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Enhanced Valsa canker resistance conferred by expression of MdLecRK-S.4.3 in Pyrus betulifolia is largely suppressed by PbePUB36

文献类型: 外文期刊

作者: Sun, E. 1 ; Yu, Hongqiang 1 ; Chen, Zhongjian 2 ; Cai, Minrui 1 ; Mao, Xia 1 ; Li, Yanyan 1 ; Zuo, Cunwu 1 ;

作者机构: 1.Gansu Agr Univ, Coll Hort, Lanzhou 730070, Gansu, Peoples R China

2.Guangdong Acad Agr, Agrobiol Gene Res Ctr, Guangzhou 510640, Peoples R China

3.State Key Lab Aridland Crop Sci, Lanzhou 730070, Peoples R China

关键词: Apple; co-expression analysis; gene duplication; L-type lectin receptor-like kinases; Malus domestica; pattern recognition receptors; pear; Pyrus betulifolia; reciprocal confrontation role; Valsa canker

期刊名称:JOURNAL OF EXPERIMENTAL BOTANY ( 影响因子:6.9; 五年影响因子:8.0 )

ISSN: 0022-0957

年卷期: 2023 年 74 卷 14 期

页码:

收录情况: SCI

摘要: MdLecRK-S.4.3-induced resistance to Valsa canker in pear is compromised by PbePUB36, and MdLecRK-S.4.3 interacts with PbePUB36 and/or MdBAK1 to mediate immune responses. L-type lectin receptor-like kinases (L-LecRKs) act as sensors of extracellular signals and as initiators for plant immune responses; however, the function of LecRK-S.4 in plant immunity has not yet been extensively investigated. In the present study we found that MdLecRK-S.4.3 in apple (Malus domestica), a homologous gene of LecRK-S.4, was differentially expressed during infection by Valsa mali and Valsa pyri. Overexpression of MdLecRK-S.4.3 facilitated the induction of immune responses and enhanced the resistance to Valsa canker of fruits of apple and pear (Pyrus betulifolia), and of suspension cells of pear 'Duli-G03'. The expression of PbePUB36, a RLCK XI sub-family member, was significantly repressed in the MdLecRK-S.4.3-overexpressing cell lines. Overexpression of PbePUB36 interfered with the resistance to Valsa canker and the immune response caused by up-regulation of MdLecRK-S.4.3. In addition, we found that MdLecRK-S.4.3 interacted with BAK1 and/or PbePUB36 in vivo. Thus, whilst MdLecRK-S.4.3 activated various immune responses and positively regulated Valsa canker resistance, this could be largely compromised by PbePUB36. MdLecRK-S.4.3 interacted with PbePUB36 and/or MdBAK1 to mediate the immune responses. Our finding provides a basis for further examination of the molecular mechanisms underlying resistance to Valsa canker, and can contribute to resistance breeding.

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