Characterisation of Eucalyptus grandis SWEET and SWI/SNF proteins during symbiosis with Pisolithus microcarpu

Eucalyptus grandis, an economically important bioenergy tree, is constantly bombarded by different fungal lifestyles seeking to acquire photosynthetically fixed sugar. How the plant immune system filters beneficial fungi from pathogenic is poorly understood. This thesis investigates two aspects of plant immunity: shuttling of sugar and interference by fungal effectors. Plant sugars are known to play a dual role in plant-microbe interactions: they can either feed the microbe with growth-limiting carbon or they can act as fuel for plant secondary metabolism and, subsequently, plant defence. In my first study I consider how hexose SWEET transporters respond at the transcriptomic level in E. grandis roots during challenge by different microbes covering the fungal lifestyles from pathogenic through mutualistic. Further, I characterise four E. grandis SWEET proteins that share sequence homology to previously identified SWEET proteins and determine their cellular localization, their sugar transport capabilities and their role in shuttling carbon during plant-microbe interactions. In the second part of my thesis, I investigate how a mutualistic fungus attempts to manipulate plant defences through the use of effector like proteins. Specifically, I characterise the role of Pisolithus albus MiSSP9.7, a highly induced secreted fungal protein of unknown function. I demonstrate that it interacts with a member of the SWI/SNF protein complex previously identified as being responsible for the regulation of plant hormone signalling pathways used in immune responses against microbes. Increased expression of SWI3D in E. grandis roots is tied to the colonisation process and may regulate a key aspect of plant immunity towards mutualistic fungi. Taken together, my work provides a better understanding of the controls used by plants to modulate plant-microbe interactions and the counter-measures utilized by fungi to overcome host immunity.