Abstract
My group is addressing fundamental questions in evolutionary biology, using both genome-first and phenotype-first approaches. A few years ago, we discovered that Arabidopsis thaliana is a great model for the study of hybrid necrosis. This widespread syndrome of hybrid failure in plants is caused by plant paranoia – regardless of the presence of enemies, plants “think” they are being attacked by pathogens. The consequence is autoimmunity, which can be extreme enough to kill plants before they set seeds. Over the past decade, we have studied in detail the underlying genetics, finding that often only one or two loci are involved, with most of them encoding NLR immune receptors. The NLR gene family is the most variable gene family in plants, and it is thus not surprising that they are often involved in genome-genome conflict, with alleles at one locus greatly changing the activity of alleles at another locus. Similarly, we have found that autoimmunity due to allelic variation at the ACD6 locus, which probably encodes a channel, is modulated by a slew of extragenic suppressors. I will describe what we have learned and how our unique angle on studying the plant immune system has led to insights that were not obtained with conventional laboratory genetics. Our goal for the next decade is to understand the genomic and geographic patterns of immune system diversity. Together with collaborators Jeff Dangl, Jonathan Jones and Brian Staskawicz, we have been describing species-wide diversity of NLR immune receptor genes. In parallel, we have been describing with collaborator Eric Kemen the local diversity on A. thaliana plants of the microbial pathogen, Pseudomonas, on A. thaliana plants. This year, we initiated an ambitious new project, Pathodopsis (Pathogens in Arabi]dopsis), in which we aim to describe genetic diversity in the host and two important pathogens, the generalist Pseudomonas and the specialist Hyaloperonospora arabidopsidis. The long-term vision is to produce maps of resistance alleles in the host, and of effector alleles in the pathogens, in order to learn who normally wins in a wild plant pathosystem – the host or the pathogen.
