Author
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RASHID, KHALID - AGRI & AGRI-FOOD CANADA |
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Seiler, Gerald |
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Submitted to: World Wide Web
Publication Type: Other Publication Acceptance Date: 1/18/2006 Publication Date: 1/20/2006 Citation: Rashid, K.Y., Seiler, G.J. 2006. Updates on epidemiology and resistance to Sclerotinia head rot in wild sunflower species. Poster presented at Sclerotinia Initiative Annual Meeting, January 18-20, 2006, Bloomington, MN. Available: http://www.whitemoldresearch.com/posters2005/Rashid2006-02.pdf Interpretive Summary: Sunflower head rot (white mold) results from infection by spores that are produced by the germination of hard gray-black sclerotia when soil moisture is abundant. Lack of genetic resistance has led to a steady rise in prevalence and severity of head rot losses (up to 80%) in the Red River Valley of North Dakota and Minnesota. Field trials were conducted in 2002 to 2005 to understand how head rot infects wild sunflower species, identify sources of resistance in the wild species populations, and establish infection methodology for head and stem rot in wild sunflower germplasm. In 2002-2003, 96 populations of perennial wild sunflower species of Maximilian and Nuttall sunflower were tested in a four replicated randomized complete block design trial with various inoculum types, inoculation at three growth stages, and three types of head covering. Ground sclerotinia-infected millet seed and spores were used to inoculate wild species at the mid-flowering stage, and heads were covered with light brown paper bags, which proved to be the most appropriate method to create disease epidemics to differentiate between susceptible and resistant populations. In 2004-2005, 400 populations of the perennial wild sunflower species were evaluated using the standard artificial inoculation procedure established in previous years. Different groups of plants (5 to 10) from each population were inoculated at the early-flowering and late-flowering stages, and were covered with light brown paper bags. The typical symptoms of Sclerotinia infection on wild sunflower plants were stem bleaching, shredding, and the formation of tiny cylindrical sclerotia inside the stems, while the heads were shriveled and dry with little or no seed set. Some changes were observed in the reaction of several populations from year to year; however, most wild populations identified with resistance to head rot in 2002-2003 remained resistant in 2004 and 2005. Seven populations of Maximilian and six of Nuttall sunflower were identified with no Sclerotinia infection in the head or mid-stems. These populations are believed to have genetic resistance to Sclerotinia head rot and mid-stem infection. Present research is focusing on the transfer of the resistance genes into sunflower breeding lines and studying the genetics of the resistance for future hybrid development. Technical Abstract: Sunflower head rot results from infection by ascospores that are produced by carpogenic germination of sclerotia of Sclerotinia sclerotiorum under saturated soil moisture conditions. Lack of genetic resistance has led to a steady rise in prevalence and severity of head rot losses (up to 80%) in the Red River Valley of North Dakota and Minnesota. This study was undertaken to understand the epidemiology of head rot in wild sunflower species, and identify source of resistance in the wild populations. Field trials were conducted in 2002 to 2005 to understand the epidemiology of the Sclerotinia infection in wild sunflower heads and stems, to establish methodology for assessing wild sunflower germplasm, and to identify sources of resistance. In 2002-2003, 96 accessions of perennial wild sunflower species of Helianthus maximiliani and H. nuttallii were tested in a four replicated randomized complete block design trial with various inoculum types, inoculation at three growth stages, and three types of head covering. Ground Sclerotinia-infected millet seed and ascospores inoculated at the mid-flowering stage and covered with light brown paper bags proved to be the most appropriate method to create disease epidemics to differentiate between susceptible and resistant genotypes. In 2004-2005, 400 accessions of the perennial wild sunflower species were evaluated using the standard artificial inoculation procedure established in previous years with a combination of ascospores and ground Sclerotinia-infected millet seed. Different groups of plants (5 to 10) from each accession were inoculated at the early-flowering and late-flowering stages, and were covered with light brown paper bags. The typical symptoms of Sclerotinia infection on wild sunflower plants were stem bleaching, shredding, and the formation of tiny cylindrical sclerotia inside the stems, while the heads were shriveled and dry with little or no seed set. Some changes were observed in the reaction of several accessions from year to year; however, most wild accessions identified with resistance to head rot in 2002-2003 remained resistant in 2004 and 2005. Seven accessions of H. maximiliani and six of H. nuttallii were identified with no Sclerotinia infection in the head or mid-stems. These accessions are believed to have genetic resistance to Sclerotinia head rot and mid-stem infection. Present research is focusing on the transfer of the resistance genes into sunflower breeding lines and studying the genetics of the resistance for future hybrid development. |
