The needle and the damage done: type III effectors and the plant immune response

TitleThe needle and the damage done: type III effectors and the plant immune response
Publication TypeBook Chapter
Year of Publication2009
AuthorsLewis JD, Schreiber K, Desveaux D
Book TitleMolecular Plant-Microbe Interactions, edited by Bouarab K, Brisson N and Daayf F
VolumeChapter 8
Pagination p. 179-210
PublisherCAB International
AbstractThe intimate interactions between plant pathogenic bacteria and their hosts have resulted in an evolutionary arms race between host immune responses and pathogen virulence strategies. Successful pathogens are continuously under pressure to diversify their mechanisms to thwart host defences and optimize nutrient availability, while at the same time avoiding recognition by host surveillance systems. In turn, these virulence mechanisms have shaped the evolution of plant innate immunity. The needle-like structure known as the type III secretion system is used by numerous Gram-negative bacterial pathogens to inject diverse sets of effector proteins into host cells where they have been demonstrated to dampen host immune responses and promote virulence. Not surprisingly, type III effector molecules are prime ‘non-self’ molecules and plants have evolved to recognize their presence and deploy effective defence responses. Type III effector proteins are the direct molecular interface between pathogen and host and their study has yielded invaluable information about the evolution of host / pathogen interactions. In this Chapter, we discuss recent advances in understanding the diverse virulence and avirulence functions of the type III effector proteins of plant pathogenic bacteria. We discuss how their biochemical activities on host targets can contribute to the recognition of ‘modified self’ by the host and the activation of plant innate immunity. Further, we describe how type III effectors can usurp host proteins for their activation and also their use of structural mimicry of eukaryotic proteins as a virulence strategy. Finally, we address the evolutionary pressures and diversification mechanisms of type III effectors and the functional consequences for adaptation of pathogens and their hosts.