Blackleg resistance breaking down
By Bruce Barker
Anastasia Kubinec, the oilseeds specialist for Manitoba Agriculture, Food and Rural Initiatives, has seen the effects of tight canola rotations first-hand. In the past several years, she has had the misfortune of seeing fields planted to resistant blackleg canola varieties that were infected with blackleg. “You may think you don’t have a blackleg problem, but can you explain reduced yields in some fields and premature ripening when the field looked great all year long and you did everything ‘right?’” asks Kubinec.
She cites three examples that she saw first-hand in 2009, where yields were severely compromised. Case 1 was a field with a new resistant variety planted; it was infected with blackleg. Kubinec says that the field had a history of canola-wheat rotations, which likely selected for the development of a new strain of blackleg that overcame the single-gene resistance in the variety.
Two other cases in 2009 also highlighted the changing nature of blackleg pathogens. One field had 40 percent blackleg infection and the other had close to 75 percent infection, yet both fields had canola with a resistant rating. “In Europe, five specific resistance genes have lost their effectiveness since the late 1960s, so if one considers that intensive production of this crop has been only in the last 40 years or so, on average, the effectiveness of a resistant gene was lost every eight to nine years,” says Dr. Randy Kutcher, a plant pathologist with Agriculture and Agri-Food Canada at Melfort, Saskatchewan. He has been studying the blackleg pathogen for several decades, and says that the blackleg pathogen in Western Canada is changing, as it has in Europe and Australia.
Blackleg is the second most prevalent disease in Manitoba canola fields based on canola disease surveys in the past few growing seasons, and it is common in Saskatchewan and Alberta, as well. For example, in 2009, blackleg was found in 56 percent of Manitoba fields surveyed in the canola disease survey (140 fields total), with a four percent incidence. The 2010 survey results have yet to be compiled.
Blackleg disease of canola (Brassica napus), is caused by two Leptosphaeria species: L. maculans and L. biglobosa; however, it is L. maculans that is responsible for significant yield loss of canola or oilseed rape, worldwide. During the 1980s in Manitoba and Saskatchewan, only two pathogenicity groups (PG) were observed, those of PG1 and PG2. However, in Australia and other parts of the world, PG2, PG3 and PG4 have been reported, indicating a greater variation of disease. PG1 has since been determined to be L. biglobosa, and all other PGs, L. maculans.
By 2003, five PGs had been identified in Western Canada: PG1, PG2, PGT, PG3 and PG4. The relative frequency was also changing, with a shift away from PG1, to the largest percentage being PG2, with increasing percentages of PGT, PG3 and PG4.
However, the traditional method of identifying PGs of L. maculans, which is determined by reaction of the pathogen on only two varieties, can only identify four PG types (PG2, PG3, PGT and PG4). More recent research has identified as many as 14 resistance genes in canola or other Brassica species to L. maculans. Kutcher says that by using varieties or lines of Brassica species carrying these 14 resistance genes, isolates of L. maculans can be characterized into races based on the reactions observed. He conducted a study of 96 Western Canadian isolates of L. maculans using 10 resistance genes, and found considerable variation in the pathogen population for many of the genes.
Management practices and resistance breeding are key
Kutcher says that knowing the races of the pathogen and where these races occur across the Prairies will help plant breeders stay one step ahead of the disease. By identifying specific resistant genes in current varieties, better breeding strategies can be implemented. These could include rotation of resistant genes, by periodically changing the production of varieties that carry the same resistance gene to varieties that carry a different resistance gene. Another method is by gene pyramiding, where one variety carries more than one resistant gene, or the development of resistance based on the combination of quantitative (multiple-site) resistance with qualitative (single-site) resistance.
However, Kutcher says resistant varieties are not the magic bullet. Cultural control such as using crop rotations of at least three years between canola crops will be important to maintain varietal resistance. A rotation of this length allows most of the residue of the previous crop to break down before the next canola crop is grown. This is extremely important because it is on the residue that the pathogen survives and reproduces, which provides the opportunity for the pathogen to form new races. “In Europe, surveys of the pathogen have indicated that the effectiveness of resistance genes Rlm1 through Rlm4 and Rlm9 have been lost. They do not appear to be of any use there now,” says Kutcher.
He says examples of rapid loss of resistance in France and Australia due to dependence on specific resistance genes have demonstrated that specific resistance genes exert strong selection pressure on pathogen populations. “Monitoring of L. maculans populations for shifts in virulence should provide advance warning of new virulent races with the potential to overcome specific resistance genes. The use of management strategies such as variety selection or rotation of resistance genes over time, in combination with good quantitative resistance and best agronomic practices, will be needed to manage blackleg for successful canola production,” explains Kutcher.
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