PROGRAM OBJECTIVES

Host-Pathogen Interaction and Variability of Colletotrichum lindemuthianum

Maeli Melotto¹, Ricardo S. Balardin², and James D. Kelly³

¹Universidade de Sao Paulo,
ESALQ, Piracicaba, Sao Paulo, Brazil

²Universidade Federal de Santa Maria,
Santa Maria, Rio Grande de Sul, Brazil

³Crop and Soil Sciences, Michigan State University,
East Lansing, MI 48824, USA

ABSTRACT

A better resolution of the structure of the variability in Colletotrichum lindemuthianum is obtained by combining virulence and molecular analyses. Unfortunately, virulence analysis based on local codes and different cultivar differential series has limited the understanding of the broad variability within this pathogen worldwide. The imbalance among cultivars from the two Phaseolus vulgaris gene pools in the new differential series might favor identification of races belonging to the Middle American reaction group. In addition, the multigenic resistance in some differentials such as G 2333 might select races with multiple avirulence genes. Therefore, information related with virulence may still be biased. Developing durable resistance to C. lindemuthianum must be based on reliable characterization of variability in this pathogen. Neutral molecular markers may sample a large portion of the genome and be more informative in assessing variability of organisms. No congruence was observed between data obtained by RAPD/AFLP and virulence analyses. Likewise, RFLP and sequence analyses of the variable ITS region in the rRNA genes in C. lindemuthianum have not supported the virulence data or shown a strong association with host gene pools or the geographic origin of isolates. The intra-specific variability shown by molecular analysis is evidence of limitations of virulence analysis. Combining virulence data and molecular markers for characterizing variability in C. lindemuthianum may have limited value in identifying new sources of resistance for local breeding programs. Pyramiding and deploying resistance genes according to host gene pools and specific geographic regions may result in the development of more durable resistance to C. lindemuthianum.

Abstracted from Melotto, M.,  R.S. Balardin and J.D. Kelly. 2000. Host-pathogen interaction and variability of Colletotrichum lindemuthianum. In: D. Prusky, S. Freeman, and M.B. Dickman, Eds,  pp 346-361. APS press St. Paul, MN. www.apsnet.org

James D. Kelly and Veronica A. Vallejo, Crop and Soil Sciences, Michigan State University, East Lansing, MI 48824, USA

Resistance to anthracnose in common bean is conditioned primarily by nine major independent genes, Co-1 to Co-10 as the Co-3/Co-9 genes are allelic. With the exception of the recessive co-8 gene, all other nine are dominant genes and multiple alleles exist at the Co-1, Co-3 and Co-4 loci. A reverse of dominance at the Co-1 locus suggests that an order of dominance exists among individual alleles at this locus. The nine resistance genes Co-2 to Co-10 are Middle American in origin and Co-1 is the only locus from the Andean gene pool. Seven resistance loci have been mapped to the integrated bean linkage map and Co-1 resides on linkage group B1; Co-2 on B11, Co-3 on B4; Co-4 on B8; Co-6 on B7; and Co-9 and Co-10 are located on B4 but do not appear to be linked. Three Co-genes map to linkage groups B1, B4 and B11 where clusters with genes for rust resistance are located (fig 1). In addition, there is co-localization with major resistance genes and QTL that condition partial resistance to anthracnose. Other QTL for resistance may provide putative map locations for the major resistance loci still to be mapped. Molecular markers linked to the majority of major Co-genes have been reported and these provide the opportunity to enhance disease resistance through marker-assisted selection and gene pyramiding. The ten Co-genes are represented in the anthracnose differential cultivars, but are present as part of a multi-allelic series or in combination with other Co-genes, making the characterization of more complex races difficult. Although the Co-genes behave as major Mendelian factors, they most likely exist as resistance gene clusters as has been demonstrated on the molecular level at the Co-2 locus. Since the genes differ in their effectiveness in controlling the highly variable races of the anthracnose pathogen, the authors discuss the value of individual genes and alleles in resistance breeding and suggest the most effective gene pyramids to ensure long-term durable resistance to anthracnose in common bean.

Abstracted: Kelly, J.D. and V.A. Vallejo. 2004. A Comprehensive Review of the Major Genes Conditioning Resistance to Anthracnose in Common Bean. HortScience 39:(in  press).

Anthracnose differential series, resistance genes, host gene pool, and the binary number of each cultivar used to characterize races of anthracnose in common bean.

Differential Cultivar	Host Genes1	Gene Pool2	Binary Number3
Michelite	--	MA	1
Michigan D.R.Kidney	Co-1	A	2
Perry Marrow	Co-13	A	4
Cornell 49242	Co-2	MA	8
Widusa	Co-9?	MA	16
Kaboon	Co-12	A	32
Mexico 222	Co-3	MA	64
PI 207262	Co-43, Co-9	MA	128
TO	Co-4	MA	256
TU	Co-5	MA	512
AB 136	Co-6, co-8	MA	1024
G 2333	Co-42, Co-5, Co-7	MA	2048

¹Not all resistance genes have been characterized.

²MA: Middle American gene pool; A: Andean gene pool of Phaseolus vulgaris

³Binary number: 2ⁿ, n is equivalent to the place of the cultivar within the series. The sum of cultivars with susceptible reaction will give the binary number of a specific race.

For example race 17 is virulent on Michelite [1] + Widusa [16].