Submitted to: Euphytica
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/22/1999
Publication Date: N/A
Citation: Interpretive Summary: Fusarium wilt is an important disease of chickpea in the world including the U.S. The disease is especially difficult to overcome due to the presence of several pathogenic races of the pathogen that are capable of differential reactions in the chickpea host. Because of the difficulties of incorporating resistance into improved varieties, we wanted to find markers sfor the resistance genes that could be used in marker assisted selection. If markers could be found they can be used to select for resistant plants in the absence of the disease. In this study we identify markers for the gene for resistance to race 4 of the pathogen and we report the location in the Cicer genome. The markers indicate a clustering of resistance genes. The information is especially useful for geneticists and breeders of chickpea attempting to overcome fusarium wilt. The information also contributes to the development of a comprehensive gene map of chickpea.
Technical Abstract: Several races of Fusarium oxysporum Schlechtend.:Fr f. Sp. Ciceris (Padwick) Matuo and K. Sato cause economic losses from wilting disease of chickpea (Cicer arietinum L.). While the genetics of resistance to race 1 have been reported, little is known of the genetics of resistance to race 4. We undertook a study to determine the inheritance of resistance and identified random amplified polymorphic DNA markers (RAPDs) linked to the gene for resistance. For the investigation, we used 100 F5 derived F7 recombinant inbred lines (RILs) that had been developed from the cross of breeding lines C-104 x WR-315. Results indicated that resistance is controlled by a single recessive gene. The RAPD makers previously shown to amplify fragments linked to race 1 resistance also amplified fragments associated with race 4 resistance. The RAPD loci, CS-27 700, UBC-170 550 and the gene for resistance to race 4 segregated in 1:1 ratios expected for rsingle genes. Both RAPD markers were located 9 map units from the race 4 resistance locus and were on the same side of the resistance gene. Our results indicated that the genes for resistance to race 1 and 4 and 5 map units apart. The need to determine the genomic locations of race specific resistance genes and the possibility that these genes are clustered to the same genomic region should be investigated.