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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.

The Arabidopsis RNA Polymerase II Carboxyl Terminal Domain (CTD) Phosphatase-Like1 (CPL1) is a biotic stress susceptibility gene