Abstract
Pathogen-induced cell death is closely related to plant disease susceptibility and resistance. The cucumber (Cucumis sativus L.) mildew resistance locus O (CsMLO1) and calmodulin (CsCaM3) genes, as molecular components, are linked to nonhost resistance and hypersensitive cell death. In this study, we demonstrate that CsMLO1 interacts with CsCaM3 via yeast two-hybrid, firefly luciferase (LUC) complementation and bimolecular fluorescence complementation (BiFC) experiments. A subcellular localization analysis of green fluorescent protein (GFP) fusion reveals that CsCaM3 is transferred from the cytoplasm to the plasma membrane in Nicotiana benthamiana, and CsCaM3 green fluorescence is significantly attenuated via the coexpression of CsMLO1 and CsCaM3. CsMLO1 negatively regulates CsCaM3 expression in transiently transformed cucumbers, and hypersensitive cell death is disrupted by CsCaM3 and/or CsMLO1 expression under Corynespora cassiicola infection. Additionally, CsMLO1 silencing significantly enhances the expression of reactive oxygen species (ROS)-related genes (CsPO1, CsRbohD, and CsRbohF), defense marker genes (CsPR1 and CsPR3) and callose deposition-related gene (CsGSL) in infected cucumbers. These results suggest that the interaction of CsMLO1 with CsCaM3 may act as a cell death regulator associated with plant immunity and disease.
Highlights
In natural environments, plants are exposed to attack from a variety of microbial pathogens
The analysis demonstrated that CsMLO1 stably interacted with CsCaM3 via yeast two-hybrid, firefly luciferase (LUC) complementation and bimolecular fluorescence complementation (BiFC) experiments
The sequences of calmodulin-7 (A0A0A0KWT3) were aligned with the cucumber genome database using the service provided by http://cucurbitgenomics.org/BLAST
Summary
Plants are exposed to attack from a variety of microbial pathogens. Plant pattern-recognition receptors (PRRs) recognize conserved pathogen-associated molecular patterns (PAMPs) of microorganisms, and PAMP-triggered immunity (PTI) is usually strong enough to prevent the colonization of most microbial pathogens. In the second stage, evolved pathogens secrete virulence factors that inhibit PTI to cause effector-triggered susceptibility (ETS) in plants. Plants express a specific R gene to directly or indirectly recognize pathogen-specific effector factors, and effector-triggered immunity (ETI) accelerates and amplifies PTI to cause disease resistance in plants. Under the pressure of natural selection, the pathogen is forced to produce new effector factors to inhibit ETI, plants produce new R genes to activate ETI to maintain their survival [1,2,3]. Upon recognition of certain effector proteins, host cells undergo rapid programmed cell death, namely, the hypersensitive response (HR), which in turn inhibits pathogen infection [4]
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