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ARS Home » Pacific West Area » Pullman, Washington » Grain Legume Genetics Physiology Research » Research » Publications at this Location » Publication #193876
Title: EVIDENCE OF MINOR GENES IN CHICKPEA 'SPANISH WHITE' FOR RESISTANCE TO ASCOCHYTA RABIEI PATHOTYPE II

Author
item Chen, Weidong
item Muehlbauer, Frederick

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 3/15/2006
Publication Date: 6/28/2006
Citation: Chen, W., Muehlbauer, F.J. 2006. Evidence of minor genes in chickpea 'spanish white' for resistance to ascochyta rabiei pathotype ii. Meeting Abstract.

Interpretive Summary:

Technical Abstract: BACKGROUND and OBJECTIVES Isolates from the United States of Ascochyta rabiei, the causal agent of chickpea Ascochyta blight, were divided into two pathotypes (I and II). Cultivar ‘Spanish White’ is susceptible to both pathotypes and ‘Dwelley’ is resistant to pathotype I but susceptible to pathotype II. Resistance to pathotype I is conditioned by a major gene and resistance to pathotype II is conditioned by at least two quantitative trait loci (minor genes). In pathogenicity assays, ‘Spanish White’, being susceptible to both pathotypes, consistently did better against pathotype II than against pathotype I, and also consistently did better against pathotype II than did ‘Dwelley’. It was hypothesized that ‘Spanish White’ carries minor resistance gene(s) to pathotype II. Experiments were designed and carried out to test this hypothesis. MATERIALS and METHODS Chickpea cultivars ‘Spanish White’ and “Dwelley’ were planted (2 seeds/pot) in a greenhouse. Conidia of Ascochyta rabiei isolates AR19 (pathotype I) and AR628 (pathotype II) were collected from 2-week old V8 agar plates and were adjusted to three concentrations (103, 104 and 105 spores/ml), and were used to inoculate 2-week old plants using the mini-dome technique. Disease severity was rated two weeks after inoculation using the 1-to-9 rating scale. The experiment was performed twice. RESULTS Disease severity ratings of ‘Spanish White’ when inoculated with isolate AR19 at the three inoculum concentrations 103, 104 and 105 spores/ml were 3.4, 6.0, and 8.0, respectively, and when inoculated with isolate AR628 at the three inoculum concentrations were 1.8, 3.2 and 6.0, respectively. Disease severity ratings of ‘Dwelley’ when inoculated with isolate AR19 at the three inoculum concentrations were 1.8, 2.8, 3.2, and when inoculated with isolate AR628 were 2.7, 4.8 and 6.8, respectively. The evidence for minor resistance genes in ‘Spanish White’ to pathotype II (AR628) became obvious and statistically significant at lower disease pressure (104 spores/ml). CONCLUSIONS Employing host resistance is an important means in managing Ascochyta blight, but resistance sources are limited in chickpea. Identifying minor genes in susceptible cultivars will provide additional resistance sources for pyramiding resistance genes in chickpea breeding programs. Additionally, the differential response of the two cultivars to the pathotypes provides additional evidence of separating the two pathotypes.