Mechanisms of glacial‐to‐future atmospheric CO (2) effects on plant immunity

The impacts of rising atmospheric CO(2) concentrations on plant disease have received increasing attention, but with little consensus emerging on the direct mechanisms by which CO(2) shapes plant immunity. Furthermore, the impact of sub‐ambient CO (2) concentrations, which plants have experienced repeatedly over the past 800 000 yr, has been largely overlooked. A combination of gene expression analysis, phenotypic characterisation of mutants and mass spectrometry‐based metabolic profiling was used to determine development‐independent effects of sub‐ambient CO (2) (sa CO (2)) and elevated CO (2) (eCO (2)) on Arabidopsis immunity. Resistance to the necrotrophic Plectosphaerella cucumerina (Pc) was repressed at sa CO (2) and enhanced at eCO (2). This CO (2)‐dependent resistance was associated with priming of jasmonic acid (JA)‐dependent gene expression and required intact JA biosynthesis and signalling. Resistance to the biotrophic oomycete Hyaloperonospora arabidopsidis (Hpa) increased at both eCO (2) and sa CO (2). Although eCO (2) primed salicylic acid (SA)‐dependent gene expression, mutations affecting SA signalling only partially suppressed Hpa resistance at eCO (2), suggesting additional mechanisms are involved. Induced production of intracellular reactive oxygen species (ROS) at sa CO (2) corresponded to a loss of resistance in glycolate oxidase mutants and increased transcription of the peroxisomal catalase gene CAT2, unveiling a mechanism by which photorespiration‐derived ROS determined Hpa resistance at saCO(2). By separating indirect developmental impacts from direct immunological effects, we uncover distinct mechanisms by which CO (2) shapes plant immunity and discuss their evolutionary significance.