Peter Balint-Kurti was born in Boston MA, attended Cambridge University (UK) as an undergraduate and received his Ph.D. at the Sainsbury Laboratory, John Innes Centre, University of East Anglia in Norwich, UK (1990-1994). He held post-doctoral appointments at the National Institutes of Health and the Boyce Thompson Institute at Cornell University, and worked at two biotechnology companies before joining the USDA-ARS in 2003 as a research geneticist where he remains today. He also holds the position of USDA Professor in the Department of Plant Pathology at North Carolina State University.
Balint-Kurti is internationally recognized for his work on the genetics of disease resistance and defense response in plants. Early in his career, he contributed to the cloning of the disease resistance genes Cf-4 and Cf-9 in tomato, which are among the first plant major resistance genes to be identified. Since 2003, Balint-Kurti has focused on elucidating the genetics controlling quantitative disease resistance (QDR) and the defense response in maize, a model genetic system and a vital crop. QDR, also known as partial resistance, is the predominant form of disease resistance deployed in agriculture and the only form of resistance for most necrotrophic pathogens. In contrast to qualitative resistance, QDR tends to be durable, and seldom overcome by pathogens in the field. However, molecular and genetic bases of QDR are poorly understood, in part due to difficulties inherent in studying alleles with small and often environmentally dependent effects.
Focusing on the foliar fungal diseases Southern leaf blight (SLB, caused by Cochliobolus heterostrophus), Northern leaf blight (NLB, caused by Exserohilum turcicum) and Gray leaf spot (GLS, caused by Cercospora zeae-maydis), and using large mapping populations, careful phenotyping, and powerful genetic analysis resources available for maize, Balint-Kurti and colleagues have elucidated the genetic architecture controlling natural variation in QDR to these diseases in unprecedented detail. An emphasis on natural (as opposed to mutational) variation is important since this is the variation with which breeders generally work to improve crops.
Balint-Kurti’s group has now identified several genes affecting a variety of different pathways which, when disrupted, alter the observed symptoms associated with SLB, showing that the mechanistic bases of QDR are numerous and relatively non-specific. This non-specificity has been largely considered at the level of isolates within a species, but the work of Balint-Kurti and his colleagues has shown that, in some cases, QDR is not specific to particular diseases either. Multiple disease resistance (MDR), the phenomenon whereby genes or loci confer QDR to more than one disease had not previously been systematically investigated in plants. Their work has identified the presence of genetic factors conferring MDR to GLS, SLB and NLB in maize. They have also identified several QTL alleles and two specific genes associated with enhanced levels of resistance to more than one disease. Building on these findings, Balint-¬Kurti and colleagues identified alleles from teosinte, the ancient progenitor of cultivated maize, that confer superior levels of QDR and, in one case, MDR to both GLS and SLB.
Balint-Kurti’s and collaborators also used a novel technique called MAGIC (mutant-assisted gene identification and characterization) to characterize the genetic control of the hypersensitive response (HR) in maize. The HR, a rapid, localized cell death in response to pathogen penetration, is a ubiquitous and vital component of the classical qualitative disease resistance response in higher plants. Little is known about how the strength of the HR varies in natural populations or the genetic architecture controlling this variation. Balint-Kurti’s team developed and used massive mapping populations combined with precise phenotyping to identify sets of specific genes and pathways associated with natural variation in the strength of HR. As part of this work, Balint-Kurti demonstrated that the genetic bases of variation in QDR and HR partially overlap, and that they also share some genetic basis with variation in the strength of a mild leaf flecking trait often observed in maize lines.
Studying Rp1, a major maize resistance (R-) gene that triggers HR upon pathogen recognition, Balint-Kurti’s group showed that the Rp1 protein interacts directly with two proteins in the phenylpropanoid pathway, a crucial pathway in plant defense, and that these interactions modulate Rp1 activity. Balint-Kurti’s group is investigating how natural allelic variation in some of these proteins alters the strength of the HR elicited. This work also identified several novel features concerning the control of R-gene regulation and sub-cellular localization which are likely important in numerous plant-pathogen systems.
Balint-Kurti has published his findings in high-impact journals including Science, Proceedings of the National Academy of Sciences, Plant Cell, Plant Journal, Plant Physiology, Genetics, PLoS Genetics, and PLoS Pathogens. He has contributed to several reviews summarizing the state of the art in the genetics of plant disease resistance. He was the Chair of the inaugural and, respectively co-Chair and co-organizer of the second and third Maize Plant-Microbe interactions workshops held in 2011, 2013 and 2016. He has been PI or Co-PI on grants totaling more than $12.5M. His outreach work on plant genetics with the North Carolina Museum of Natural Sciences has reached thousands of students across North Carolina. He has been an associate and senior editor for Phytopathology, is a senior editor for Plant Pathology and was a member of the maize genetics steering committee. The MAGIC technique that he helped pioneer has been used by many other research groups investigating a variety of traits.
Balint-Kurti’s sustained contributions to the field of maize disease resistance and defense response have provided a framework for the understanding and further investigation of this phenomenon in plants. His work in bringing the maize disease community together has resulted in a more robust scientific community able to better tackle disease problems in one of our most important crops.