Evasion of chitin-triggered immunity by fungal plant pathogens

Plants establish intricate relationships with microorganisms that range from mutualistic to pathogenic. In order to prevent colonization by potentially harmful microbes, plant hosts employ surface-localized receptor molecules that perceive ligands, which are either microbe-derived or result from microbe-mediated plant manipulation. This recognition ultimately leads to the activation of host immunity. In order to circumvent recognition or suppress immune responses, microbes secrete effector proteins that deregulate host physiological processes. While the number of identified putative effectors has rapidly increased in recent years, their functions and the mechanisms governing their recognition have largely remained unexplored. To enhance our understanding of the molecular interplay between host and microbe, the work presented here was designed to identify further components involved in the recognition of the two fungal pathogens Verticillium dahliae and Cladosporium fulvum, as well as to characterize the functions of effector proteins produced by these pathogens during tomato infection.