期刊
MOLECULAR PLANT PATHOLOGY
卷 23, 期 2, 页码 188-203出版社
WILEY
DOI: 10.1111/mpp.13153
关键词
cell death; E3 ligase; effector; effector-triggered immunity; Nicotiana; Ralstonia solanacearum; RipAW
资金
- Shaanxi the Nature Science Basic Research Plan [2020JM-160]
- Fundamental Research Fund for the Central Universities of China [Z109021706]
- State administration of Foreign Experts Affairs [B18042]
- External Science and Technology Cooperation Program of Ningxia Academy of Agriculture and Forestry Sciences [DW-X-2018012]
- Start-up Funds of Northwest AF University [Z111021601]
- National Natural Science Foundation of China [31901573]
- Special Research project from Shaanxi province [F2020221001]
- Key Research and Development plan of Ningxia Province [021BEF02033]
This study demonstrated that the RipAW effector triggers effector-triggered immunity (ETI) in two evolutionally related species, Nicotiana benthamiana and Nicotiana tabacum. The research showed that there are commonalities and specificities in RipAW-activated ETI between these two species, suggesting Nicotiana species have acquired different abilities to perceive RipAW and activate plant defenses during plant-pathogen co-evolution.
Diverse pathogen effectors convergently target conserved components in plant immunity guarded by intracellular nucleotide-binding domain leucine-rich repeat receptors (NLRs) and activate effector-triggered immunity (ETI), often causing cell death. Little is known of the differences underlying ETI in different plants triggered by the same effector. In this study, we demonstrated that effector RipAW triggers ETI on Nicotiana benthamiana and Nicotiana tabacum. Both the first 107 amino acids (N1-107) and RipAW E3-ligase activity are required but not sufficient for triggering ETI on N. benthamiana. However, on N. tabacum, the N1-107 fragment is essential and sufficient for inducing cell death. The first 60 amino acids of the protein are not essential for RipAW-triggered cell death on either N. benthamiana or N. tabacum. Furthermore, simultaneous mutation of both R75 and R78 disrupts RipAW-triggered ETI on N. tabacum, but not on N. benthamiana. In addition, N. tabacum recognizes more RipAW orthologs than N. benthamiana. These data showcase the commonalities and specificities of RipAW-activated ETI in two evolutionally related species, suggesting Nicotiana species have acquired different abilities to perceive RipAW and activate plant defences during plant-pathogen co-evolution.
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