Mechanisms linking nutrient acquisition and water-soaking during bacterial infection of plants

点击翻译按钮获取中文摘要

Plant pathogens negatively affect production of food, fiber, biofuel and aesthetic crops. Water-soaking, which is the accumulation of fluid in extracellular spaces of infected plant tissues, is a hallmark symptom of diseases caused by pathogenic fungi, oomycetes and bacteria. Plant pathogens must also obtain nutrients from infected host tissues. Despite their central roles in pathogenesis, mechanistic explanations for how infecting microbes induce water-soaking and acquire nutrients are lacking. Bacterial pathogens that causes bacterial speck disease in tomato, the model plant Arabidopsis, and maize rely on a single, key virulence factor to induce water-soaking. In maize, the accumulating fluids are also rich in nutrients that support pathogen proliferation, indicating an inter-relationship in the key processes of water and nutrient acquisition. These findings along with identification of intracellular host targets of the virulence factor enable the proposed studies to elucidate molecular mechanisms underlying the liberation of water and nutrients from infected plant tissues. The acquired fundamental knowledge of this key step in pathogenesis will in turn enable breeding and biotechnological approaches for development of disease resistant plants. Because the key virulence factor is broadly conserved among diverse plant-pathogenic bacteria, these strategies will extend beyond tomato and maize to a multitude of agriculturally important plants.Prevailing speculation posits that pathogen-induced release of water and nutrients into extracellular spaces results from damage to plant cells. However, preliminary data indicate that Pseudomonas syringae pv. tomato (Pst) and Pantoea stewartii subsp. Stewartii (Pnss) deploy AvrE-family type III effector proteins that induce water-soaking and increase the extracellular abundance of nutritive metabolites prior to disrupting the integrity of infected plant cells. Additionally, pathogenicity of Pnss depends on AvrE-family effector induced perturbation of host phenylpropanoid metabolism, including accumulation of hydroxycinammic acid amides (HCAAs). Existing and newly generated mutant plants lacking AvrE-family effector targets, including plasma membrane-localized phosphatases, plasma membrane-spanning receptor-like kinases, and HCAA biosynthetic enzymes, will reveal the contribution of these host targets to effector-induced water and nutrient accumulation outside of intact plant cells. Comparisons of the plasma membrane (phospho)proteomes of wild-type plants with mutants that do not fully support the virulence activity of the AvrE-family effectors will enable identification of changes in protein phosphorylation or abundance that are genetically linked to these effector-induced perturbations of host physiology. These physiological, metabolomic, proteomic and genetic analyses will reveal mechanisms through which AvrE-family effectors regulate the movement of water and nutrients across the plasma membrane of host cells and place these mechanisms in the context of the disease state produced by Pst and Pnss in their dicot and monocot hosts, respectively. More generally, the findings will advance understanding of how plant pathogens induce water-soaked and nutritive extracellular spaces in their hosts.This award reflects NSF's statutory mission and has been deemed worthy of support through evaluation using the Foundation's intellectual merit and broader impacts review criteria.