Professor of PPPMB
The Martin laboratory studies the molecular basis of bacterial infection processes, plant disease susceptibility, and plant immunity.
The Martin laboratory studies the molecular basis of bacterial infection processes and the plant immune system. The research focuses on speck disease which is caused by the infection of tomato leaves with the bacterial pathogen Pseudomonas syringae pv. tomato. This is an economically important disease that can decrease both the yield and quality of tomato fruits. It also serves as an excellent system for studying the mechanisms that underlie plant-pathogen interactions and how they have evolved. Many experimental resources including an increasing number of genome sequences are available for both tomato and P. s. pv. tomato. Current work relies on diverse experimental approaches involving methods derived from the fields of biochemistry, bioinformatics, cell biology, forward and reverse genetics, genomics, molecular biology, plant breeding, plant pathology, and structural biology.
In the tomato-Pseudomonas interaction, the plant responds rapidly to a potential infection by detecting certain conserved molecules expressed by the pathogen. At this stage the pathogen uses a specialized secretion system to deliver virulence proteins, such as AvrPto and AvrPtoB, into the plant cell. These proteins suppress early host defenses and thereby promote disease susceptibility. Some tomato varieties express a resistance gene, Pto, which encodes a protein that detects the presence of AvrPto or AvrPtoB and activates a second strong immune system that halts the progression of bacterial speck disease.
The Martin lab is currently studying many aspects of the molecular mechanisms that underlie the bacterial infection process and the plant response to infection. One project takes advantage of the genetic natural variation present in wild relatives of tomato to identify new genes that contribute to plant immunity. These genes provide insights into the plant immune system and also can be bred into new tomato varieties to enhance disease resistance. A second project relies on next-generation sequencing methods to identify tomato genes whose expression increases during the interaction with P. s. pv. tomato. The expression of these genes is then reduced by using virus-induced gene silencing or they are mutated using CRISPR/Cas9 to test whether they make a demonstrable contribution to immunity. A third project uses photo-crosslinking and other biochemical methods to characterize plant proteins that play a direct role in recognizing the conserved bacterial molecules that activate the early plant immune system.
The long-term goal in this research is to use the knowledge gained about the molecular basis of plant-pathogen interactions to develop plants with increased natural resistance to diseases. Such plants would require fewer applications of pesticides producing economic and environmental benefits while providing food for consumers with less pesticide residue.
PLPA 452.1 / PLPA 662.1 Molecular Plant-Microbe Interactions: Plant Responses to Pathogen Attack. 4-week module (1 credit. Taught in even-numbered years.
- Wei, H. L., Chakravarthy, S., Mathieu, J., Helmann, T., Stodghill, P., Swingle, B., Martin, G. B., & Collmer, A. (2015). Pseudomonas syringae pv. tomato DC3000 Type III secretion effector polymutants reveal an interplay between HopAD1 and AvrPtoB. Cell Host & Microbe. 17:752-762.
- Mathieu, J., Schwizer, S., & Martin, G. B. (2014). Pto kinase binds two domains of AvrPtoB and its proximity to the effector E3 ligase determines if it evades degradation and activates plant immunity. PLoS Pathogens. 10:e1004227.
- Pombo, M. A., Zheng, Y., Fernandez-Pozo, N., Dunham, D. M., Fei, Z., & Martin, G. B. (2014). Transcriptomic analysis reveals tomato genes whose expression is induced specifically during effector-triggered immunity and identifies the Epk1 protein kinase which is required for the host response to three bacterial effector proteins. Genome Biology. 15:492.
- Rosli, H. G., Zheng, Y., Pombo, M. A., Zhong, S., Bombarely, A., Zhangjun, Z., Collmer, A., & Martin, G. B. (2013). Transcriptomics-based screen for genes induced by flagellin and repressed by pathogen effectors identifies a cell wall-associated kinase involved in plant immunity. Genome Biology. 14:R139.
- Bombarely, A., Rosli, H. G., Vrebalov, J., Moffett, P., Mueller, L. A., & Martin, G. B. (2012). A draft genome sequence of Nicotiana benthamiana to enhance molecular plant-microbe biology research. Molecular Plant-Microbe Interactions. 25:1523-1530.
- Cunnac, S., Chakravarthy, S., Kvitko, B. H., Russell, A. B., Martin, G. B., & Collmer, A. (2011). Genetic disassembly and combinatorial reassembly identify a minimal functional repertoire of type III effectors in Pseudomonas syringae pv. tomato DC3000. PNAS: Proceedings of the National Academy of Sciences of the United States of America. 108:2975-2980.
- Oh, C., Pedley, K., & Martin, G. B. (2010). Tomato 14-3-3 protein 7 (TFT7) positively regulates immunity-associated programmed cell death by enhancing protein abundance and signaling ability of MAPKKKα. The Plant Cell. 22:260-272.
- Shan, L., He, P., Li, J., Heese, A., Peck, S., Numberger, T., Martin, G. B., & Sheen, J. (2008). Bacterial effectors target BAK1 to disrupt MAMP receptor signaling complexes and impede plant innate immunity. Cell Host & Microbe. 4:17-27.
- Rosebrock, T. R., Zeng, L., Brady, J. J., Abramovitch, R. B., Xiao, F., & Martin, G. B. (2007). A bacterial E3 ubiquitin ligase targets a host protein kinase to disrupt plant immunity. Nature. 448:370-374.
- Abramovitch, R. B., Anderson, J. C., & Martin, G. B. (2006). Bacterial elicitation and evasion of plant innate immunity. Nature Reviews Molecular Cell Biology. 7:601-611.