Our research is largely (though not entirely) in two related areas:

1. Identification and characterization of loci and genes which confer quantitative (or partial) disease resistance in maize.

For this we work mainly with three foliar fungal maize diseases; Southern corn leaf blight (SLB—causal agent Bipolaris maydis), Gray leaf spot (GLS - causal agent Cercospora zeae-maydis) and Northern leaf blight (NLB– causal agent Exserohilum turcicum).  We also work occasionally with various other maize diseases caused.

This work is funded largely by our base ARS funding, funding from NC Corn Growers and a recent NSF grant : “Genetic and Histological Dissection of Phenotypic Variation in Quantitative Resistance to Maize Diseases”.  This grant is a collaboration with Randall Wisser (PI),  Rebecca Nelson, Nick Lauter, Jim Holland, Kirk Czymmek and their groups.


2. Characterization of the genetic architecture controlling the maize defence response.

For this work we are using maize mutants with an extreme “auto-immune” phenotype to look at genetic factors modifying the maize defence response.

This work is also funded by our base ARS funding and another NSF grant: “Mutant-assisted exploration of natural variation underlying R gene-mediated immunity in maize “ and is a collaboration with Guri Johal at Purdue University.

For more specific details see below, or contact us.





As a starting point for our research, we identified regions of the genome (called quantitative trait loci or QTL) that confer quantitative resistance to SLB, NLB and GLS  in several segregating maize populations provided by collaborators (we’ve published a lot of this) .

In particular , we used the Maize IBM mapping population , an advanced intercross line population and the nested association mapping (NAM) population, developed under the NSF Molecular and Functional Diversity of the Maize Genome program.  In collaboration with Jim Holland we used the NAM to identify a set of genes strongly associated with resistance.  We are presently working with the loci identified in the NAM and IBM populations; fine-mapping the genes, validating their roles and investigating their function. 

           We are particularly interested to see whether there are common loci conferring resistance to all three diseases.  In some  cases we have identified common QTL for SLB and GLS. In collaboration with Rebecca Nelson’s and Randy Wisser’s groups, we phenotyped a 303-line collection of diverse maize germplasm for resistance to SLB, NLB and GLS .   We observed that in this population there was a significant genetic correlation between resistance to the three different diseases– implying the existence of genes for multiple disease resistance.  Through association mapping we identified a SNPs associated with multiple disease resistance in a Glutathione-S-transferase gene.

 We have also identified correlations between resistance to multiple diseases in the IBM and other populations.

In collaboration with Randy Wisser we are producing a set of Near-Isogenic Line populations designed specifically for investigating the genetic bases of multiple disease resistance, with multiple disease resistant lines as the donor parent and multiple disease susceptible lines as the recurrent parents


Identification of QTL for single and multiple disease resistance

Research Program

Text Box: Southern leaf blight (left) and Gray leaf spot (right) , in North Carolina in 2005

Certain alleles of major resistance genes (R-genes) confer a mutant, “disease lesion mimic” phenotype, where the Hypersensitive resistance response is triggered inappropriately.   We are using one of these genes, Rp1-D21 as a reporter for the maize defence response.

           Disease lesion mimic genes confer different phenotypes in different genetic backgrounds (see below) .  By mapping the loci responsible for these differences, we hope to gain an insight into the mechanics of the defence response in maize.  We have identified several loci that moderate the lesion mimic phenotype (Figure 10).    We are also interested in how the Rp1-D21 gene works and we are taking several approaches to examine this.

This work is funded by an NSF grant  and is a collaboration with Guri Johal. See the project website for more info.

Use of a disease lesion mimic to investigate the genetic architecture of the maize defence response

Identification of disease resistance genes from exotic germplasm

X CML322


X B73


Example of different phenotypes conferred by the Rp1-D21 gene in different genetic backgrounds

Peter Balint-Kurti


Dept. of Plant Pathology,

NC State University

Raleigh NC 27695-7616

Phone: 919-515-3516

Lab: 919 515 7376


E-mail: peter_balintkurti@ncsu.edu




USDA-ARS Maize Disease Resistance Genetics at NC State

We are interested in optimization of a viral induced silencing system in maize.  This is a collaboration with Rick Nelson at the Noble Foundation, Ardmore OK and Peg Redinbaugh in Wooster OH.  We have focused on improving Dr. Nelson’s VIGS sytem using BMV (see Mol. Plant-Microbe Interact. 19, 1229-1239 ), looking both at various hosts and different ways of delivering the virus.


Viral Induced Gene silencing in Maize

Demonstration of VIGS in maize (L. Benavente and P. Balint-Kurti unpublished).  Photobleaching (white areas) resulting from the silencing of phytoene desaturase by seed infection vascular puncture of a VIGS construct in maize inbred lines (A) Ki3 and (B) Oh7B.

Text Box: Scatter plot of breeding values for resistance to SLB , GLS and NLB. Dots indicate genotypic breeding values or E-MBLUPs .  Axes span the full range of the measurement scale for each disease and resistance increases with increasing values.  A color scale is used to indicate the breeding values for northern NLB resistance.

           We are using a number of approaches to try to identify gene alleles for disease resistance from exotic sources.  Such alleles are likely not present in the genetic pool used in most US breeding programs and are therefore more likely to be useful.

            Both the Association and NAM populations are rich sources of exotic alleles and we are using both these populations extensively (see above).  In addition we are screening a population of ~700 Near-Isogenic lines in which segments of chromosomes from various teosinte accessions (the progenitor of maize) are introgressed into a standard maize background.  This population was provided by our collaborator Sherry Flint-Garcia .    We have found several loci associated with resistance to both GLS and SLB

Text Box: Teosinte and primitive maize