Figure 5.  The individual effects on SLB resistance of  each single introgression that differentiates B73 and NC292.  A bar below the x-axis indicates increased resistance.

Our projects are centered around identifying and characterizing loci and genes which confer quantitative (or partial) disease resistance in maize (corn) and identifying maize lines with superior disease resistance.

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 with other diseases caused by fungal pathogens including :  Aspergillus ear rot (causal agent Aspergillus flavus), Fusarium ear rot (Fusarium verticillioides) and maize common rust (Puccinia sorghi).

 

 

 

 

 

 

 

 

 

As a starting point for our research, we are identifying regions of the genome (called quantitative trait loci or QTL) that confer quantitative resistance to SLB, NLB and GLS  in several segregating maize populations which have been provided by collaborators (see Publications).

           We are particularly interested to see whether there are common loci conferring resistance to both diseases.  In some  cases we have identified common QTL for SLB and GLS (Figure 2)

 

Identification of Quantitative Trait Loci for disease resistance in maize segregating populations

Research Program

Figure 1. Southern leaf blight (left) and Gray leaf spot (right) , in North Carolina in 2005

      We have been phenotyping a 303-line collection of diverse maize germplasm for resistance to SLB, NLB (in collaboration with Rebecca Nelson’s and Randy Wisser’s groups) and GLS for several years.   This population is also used for association mapping and we have used it to identify several snps potentially associated with resistance .  We have shown that, in this population,  there is a significant genetic correlation between resistance to the three different diseases– implying that genes for multiple disease resistance exist (Figure 8).We have also identified correlations between resistance to multiple diseases in the IBM and other populations.

 We also screen germplasm for the USDA GEM program.

                     

 

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 interested in these genes from two perspectives;

· Some disease lesion mimic genes seem to confer non-specific, quantitative resistance.

· Disease lesion mimic genes confer different phenotypes in different genetic backgrounds (Figure 9) .  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 shown that a locus on chromosome 10 moderates the lesion mimic phenotype caused by the aberrant resistance gene Rp1-D21 (Figure 10).    We have recently been awarded a grant by NSF to continue this work.  This is a collaboration with Guri Johal and Cliff Weil.

 

         We are using Near-Isogenic Line pairs for fine mapping of the resistance loci with the eventual goal of cloning the genes involved.  Presently we are concentrating on cloning genes in bins 3.04 and 6.01.  We are also making a detailed study of the pathogenesis process on these pairs to determine where in the pathogenesis process resistance conferred by each QTL is manifested (Figure 6, 7).

Use of Disease Lesion Mimics to investigate the genetic architecture of the Maize Hypersensitive Response

Diverse Germplasm Survey/Multiple Disease Resistance/Association Mapping

B73

NC330

X CML322

 

X B73

 

Figure 9. An example of the different phenotypes conferred by the Rp1-D21 gene in different genetic backgrounds

         Our projects incorporate quantitative genetics, molecular biology and plant pathology.  Some of the major questions/goals we are addressing include:

· Where are disease resistance quantitative trait loci (dQTL) located in maize?

· Are there dQTL hotspots in the genome?

· Do dQTL confer resistance to more than one disease (multiple disease resistance)?

· What is the molecular identity of genes conferring quantitative resistance, and how are they working?  

· Are there similarities between quantitative and qualitative resistance mechanisms?

· What genetic pathways are involved in maize disease resistance?

· Can we identify superior disease resistant germplasm for incorporation into breeding programs?

Peter Balint-Kurti

USDA-ARS

Dept. of Plant Pathology,

NC State University

Raleigh NC 27695-7616

Phone: 919-515-3516

Lab: 919 515 7376

Fax:919-856-4816

E-mail: peter_balintkurti@ncsu.edu

 

 

 

We have surveyed the maize quantitative disease resistance literature to look for possible patterns and identify hotspots in the genome for disease resistance.  We plan to repeat these surveys on a periodic basis.  See Wisser et al. 2006.

Literature surveys and Reviews

Consensus map of resistance loci in maize. Chromosome 3 is shown here for illustration purposes.  At the bottom of the diagram is a histogram summarizing the QTL frequency per centiMorgan.  The thicker line shows the frequency of dQTL and the thinner line maturity QTL.  dQTL hotspots (taking into account gene density) are indicated as white areas in the histogram.  On chromosome 3 there are two such hotspots, 3a and 3b.

 

Production and characterization of Near-Isogenic Lines

Once we have identified QTL we want to move them into a common genetic background in order to characterize and fine-map them.     We have done this in a number of ways , through our own crossing programs (Figure 4) and through collaborations with Peg Redinbaugh, Owen Hoekenga, Mike Kolomiets,  Jim Holland, Roberto Tuberosa and Sherry Flint-Garcia.

           John Zwonitzer has created a series of B73 NILs in which different QTL loci from the elite resistance source NC250 are introgressed (Figure 4).   Several of these introgressions cause significant levels of SLB resistance (Figure 5).

Figure 4. The lines NC292 and NC330 were developed as B73-NILs (~95% B73 background) with contributions from the line NC250 which conferred greatly enhanced SLB resistance compared to B73.   We have characterized these line to identify the introgressions derived from NC250 in NC292 and NC330 and have created a set of single introgression lines in B73 background each carrying one of these introgressions

In particular , we have been using the Maize IBM mapping population , an advanced intercross line population that allows the quite precise mapping of QTL, to map QTL for resistance to SLB, NLB and GLS.   We are now using the nested association mapping (NAM) population, developed under the NSF Molecular and Functional Diversity of the Maize Genome program. We anticipate this will soon allow us to map SLB QTL down to the gene or several-gene level.

We are involved in the following specific projects:

 

·  Identification of QTL for disease resistance in maize segregating populations

· Production and characterization of Near-Isogenic Lines

· Diverse Germplasm Survey/Multiple Disease Resistance/Association Mapping

· Use of Disease Lesion Mimics to investigate the genetic architecture of the Maize Hypersensitive Response

· Literature Reviews

·  Viral Induced Gene Silencing in Maize

Figure 10.  Identification of a QTL that modifies the Rp1-D21 phenotype on maize chromosome 10.  A B73 allele represses the phenotype and a M017 allele enhances it.

         Rp1-D21 was crossed into the maize IBM population and the resulting F1 families were assessed in North Carolina , Indiana and in the greenhouse.  The QTL was identified in each environment.

We have also written reviews on maize disease resistance, gene discovery using mutants and quantitative resistance, see publications.

USDA-ARS Maize Disease Resistance Genetics at NC State

We have recently received a grant to work on optimization of a viral induced silencing system in miaze.  This is a collaboration with Rick Nelson at the Noble Foundation, Ardmore OK and will initially focus on improving his VIGS sytem using BMV (see Mol. Plant-Microbe Interact. 19, 1229-1239 ).

We are currently looking for a post-doctoral associate to work on this project– further details available on request.

Viral Induced Gene silencing in Maize