- American Association for the Advancement of Science (2010)
- American Association for the Advancement of Science
Indiana University Bloomington
College of Arts and Sciences
Department of Biology
BIOGRAPHYRoger Innes is Professor and Chair of Biology at Indiana University Bloomington. His research interests include: Eukaryotic Cell Biology, Cytoskeleton and Signaling, Microbial Interactions and Pathogenesis, and Plant Molecular Biology. His PhD is from the University of Colorado (1988) and he completed postdoctoral work at the University of California, Berkeley (1988-1991).
Dr. Innes' research and lab work is primarily interested in understanding the genetic and biochemical basis of disease resistance in plants. Plants are able to specifically recognize pathogens and actively respond. We are investigating how this specific recognition is accomplished and how recognition is translated into a resistant response. Our research is funded by two grants from the NIH and has recently been featured in the European journal International Innovation.
To address these questions we take a molecular genetic approach. We use the small mustard Arabidopsis thaliana as our standard host plant, and the bacterial pathogen Pseudomonas syringae as our standard pathogen. Recognition of specific P. syringae strains by Arabidopsis is mediated by specific disease resistance ( R ) genes of Arabidopsis. These R genes are thought to encode receptors that detect a signal produced directly or indirectly by bacterial proteins that are injected into the plant cell. The molecular mechanism of this detection step is poorly understood, however. Understanding this mechanism is a major goal in plant biology as it will likely lead to new approaches for engineering disease resistance in plants, as well as provide critical insights into how pathogens evolve to escape recognition and cause disease.
To uncover the molecular basis of pathogen recognition we have focused on identifying genes in both the plant and the pathogen that are required for the recognition event. This has been accomplished by screening for plant mutants that fail to respond to bacteria expressing specific effector proteins that are secreted into the plant cells. To date we have cloned two R genes ( RPM1 and RPS5 ) and have identified six additional genes ( PBS1 , PBS2 , PBS3 , EDR1 , EDR2 , and EDR3 ) believed to mediate signal transduction events. RPM1 and RPS5 belong to a very large gene family in plants. Each member of this family mediates recognition of a specific pathogen molecule. All members of this R gene family contain a nucleotide binding site (e.g. ATP) and leucine rich repeats (LRRs). The LRRs are thought to mediate protein:protein interactions, and may possibly participate in binding pathogen molecules or the targets of pathogen molecules. We have shown that the PBS1 protein is a target of the P. syringae protease AvrPphB, and that cleavage of PBS1 somehow activates the RPS5 protein. We are now using a combination of biochemical and genetic approaches to determine how this activation occurs. In addition, we have recently isolated a disease resistance gene from soybean, Rpg1 , that has the same specificity as RPM1 . We have shown that Rpg1 and RPM1 evolved independently in soybean and Arabidopsis, but recent data suggest that the recognition mechanism may be the same in soybean and Arabidopsis. These analyses may allow us to develop "designer R genes" that have novel specificities for use in real world agriculture.