George W. Sundin was born in Philadelphia, Pennsylvania, and grew up in southern New Jersey. He received his B.S. degree in biology at Penn State University and credits William Merrill with stimulating his interest in plant pathology. Sundin received an M.S. degree in plant pathology from Michigan State University (MSU) and a Ph.D. degree in plant pathology from Oklahoma State University. He conducted post-doctoral research at the University of Illinois-Chicago in environmental microbiology. In 1997, Sundin joined the faculty in the Department of Plant Pathology & Microbiology at Texas A&M University with a research emphasis in phytobacteriology. He was tenured in 2002. Later that year, Sundin joined the Department of Plant Pathology at MSU, where he is currently a professor and extension specialist with responsibilities in tree fruit disease management.
Sundin’s current research is focused on basic and applied research on the fire blight pathogen Erwinia amylovora. Sundin’s research goals are to obtain a comprehensive genetic understanding of E. amylovora–apple interactions and to research and optimize new control measures for fire blight. Sundin is part of a team that has made recent discoveries (detailed below) and has begun extensive genome-scale studies to understand the regulation of pathogenesis in E. amylovora by small noncoding RNAs and the second messenger compound cyclic di-GMP. Sundin’s group also performs research focused on disease management of fungal tree fruit diseases and on the genetics and mechanisms of fungicide resistance.
Sundin is committed to graduate education and has served as major advisor for eight M.S. and nine Ph.D. graduate students and ten post-doctoral research associates. Sundin has also mentored three Ph.D. graduate students from Spain who have studied in his lab at MSU. Sundin teaches a graduate course in phytobacteriology and also provides guest lectures for other graduate courses in plant pathology and in the Microbiology Department.
Sundin was an associate editor (2004–2006) and a senior editor (2009–2011) for Phytopathology and is currently editor-in-chief (2012–2014) and a member of the APS Publications Board. He has served the North Central Division as councilor and divisional forum representative (2009–2012) and was the inaugural chair of the APS Divisional Forum (2010–2011). He has also served on the APS Bacteriology and Phyllosphere Microbiology Committees.
Sundin is recognized specifically for his research on the fire blight disease and pathogen. Fire blight is a significant problem in most apple- and pear-growing regions of the world. It can be devastating, and management efforts are impacted by the evolution of resistance in the pathogen to the main chemical control compound streptomycin. Sundin has attacked fire blight from many research angles. Since 2006, Sundin and colleagues have published eight fire blight articles in APS journals. In addition, Sundin has published 19 fire blight research reports in Plant Disease Management Reports (PDMR) and contributed the fire blight chapter in the upcoming APS Compendium of Apple and Pear Diseases and Pests, Second Edition.
Sundin’s applied research, published in Phytopathology, Plant Disease, and PDMR, has contributed to an understanding of the mechanism of streptomycin resistance in E. amylovora strains in Michigan and the spread of streptomycin-resistant strains, the development of the agricultural antibiotic kasugamycin for fire blight management, and a thorough evaluation of the potential for biological control for managing fire blight in the eastern United States. Sundin’s basic research, published in Molecular Plant-Microbe Interactions (MPMI) and Phytopathology, has contributed to our knowledge of critical virulence determinants of E. amylovora and a better understanding of host–pathogen interactions. His basic research has laid a strong foundation for long-term efforts by Sundin’s group to develop novel controls that target critical pathogenicity mechanisms of E. amylovora.
In 2011, Sundin and his research team demonstrated that streptomycin-resistant (SmR) strains of E. amylovora had spread throughout major apple-growing areas in Michigan between 2004 and 2010. Genetic characterization of strains indicated that only two genotypes were responsible for the streptomycin resistance, even though the SmR genes in E. amylovora in Michigan are located on a transposable element that was acquired by horizontal gene transfer. The significance of this work was the finding that E. amylovora is apparently not a ready partner for gene transfer events in agricultural habitats. These results have important implications for the use of streptomycin in Michigan in areas that are not yet impacted by streptomycin resistance. Sundin’s group also published results demonstrating the field efficacy of kasugamycin and has demonstrated that laboratory-derived spontaneous kasugamycin-resistant mutants of E. amylovora were reduced in fitness and virulence development. The results enabled Sundin and the Michigan Department of Agriculture to obtain a Section 18 Specific Exemption (2010–2013) from the EPA for kasugamycin use in orchards in Michigan that are impacted by streptomycin resistance. This helped growers avert potential catastrophic losses.
Sundin’s other recent work published in Phytopathology includes a 2009 paper demonstrating the importance of biofilms to infection by E. amylovora and that biofilm formation plays a critical role in xylem invasion and systemic movement of the pathogen in apple. The establishment of biofilms as an important virulence mechanism of E. amylovora has set new work in motion by Sundin’s group toward finding inhibitors of biofilm formation that could be used for fire blight management. In a second 2009 paper, Sundin’s group determined the mechanism of action of prohexadione-calcium (ProCa), an important growth regulator of apple that is also active in shoot blight control. This work demonstrated that ProCa treatment results in the thickening of apple cell walls that subsequently limit E. amylovora infection and migration between parenchymal cells into host xylem tissue. A hypothesis was presented that thickened cell walls are recalcitrant to E. amylovora infection because the type III secretion Hrp pilus is not as thick as the average cell wall width of ProCa-treated apple cells.
Sundin’s basic research published in MPMI included work leading to the identification of a new type III effector in E. amylovora, termed AvrRpt2Ea. This effector was similar to a type III effector from Pseudomonas syringae that has been studied quite extensively and is known to trigger resistance in Arabidopsis thaliana via a known resistance gene. This work lead to a recent finding by Sundin, in collaboration with Andreas Piel at the University of Dresden in Germany, of a gene-for-gene interaction between Malus × robusta 5 and E. amylovora, in which AvrRpt2Ea is specifically recognized triggering a host resistance response. A second study published in MPMI deduced the role of the type III chaperone DspF in the secretion and translocation of the effector DspE. These studies have further unraveled the critical events during pathogenesis of E. amylovora in apple and provide potential targets for novel future disease control efforts.