How does a pathogen unlock the plasmodesmatal gates between neighbouring cells?

Cell-to-cell communication is fundamental to multicellular organisms. The exchange of information and resources between cells and tissues enables co-ordination of responses to environmental and developmental signals. In plants, the cytoplasm of adjacent cells is connected by intercellular ‘tunnels’ that cross the cell wall, generating cytoplasmic continuity between cells and tissues, and allowing for direct, intercellular exchange of molecules. This interconnected cytoplasm is termed the symplast and is unique to plants. The ‘tunnels’ between plant cells are plasma-membrane lined pores called plasmodesmata (PD) which effectively serve as ‘sluice gates’ that regulate the flux of soluble molecules between adjacent cells, and thus regulate symplastic communication.
Plant defence and pathogen infection are antagonistic processes. Both pathogens and host alike have something at stake in regulation of symplastic connectivity in the host tissues: we have found that the host tries to close PD in response to pathogen perception while the pathogen tries to suppress this. That pathogens actively compete with their hosts for control of PD compels us to ask what they gain from this: do pathogens aim to maintain symplastic connectivity to allow transit of molecules (effectors) to non-infected cells to suppress host immune responses, or to maximise pathogen access to host nutrients, or both?
This project will explore how the Arabidopsis fungal pathogen Colletotrichum higginsianum manipulates the plasmodesmata to gain access to the host symplast. Specifically, the project will firstly investigate how pathogens manipulate PD. We have identified Colletotrichum proteins that are secreted into plant cells and localise at plasmodesmata - using these proteins as bait the student will use biochemical methods to identify the host PD proteins that they target and manipulate. Secondly, the project will investigate the critical question of what a pathogen gains from manipulating PD. By manipulating the expression of these effectors during infection (by gene editing of the pathogen or host induced gene silencing), the student can compare the rate of infection and use transcriptional analysis to identify the processes that the presence of effector regulates during infection.
The project will also address whether we can we control infection success by cutting off a pathogen’s access to surrounding cells. By tuning the rate of callose synthesis that blocks PD (with genetically encoded inducible enzymes), the student can induce plasmodesmal closure and opening to determine the impact of increased isolation or connectivity between host cells on infection outcomes and immune responses. By using a range of pathogens this will enable the student to ask questions relating to whether symplastic connectivity contributes equally to different pathogen lifestyles.