PRJNA767202
A photoperiod-dependent lesion-mimic mutant reveals the role of shikimate pathway in programmed cell death
Programmed cell death (PCD) is essential for both plant development and stress responses. However, how plants control PCD is not well-understood. The shikimate pathway is one of the most important metabolic pathways in plants, but its relationship to PCD is unknown. Here we show that shikimate can induces PCD in Arabidopsis. We identify a photoperiod-dependent lesion-mimic mutant named lis, which forms spontaneous lesion in short-day condition. Map-based cloning and whole-genome resequencing reveal that LIS encodes MEE32, a bifunctional enzyme in the shikimate pathway. Metabolic analysis shows that the level of shikimate is dramatically increased in lis. Through genetic screening, three Suppressors of lis (slis) are identified and the causal genes are cloned. SLISs encode proteins upstream of MEE32 in the shikimate pathway. Furthermore, exogenous shikimate treatment causes PCD. Our study not only uncovers that shikimate is an inducer of PCD, but also suggests that the accumulation of shikimate contributes to the efficacy of glyphosate, the most successful herbicide.