Evolutionarily conserved bacterial effectors hijack abscisic acid signaling to induce an aqueous environment in the apoplast

High atmospheric humidity levels profoundly impact host-pathogen interactions in plants by enabling the establishment of an aqueous living space that benefits pathogens. The effectors HopM1 and AvrE1 of the bacterial pathogen Pseudomonas syringae have been shown to induce an aqueous apoplast under such conditions. However, the mechanisms by which this happens remain unknown. Here, we show that HopM1 and AvrE1 work redundantly to establish an aqueous living space by inducing a major reprogramming of the Arabidopsis thaliana transcriptome landscape. These effectors induce a strong abscisic acid (ABA) signature, which promotes stomatal closure, resulting in reduced leaf transpiration and water-soaking lesions. Furthermore, these effectors preferentially increase ABA accumulation in guard cells, which control stomatal aperture. Notably, a guard-cell-specific ABA transporter, ABCG40, is necessary for HopM1 induction of water-soaking lesions. This study provides molecular insights into a chain of events of stomatal manipulation that create an ideal microenvironment to facilitate infection.

Automated summary

High atmospheric humidity levels facilitate bacterial pathogens in plants by inducing an aqueous living space, as shown by the effectors HopM1 and AvrE1. This study reveals that these effectors work together to reprogram the transcriptome of Arabidopsis thaliana, leading to the accumulation of abscisic acid (ABA) and subsequent stomatal closure, reduced leaf transpiration, and water-soaking lesions. Moreover, these effectors preferentially increase ABA accumulation in guard cells, with the ABA transporter ABCG40 playing a crucial role in the induction of water-soaking lesions. These findings provide molecular insights into the manipulation of stomatal responses during infection.