HOPESEE · How do pathogens exploit the symplast to promote disease?

How do pathogens exploit the symplast to promote disease?

It is well established that pathogens invade plant cells to establish an infection. Part of a biotrophic pathogen’s infection strategy is to secrete their own protein effectors into host cells to manipulate the host cellular processes to the pathogen’s benefit. It has been observed that some effectors can move from cell-to-cell in the host and this suggests that a pathogen can invade and exploit cells surrounding the immediate infection site. To further support this hypothesis, my host lab observed that pathogen-induced plasmodesmata (PD) closure is suppressed in some virulent infections, suggesting pathogens attempt to keep intercellular connections open; some pathogens must maintain intercellular symplastic connectivity by counteracting pathogen-induced PD closure to promote disease. This proposes the question: why does a pathogen want PD open? We hypothesise that open PD allow pathogen effectors to move into non-infected cells where they target host processes to promote infection and allow pathogen access host resources such as sugars. In this study, I will use the Hyaloperonospora arabidopsidis (Hpa) – Arabidopsis interaction to identify cell-to-cell mobile effectors and their host targets. I will identify global changes of host gene regulation that are associated with cell-to-cell mobile effectors and examine the effect of cell-to-cell mobile effectors on sucrose transport around an infection site. The results will give a new insight into how pathogens exploit the symplast and noninfected cells to promote infection, characterising a poorly considered element of plant-pathogen interactions. Overall objectives of HOPESEE are as follows: 1. How does Hpa access the host symplast? I will perform a large-scale screen of Hpa effectors to identify those that have intercellular mobility. To understand how cell-to-cell mobile effectors contribute to infection I will assess their impact on virulence and identify host targets for selected effectors. 2. How does Hpa manipulate non-infected cells? My host lab has recently developed a line in which infected cells are symplastically isolated from neighbouring, non-infected cells. I will compare global gene expression in this line and wild-type plants to identify host processes that are targeted by symplast mobile effectors. In a targeted approach I will further examine the regulation of genes associated with sucrose transport and distribution around infected cells and use novel cell biological tools to assess sugars (specifically sucrose) transport during infection.

Data: CORDIS, © European Union