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ARS Home » Pacific West Area » Pullman, Washington » Grain Legume Genetics Physiology Research » Research » Publications at this Location » Publication #100377

Title: DEVELOPMENT OF A DNA MARKER FOR FUSARIUM WILT RESISTANCE IN CHICKPEA

Author
item MAYER, M. - WA STATE UNIVERSITY
item TULLU, A. - WA STATE UNIVERSITY
item Simon, Charles
item KUMAR, J. - ICRISAT
item KAISER, W. - USDA-ARS (RETIRED)
item Kraft, John
item Muehlbauer, Frederick

Submitted to: Crop Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 9/19/1996
Publication Date: N/A
Citation: N/A

Interpretive Summary: Fusarium wilt resistance is a devastating disease of chickpea worldwide and selection for resistance is difficult and time consuming. The development of a genetic marker for the resistance gene would accelerate the development of resistant germplasm. In this study, we identify two genetic markers for the gene for resistance to race 1 of the disease. The markers are closely linked and can readily be used by geneticists and breeders in lieu of direct selection using screening tests. The results will accelerate the development of resistance to the disease. Also, the genes for resistance were located in the chickpea genome. The information also contributes in a large way toward the development of genetic maps for the chickpea genome.

Technical Abstract: Fusarium wilt caused by Fusarium oxysporum Schlechtend.:Fr. f. sp. ciceris (Padwick) Matuo & K. Sato is the most widely spread soilborne disease of chickpea (Cicer arietinum L.). To advance our understanding of the genetics of wilt resistance and aid chickpea breeding programs, we developed a set of F6 recombinant inbred lines (RILs) between Fusarium wilt tsusceptible (C-104) and resistant (WR-315) parents. Prior screening of selected F3 plants identified two primers (UBC-170 and CS-27) that produced random amplified polymorphic DNA (RAPD) markers associated with Fusarium wilt race 1 resistance. Analysis of the RILs with these primers yielded an estimate of 7% recombinant between the two markers and the locus for wilt resistance, and 6% recombination between the loci corresponding to the two RAPD markers. The DNA fragments were cloned and sequenced in order to construct primers that would amplify only the markers of interest. Primer pair CS-27F/CS-27R amplified a fragment linked to the allele for susceptibility to race 1 of Fusarium wilt and thus constitute allele specific associated primers (ASAPs), whereas UBC-170F/UBC-170R produced a single band for both resistant and susceptible genotypes, thus demonstrating locus specificity rather than allele specificity. The use of markers generated by the RAPD or ASAP approaches can facilitate the introgression of resistance genes into susceptible lines and expedite the screening of chickpea germplasm resources and will be useful in extending the genetic map of chickpea.