Evolutionarily conserved bacterial effectors hijack abscisic acid signaling to induce an aqueous environment in the apoplast.
Evolutionarily conserved bacterial effectors hijack abscisic acid signaling to induce an aqueous environment in the apoplast.
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DOI:
10.1016/j.chom.2022.02.006
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发表时间:
2022-04-13
影响因子:
30.3
通讯作者:
Moffett, Peter
中科院分区:
文献类型:
--
作者:
Roussin-Leveillee, Charles;Lajeunesse, Gaele;St-Amand, Meliane;Veerapen, Varusha Pillay;Silva-Martins, Guilherme;Nomura, Kinya;Brassard, Sandrine;Bolaji, Ayooluwa;He, Sheng Yang;Moffett, Peter
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. Roussin-Léveillée et al. demonstrate that two Pseudomonas syringae effector proteins induce abscisic acid (ABA) biosynthesis and signaling in Arabidopsis. Although stomatal opening early in infection allows access to the leaf apoplast, they show that ABA induces stomatal closure in later stages, leading to water soaking lesions that benefit the bacteria.
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