Understanding the mechanisms by which infectious agents cause disease has been revolutionized through the use of model genetic systems, especially in the case of plant pathogens. Evolutionary biologists have also provided significant insight into our understanding of infectious disease dynamics, including the evolution of virulence. Although hosts in nature are attacked by multiple pathogens and parasites simultaneously, such interactions are rarely studied by molecular biologists since most studies focus on a single pathogen. Conversely, although organismal biologists study these interactions with the goal of uncovering general principles underlying the ecology and evolution of host-parasite interactions, the underlying genetic or mechanistic bases of the biotic interactions mediated by host defense responses are rarely characterized. Thus, public health researchers have joined with evolutionary biologists in an effort to better understand and control infectious diseases. This proposal presents experiments designed to characterize proximate (genetic/physiological/mechanistic) and ultimate (evolutionary) mechanisms underlying two types of host defense signaling manipulation by pathogens in a model three-way pathosystem involving Arabidopsis, the pathogen Pseudomonas syringae (Ps) and insect herbivores. Ps manipulates defense signaling cross talk leading to systemic induced susceptibility (SIS) to infection by the same pathogens and increased resistance or susceptibility (SIS) to herbivory. SIS to Ps is mediated by the jasmonic acid analog coronatine (COR), which is produced by virulent Ps. However, the signal mediating the SIS to herbivory is unknown, and in both cases, the genes underlying systemic signals in the host plant are unknown. In the first aim, I will build on preliminary gene expression experiments to characterize the pathways underlying both types of SIS. In the second aim, I will investigate whether there is an adaptive basis to the two types of SIS by conducting kin selection, vector competency and other experiments.
Each aim dovetails with the cosponsors' research and my long-term career goals. Discoveries from plant- pathogen systems have led directly to a greater understanding of human-pathogen interactions. Conserved defense signaling pathways, innate immunity and many other insights that apply to all host-pathogen interactions began with studies of plants and their pathogens. Understanding the genetic, physiological and evolutionary basis of the SIS response to virulent Ps and herbivory with the goal of understanding pathogenesis and evolution of virulence is therefore directly related to the mission of the NIH. ? ? ?
| Groen, Simon C; Humphrey, Parris T; Chevasco, Daniela et al. (2016) Pseudomonas syringae enhances herbivory by suppressing the reactive oxygen burst in Arabidopsis. J Insect Physiol 84:90-102 |
| Groen, Simon C; Whiteman, Noah K; Bahrami, Adam K et al. (2013) Pathogen-triggered ethylene signaling mediates systemic-induced susceptibility to herbivory in Arabidopsis. Plant Cell 25:4755-66 |
| Whiteman, Noah K; Gloss, Andrew D; Sackton, Timothy B et al. (2012) Genes involved in the evolution of herbivory by a leaf-mining, Drosophilid fly. Genome Biol Evol 4:900-16 |
| Whiteman, Noah K; Groen, Simon C; Chevasco, Daniela et al. (2011) Mining the plant-herbivore interface with a leafmining Drosophila of Arabidopsis. Mol Ecol 20:995-1014 |
| Troemel, Emily R; Felix, Marie-Anne; Whiteman, Noah K et al. (2008) Microsporidia are natural intracellular parasites of the nematode Caenorhabditis elegans. PLoS Biol 6:2736-52 |
| Whiteman, Noah K; Pierce, Naomi E (2008) Delicious poison: genetics of Drosophila host plant preference. Trends Ecol Evol 23:473-8 |
