RNase in the pollen tube; secondly, using antisense oligonucleotide chain culture pollen tube to silence MAPK gene and then added the S-RNase protein, we will observe the pyrophosphate accumulation and pollen tube growth, to clear if it is ture that S-RNase could inhibite pollen tube growth and pyrophosphate accumulation by regulating MAPK; again, fingding the interaction protein of MAPK which might be phosphorylated by MAPK, this is to clear that if the interaction protein caused the accumulation of pyrophosphate in pollen tube; at last,we will confirm that MAPK participate in the self-incompatibility by genetic transformation. Above all, we could clarify that MAPK play a role in self-incompatibility reaction under the induction of S-RNase.