Submitted to: Crop Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 6/1/2000
Publication Date: N/A
Interpretive Summary: Fusarium wilt is one of the most devastating diseases of the chickpea crop worldwide and is also a problem in the U.S. The disease can be controlled with resistant germplasm, however there are several races of the pathogen that makes breeding for resistance difficult. Fortunately, there are genes that confer resistance to the different races. In this paper we report research that shows that resistance to the disease is conferred by single genes and that those genes are linked to selectable molecular markers. At least three of the race specific genes are closely linked in the genome and associated with markers that can be used for gene transfer to otherwise susceptible varieties. The research has important implications for the possible cloning of the resistance genes and for crop improvement efforts designed to alleviate the damage from fusarium wilt in chickpea crops.
Technical Abstract: Fusarium oxysporum Schlechtend.: Fr. f. sp. ciceris, causes a vascular wilt of chickpea (Cicer arietinum L.) and significantly limits production worldwide. Seven physiological races (0-6) of the pathogen have been reported. Recombinant inbred lines (RILs) from an interspecific cross of susceptible C. reticulatum Lad. (PI 489777) and resistant C. arietinum (ICC-4958) were used to determine the genetics of resistance to races 5 an 0, the most virulent and least virulent races of the pathogen, respectively. Seedlings of 131 F6 derived RILs were tested for reaction to races 0 and 5 and a 1 resistant: 1 susceptible segregation ratio was observed for both races indicating that resistance to each race is controlled by a single gene. Linkage analysis of the genes for resistance to races 0 and 5 with a previously identified gene for resistance to race 4 was performed. The genes for resistance to races 4 and 5 mapped to the same elinkage group and were separated by 11.21 cM. The gene for resistance to race 0 did not show linkage to the race 4 and 5 resistance genes. In addition, PCR was performed using primers that were previously shown to be linked to the genes for resistance to races 1 and 4. An allele specific associated primer (ASAP) product (CS-27R/CS-27F), developed from the CS-27 primer, was located between the two resistance genes and 7.2 cM and 4cM from the genes for resistance to races 4 and 5, respectively. Map positions of these two race specific resistance genes and the marker shown to be linked to the gene for resistance to race 1 support the hypothesis that the wilt resistance genes are clustered. That the gene conferring resistance to race 0 is found in a different region of the genome indicates that another genomic region is also responsible for resistance to wilt