Title: Genetic of virulence in Ascochyta rabiei Authors
Submitted to: Plant Pathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: February 10, 2012
Publication Date: April 6, 2012
Citation: Peever, T., Chen, W., Adbo, Z., Kaiser Jr, W.J. 2012. Genetic of virulence in Ascochyta rabiei. Plant Pathology. 61: 754-760. DOI: 10.1111/j.1365-3059.2011.02566.x. Interpretive Summary: Ascochyta rabiei causes the devastating disease Ascochyta blight of chickpea. Different classification systems have been proposed to separate the isolates into discrete categories like races, pathogenic groups or pathotypes without a clear understanding of its genetic mechanisms, which has resulted in inconsistency and confusion. In order to gain a better understanding of the genetic mechanisms of Ascochyta rabiei in causing the disease, a genetic cross was made between a highly virulent strain and a less virulent strain, and the progeny of the cross were tested for virulence on two chickpea cultivars Spanish White and Dwelley. Analysis of the results showed that the virulence of Ascochyta rabiei is under control of more than one gene or quantitative genetic control. Thus the simple classes of virulence of A. rabiei in natural populations may be due other factors like incomplete sampling and/or selection of increased virulence among contemporary A. rabiei populations.
Technical Abstract: Many attempts have been made to classify variation in virulence of the chickpea Ascochyta blight pathogen, Ascochyta rabiei, into discrete categories referred to as “pathogenic groups”, “races” or “pathotypes”. Results have been inconsistent and conflicting due to differences in host and pathogen genotypes used, lack of control of the genetic backgrounds of host and pathogen as well as environmental variation in disease assays. In order to critically test the hypothesis that virulence variation in this pathosystem is a discrete character under simple genetic control, a genetic cross was made between a highly virulent isolate of A. rabiei from Syria and a less virulent isolate from the US. Two independent virulence assays conducted by inoculating susceptible and resistant chickpea cultivars under controlled conditions with 77 progeny isolates from this cross revealed a continuous distribution of disease phenotypes. Statistical tests of the progeny phenotype distribution did not support bimodality as would be predicted for the segregation of virulence under simple genetic control. ANOVA revealed highly significant pathogen genotype X host genotype interactions demonstrating the segregation of genes controlling specialization on the two cultivars tested. These interactions could be localized to two isolates that changed virulence rank on the cultivars. We conclude that variation in virulence in the A. rabiei/chickpea interaction is under quantitative genetic control and speculate that the discrete categories of virulence variation identified in previous studies were likely due to incomplete sampling of host resistance or pathogen virulence variation and/or to selection for increased virulence in contemporary A. rabiei populations.