Abstract
Crop breeding for improved disease resistance may be achieved through the manipulation of host susceptibility genes. Previously we identified multiple Arabidopsis mutants known as enhanced stress response1 (esr1) that have defects in a KH-domain RNA-binding protein and conferred increased resistance to the root fungal pathogen Fusarium oxysporum. Here, screening the same mutagenized population we discovered two further enhanced stress response mutants that also conferred enhanced resistance to F. oxysporum. These mutants also have enhanced resistance to a leaf fungal pathogen (Alternaria brassicicola) and an aphid pest (Myzus persicae), but not to the bacterial leaf pathogen Pseudomonas syringae. The causal alleles in these mutants were found to have defects in the ESR1 interacting protein partner RNA Polymerase II Carboxyl Terminal Domain (CTD) Phosphatase-Like1 (CPL1) and subsequently given the allele symbols cpl1-7 and cpl1-8. These results define a new role for CPL1 as a pathogen and pest susceptibility gene. Global transcriptome analysis and oxidative stress assays showed these cpl1 mutants have increased tolerance to oxidative stress. In particular, components of biotic stress responsive pathways were enriched in cpl1 over wild-type up-regulated gene expression datasets including genes related to defence, heat shock proteins and oxidative stress/redox state processes.
Highlights
The second class of susceptibility genes contains many that encode negative regulators that act to keep the plant defence response under control and ready for release upon pathogen detection
To identify other susceptibility genes, we extend on our esr mutant collection to identify another class two susceptibility gene, an ESR1/K homology (KH) domain RNA-binding interacting protein partner termed Enhanced Stress Response3/RNA Polymerase II C-Terminal Domain (CTD) Phosphatase-Like[1] (CPL1)
We determined CPL1 belongs to a class of susceptibility genes encoding negative regulators, and potentially confers a broad role in susceptibility to different classes of pathogens and insect pests as we demonstrated against both root and leaf fungal pathogens and with aphid pests
Summary
The second class of susceptibility genes contains many that encode negative regulators that act to keep the plant defence response under control and ready for release upon pathogen detection. Other mutants identified from the GSTF8:LUC screen included disrupted in stress responses[1] (dsr1), encoding a positive regulator of plant defences[23] This mutant exhibited a loss of SA inducible GSTF8:LUC activity and increased susceptibility to several fungal and bacterial pathogens. The cpl[1] alleles and an independent cpl[1] T-DNA insertion mutant were functionally tested for altered oxidative stress responses and found to exhibit reduced sensitivity to the chemical oxidative stress inducer methyl viologen Combined, these results define CPL1 as a pathogen and pest susceptibility gene where it acts as a negative mediator on components of defence and redox state processes
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