Programmed cell death (PCD) is essential for several aspects of plant life, including development and stress responses. Indeed, incompatible plant-pathogen interactions are well known to induce the hypersensitive response (HR), a localized cell death. Mutational analyses have identified several key PCD components and we recently identified the mips1 mutant of Arabidopsis thaliana, which is deficient for the key enzyme catalysing the limiting step of myo-inositol (MI) synthesis. One of the most striking features of mips1 is the light-dependent formation of lesions on leaves due to Salicylic Acid (SA)-dependent PCD, revealing roles for MI or inositol derivatives in the regulation of PCD. Here, we identified a regulator of plant PCD by screening for mutants that display transcriptomic profiles opposing that of the mips1 mutant. Our screen identified the oxt6 mutant, which has been described previously as being tolerant to oxidative stress. In the oxt6 mutant, a T-DNA is inserted in the CPSF30 gene, which encodes a polyadenylation factor subunit homolog. We show that CPSF30 is required for lesion formation in mips1 via SA-dependant signalling, that the pro-death function of CPSF30 is not mediated by changes in the glutathione status and that CPSF30 activity is required for Pseudomonas syringae resistance. We also show that the oxt6 mutation suppresses cell death in other lesion mimic mutants, including lsd1, mpk4, cpr5 and cat2, suggesting that CPSF30 and, thus, the control of mRNA 3’ end processing, through the regulation of SA production, is a key component of plant immune responses.
Via Christophe Jacquet