|Santra, Dipak - NCL, PUNE, INDIA|
|Tekeoglu, Mucella - MIN. OF AG., TURKEY|
|Ratnaparkhe, Milind - NCL, PUNE, INDIA|
|Gupta, Vidya - NCL, PUNE, INDIA|
|Ranjekar, P.K. - NCL, PUNE, INDIA|
|Kaiser, Walter - RETIRED USDA-ARS|
Submitted to: Crop Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: May 31, 2000
Publication Date: N/A
Interpretive Summary: Ascochyta blight is a major disease of chickpea (garbanzo) crops in the U.S. and worldwide. The disease causes wide spread distruction of the leaves, stems, pods and seeds, sometimes causing 100% yield losses in severely affected fields. Resistant germplasm is the principal means of control. In this study we determined that resistance is quantitative and controlled by at least two regions of the chickpea genome. There also appears to be an additional minor locus that influences resistance to the disease. Knowing the inheritance of resistance and the location of the genes facilitates breeding of resistant varieties and forms a basis for isolating the gene and studying its structure and function. With this information, we plan to further study the genes for resistance and increase the genetic marker density in the region of the genes. To our knowledge, this is the first report of DNA markers linked to the ascochyta blight resistance genes in chickpea.
Technical Abstract: Ascochyta blight is a devastating disease of chickpea (Cicer arietinum L.) worldwide. Resistant germplasm has been identified and the genetics of resistance has been the subject of numerous studies. Inheritance of resistance is unclear but is reportedly controlled by more than one gene. To clarify the genetics of resistance to ascochyta blight and to identify and map the resistance genes, we used a set of F 5:6 recombinant inbred lines (RILs) obtained from a interspecific cross of C. arietinum (FLIP84- 92C, resistant parent) x C. reticulatum Lad.(PI489777, susceptible parent). The RILs were scored for disease reactions in the field over two years and were genotyped for polymorphic molecular markers (isozyme, RAPD, and ISSR) in the laboratory. The disease was scored quantitatively and used for QTL analysis. A linkage map was established that comprised 9 linkage groups containing 117 markers covering a map distance of 877cM with han average distance of 7.5cM between markers. Two QTLs, QTL-1 and QTL-2, conferring resistance to ascochyta blight, were identified which accounted for 49-57% of the estimated phenotypic variation and were mapped to linkage groups 6 and 1, respectively. Two RAPD markers flank QTL-1 and were 12cM apart while one ISSR marker, an (AG)n repeat, and an isozyme marker flank QTL-2 and were 5.1cM apart. These markers can be used for marker-assisted selection for ascochyta blight resistance in a chickpea breeding program. The markers can also be used to develop durable resistant cultivars through gene pyramiding. We infer that ascochyta blight resistance in FLIP84-92C is controlled by at least two QTLs. To our knowledge, this is the first report of molecular markers linked to ascochyta blight resistance gene(s) and their mapping in chickpea.