Inheritance of Resistance to Basil Downy Mildew (Peronospora belbahrii)

Thursday, July 31, 2014: 3:30 PM
Salon 5 (Rosen Plaza Hotel)
Robert Pyne , Rutgers University, New Brunswick
Andy Wyenandt, PhD , Rutgers Agricultural Research and Extension Center (RAREC), Bridgeton, NJ
Adolfina Koroch, PhD , Borough of Manhattan Community College, New York, NY
James E. Simon, PhD , Department of Plant Biology & Pathology, Rutgers University, New Brunswick, NJ
Sweet basil (Ocimum basilicum) is among the most important culinary herbs in the United States. Downy mildew caused by the oomycete Peronospora belbahrii has negatively impacted sweet basil production worldwide. All O. basilicum varieties screened to date are highly susceptible to basil downy mildew, while other species including O. americanum and O. x citriodorum provide resistance and tolerance, respectively. Basil accession RU329 was identified as resistant to downy mildew in field and greenhouse screenings. Pedigree information for this accession is unavailable, but it is sexually compatible with O. basilicum and the F1 generation is completely fertile. The objective of this study was to determine the mode of inheritance for resistance to downy mildew in basil using the previously unreported resistant parent RU329. Downy mildew susceptible inbred line SB22 (P1) was crossed with RU329 (P2), after two generations of inbreeding, to produce segregating generations. The total number of plants evaluated per generation was 12 per parent, 12 per F1, 12 per reciprocal F1, 300 F2 and 181 backcross. Field ratings were made on three dates at the Rutgers Research and Extension Center (RAREC) in Bridgeton, NJ during the 2013 growing season.  A disease severity index (DSI) corresponding to the estimated percentage of sporulating leaf area was generated per single plant using a five-point scale (0-4). Disease severity varied among rating dates and was greatest at the second rating, 33 days after planting, in which all susceptible SB22 parent and check plants received the highest possible disease rating (DSI=1.0; SE=0.0). RU329 parent exhibited full resistance (DSI=0.0; SE=0.0). Differences between reciprocal generations were not significant, suggesting no maternal effects and allowing these generations to be pooled. A mixed effects analysis of variance showed significant differences (P>0.0001) among generations, demonstrating genetic variation. DSI for the RU329 x SB22 population demonstrated a skewed distribution towards resistance among segregating F2 and backcross generations. Chi-square for goodness of fit was used to test observed ratios of resistant, intermediate and susceptible disease response classes against expected ratios for multiple gene models. Results suggest a dominant, complementary two-gene model in both the F2 (χ2=5.71; p<0.05) and BC1P1 (χ2=3.00; p<0.05). This is the first study to provide genetic information with respect to mechanism of resistance to basil downy mildew. Results demonstrate that resistance is highly heritable, which implies a strong potential for genetic gain through plant breeding.