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Abstract
BackgroundIdentifying new sources of disease resistance and the corresponding underlying resistance mechanisms remains very challenging, particularly in Monocots. Moreover, the modification of most disease resistance pathways made so far is detrimental to tolerance to abiotic stresses such as drought. This is largely due to negative cross-talks between disease resistance and abiotic stress tolerance signaling pathways. We have previously described the role of the rice ZBED protein containing three Zn-finger BED domains in disease resistance against the fungal pathogen Magnaporthe oryzae. The molecular and biological functions of such BED domains in plant proteins remain elusive.ResultsUsing Nicotiana benthamiana as a heterologous system, we show that ZBED localizes in the nucleus, binds DNA, and triggers basal immunity. These activities require conserved cysteine residues of the Zn-finger BED domains that are involved in DNA binding. Interestingly, ZBED overexpressor rice lines show increased drought tolerance. More importantly, the disease resistance response conferred by ZBED is not compromised by drought-induced stress.ConclusionsTogether our data indicate that ZBED might represent a new type of transcriptional regulator playing simultaneously a positive role in both disease resistance and drought tolerance. We demonstrate that it is possible to provide disease resistance and drought resistance simultaneously.
Highlights
Identifying new sources of disease resistance and the corresponding underlying resistance mechanisms remains very challenging, in Monocots
Among the various prey clones isolated, we identified KIP1 (LOC_Os01g07370), a kinase interacting protein predominantly expressed in pollen (Skirpan et al, 2001), STE11 (LOC_Os01g50400), STE20/MAPK3 (LOC_Os12g0225; Jouannic et al, 1999) and WRKY4 (LOC_Os03g55164), a transcriptional activator of rice defense responses against Rhizoctonia solani (Wang et al, 2015) (Figure 1A; ZBED auto-active controls Supplementary Figure 1)
We broaden the knowledge on the molecular function of BED domains in plants
Summary
Identifying new sources of disease resistance and the corresponding underlying resistance mechanisms remains very challenging, in Monocots. The other layer of defense, called effector-triggered immunity, is activated by direct or indirect recognition of effector molecules from the pathogen by resistance proteins of the plant and is leading to programmed cell death, preventing the spread of the pathogen in the host (Jones and Dangl, 2006). In both forms of resistance several physiological changes occur, including the generation of reactive oxygen species (ROS), ion fluxes, accumulation of defense hormones such as salicylic acid (SA), and induction of defense-related genes, such as pathogenesisrelated (PR) genes (Corwin and Kliebenstein, 2017)
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