Inositol hexakisphosphate biosynthesis underpins PAMP-triggered immunity to Pseudomonas syringae pv. tomato in Arabidopsis thaliana but is dispensable for establishment of systemic acquired resistance.

Phytic acid (inositol hexakisphosphate, InsP6 ) is an important phosphate store and signal molecule necessary for maintenance of basal resistance to plant pathogens. Arabidopsis thaliana ('arabidopsis') has three genes encoding myo-inositol phosphate synthases (IPS1-3), the enzymes that catalyse conversion of glucose-6-phosphate to InsP, the first step in InsP6 biosynthesis. There is one gene for inositol-(1,3,4,5,6)-pentakisphosphate 2-kinase (IPK1), which catalyses the final step. Previously, we showed that mutation of IPS2 and IPK1 but not IPS1 increased susceptibility to pathogens. Our aim was to better understand the InsP6 biosynthesis pathway in plant defence. Here we found that the susceptibility of arabidopsis (Col-0) to virulent and avirulent Pseudomonas syringae pv. tomato was also increased in ips3 and ips2/3 double mutants. Also, ipk1 plants had compromised expression of local acquired resistance induced by treatment with the pathogen-derived molecular pattern (PAMP) molecule flg22, but were unaffected in other responses to flg22, including Ca2+ influx and the oxidative burst, seedling root growth inhibition, and transcriptional up-regulation of the PAMP-triggered genes MITOGEN-ACTIVATED PROTEIN KINASE (MPK) 3, MPK11, CINNAMYL ALCOHOL DEHYDROGENASE 5, and FLG22-INDUCED RECEPTOR-LIKE KINASE 1. IPK1 mutation did not prevent the induction of systemic acquired resistance by avirulent P. syringae. Also, ips2 and ips2/3 double mutant plants, like ipk1, were hypersusceptible to P. syringae but were not compromised in flg22-induced local acquired resistance. The results support the role of InsP6 biosynthesis enzymes in effective basal resistance and indicate that there is more than one basal resistance mechanism dependent upon InsP6 biosynthesis.

Colonization of Barley by the Broad-Host Hemibiotrophic Pathogen Phytophthora palmivora Uncovers a Leaf Development-Dependent Involvement of Mlo.

The discovery of barley Mlo demonstrated that filamentous pathogens rely on plant genes to achieve entry and lifecycle completion in barley leaves. While having a dramatic effect on foliar pathogens, it is unclear whether overlapping or distinct mechanisms affect filamentous pathogen infection of roots. To remove the bias connected with using different pathogens to understand colonization mechanisms in different tissues, we have utilized the aggressive hemibiotrophic oomycete pathogen Phytophthora palmivora. P. palmivora colonizes root as well as leaf tissues of barley (Hordeum vulgare). The infection is characterized by a transient biotrophy phase with formation of haustoria. Barley accessions varied in degree of susceptibility, with some accessions fully resistant to leaf infection. Notably, there was no overall correlation between degree of susceptibility in roots compared with leaves, suggesting that variation in different genes influences host susceptibility above and below ground. In addition, a developmental gradient influenced infection, with more extensive colonization observed in mature leaf sectors. The mlo5 mutation attenuates P. palmivora infection but only in young leaf tissues. The barley-P. palmivora interaction represents a simple system to identify and compare genetic components governing quantitative colonization in diverse barley tissue types.

Modulation of host cell biology by plant pathogenic microbes.

Plant-pathogen interactions can result in dramatic visual changes in the host, such as galls, phyllody, pseudoflowers, and altered root-system architecture, indicating that the invading microbe has perturbed normal plant growth and development. These effects occur on a cellular level but range up to the organ scale, and they commonly involve attenuation of hormone homeostasis and deployment of effector proteins with varying activities to modify host cell processes. This review focuses on the cellular-reprogramming mechanisms of filamentous and bacterial plant pathogens that exhibit a biotrophic lifestyle for part, if not all, of their lifecycle in association with the host. We also highlight strategies for exploiting our growing knowledge of microbial host reprogramming to study plant processes other than immunity and to explore alternative strategies for durable plant resistance.