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Title: GENETICS OF PARTIAL RESISTANCE TO APHANOMYCES ROOT ROT IN PEA

Author
item PILET-NAYEL, MARIE - UMR INRA-ENSAR, FRANCE
item DORMEGNIES, THOMAS - UMR INRA-ENSAR, FRANCE
item MCGEE, REBECCA - GENERAL MILLS, MN
item ESNAULT, ROBERT - UMR INRA-ENSAR, FRANCE
item MANGIN, PIERRE - INRA, FRANCE
item ROUX-DUPARQUE, MARTINE - GSP, FRANCE
item Grunwald, Niklaus - Nik
item BARANGER, ALAIN - UMR INRA-ENSAR, FRANCE
item Coyne, Clarice - Clare

Submitted to: International Aphanomyces Symposium
Publication Type: Proceedings
Publication Acceptance Date: 8/1/2003
Publication Date: 10/1/2003
Citation: PILET-NAYEL, M.L., DORMEGNIES, T., MCGEE, R.J., ESNAULT, R., MANGIN, P., ROUX-DUPARQUE, M., GRUNWALD, N.J., BARANGER, A., COYNE, C.J. GENETICS OF PARTIAL RESISTANCE TO APHANOMYCES ROOT ROT IN PEA. International Aphanomyces Symposium. P 72-75. 2003.

Interpretive Summary: Aphanomyces root rot is considered to be one of the most damaging disease affecting pea worldwide. Breeding peas resistant to this disease remains the most effective method for controlling the disease. Different sources of resistance were characterized. Using novel molecular approaches, we identified six new genes involved in resistance to Aphanomyces root rot. These results are of considerable value to the pea industry, as they allow much more rapid development of resistant varieties than was possible with traditional breeding methods.

Technical Abstract: In order to better understand genetics of quantitative resistance to Aphanomyces euteiches in pea, this study aimed to study the consistency of 3 resistance QTL previously identified (Aph1, Aph2, and Aph3) by comparative mapping in another genetic background. A mapping population of 111 RILs, from the cross DSP (susceptible) x 90-2131 (partially resistant), was assessed for field Aphanomyces root rot resistance over 6 environments (2 US and 2 French locations, 1 to 3 years per location). A partial genetic map, consisting in 30 linked markers and covering the genomic regions including Aph1, Aph2 and Aph3, was elaborated from the RILs. A total of 6 QTL were identified from only 3 environments (2 US and 1 FR) and explained individually up to 12% of the variation. One QTL (QTL1), identified from Pullman 2000 data, co-localized with Aph1 but the others did not co-segregate with Aph1, Aph2 or Aph3. The hypothesis of the involvement in the resistance of other genetic factors in other regions of the genome is highlighted and is under investigation.