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ARS Home » Southeast Area » Charleston, South Carolina » Vegetable Research » Research » Publications at this Location » Publication #116771
Title: TOWARDS MAPPING GENES FOR DOWNY MILDEW RESISTANCE IN BRASSICA OLERACEA

Author
item Farnham, Mark
item WANG, MIN - DEFRANCESCO AND SONS
item GIOVANNELLI, JANEL - UNIVERSITY OF CHARLESTON

Submitted to: Plant and Animal Genome VX Conference Abstracts
Publication Type: Abstract Only
Publication Acceptance Date: 10/18/2000
Publication Date: 1/13/2001
Citation: Farnham, M.W., Wang, M., Giovannelli, J.L. 2001. Towards mapping genes for downy mildew resistance in brassica oleracea. Plant and Animal Genome IX. San Diego, CA. Pg 18.

Interpretive Summary:

Technical Abstract: Downy mildew is a significant disease of broccoli and other Brassica oleracea L. crops. It is caused by the fungal parasite Peronospora parasitica (Pers. Fr.) Fr. and is distributed worldwide wherever B. oleracea crops are grown. Fungicides are used to control downy mildew in broccoli, but resistant cultivars represent an alternative control method providing a practical, long-term, and environmentally-benign means to prevent damage from this disease. The ARS breeding program has developed homozygous lines of broccoli expressing high levels of resistance to downy that should prove useful in the development of resistant F1 hybrids. We have characterized lines that are susceptible at the cotyledon stage but highly resistant at the true leaf stage, and others that are highly resistant at both cotyledon and true leaf stages. Our objective is to elucidate the genes that control these different resistance phenotypes. To othis end, resistant lines were crossed to a susceptible line, and conventional (e.g., F2 and backcross) and doubled-haploid (DH) populations were developed from resulting F1s. These populations were evaluated for response to inoculation with P. parasitica. Analysis of populations segregating for true leaf resistance indicates this resistance is controlled by two complementary dominant genes. Additional evaluations of populations segregating for cotyledon resistance indicate that it is controlled by a single dominant gene. RAPD markers that cosegregate with the different resistances have been identified. Efforts are underway to develop SCAR markers from the RAPDs and to locate them on existing genetic maps.