The enhanced Valsa canker resistance conferred by MdLecRK-S.4.3 in Pyrus betulifolia can be largely suppressed by PbePUB36.

L-type lectin receptor-like kinases (L-LecRKs) act as a sensor of extracellular signals and an initiator for plant immune responses. However, the function of LecRK-S.4 on plant immunity has not been extensively investigated. At present, in the apple (Malus domestica) genome, we identified that MdLecRK-S.4.3, a homologous gene of LecRK-S.4, was differentially expressed during the occursion of Valsa canker. Over-expression of MdLecRK-S.4.3 facilitated the induction of immune response and enhanced the Valsa canker resistance of apple and pear fruit, and 'Duli-G03' (Pyrus betulifolia) suspension cells. On the contrary, the expression of PbePUB36, RLCK XI subfamily member, was significantly repressed in the MdLecRK-S.4.3 overexpressed cell lines. Over-expression of PbePUB36 interfered with the Valsa canker resistance and immune response caused by up-regulation of MdLecRK-S.4.3. Furthermore, MdLecRK-S.4.3 interacted with BAK1 or PbePUB36 in vivo. In conclusion, MdLecRK-S.4.3 activated various immune responses and positively regulate Valsa canker resistance, which could be largely compromised by PbePUB36. MdLecRK-S.4.3 interacted with PbePUB36 and/or MdBAK1 to mediate the immune responses. This finding provides a reference for studying the molecular mechanism of resistance to Valsa canker and resistance breeding.