Blackleg is not going away. In fact, AAFC researcher Dr. Garry Peng told Saskatchewan farmers at a November meeting, “we are seeing a creeping up of the disease over the last five, six years, in all provinces.”
Researchers first began to recognize blackleg in canola in the mid-70s. Blackleg incidence reached a peak in the late 80s and early 90s. Then, with changes in canola management practices and the development of blackleg resistant seed varieties in the early 90s, the degree of incidence of blackleg fell. In the future, however, we may be seeing it more often.
Peng is part of a group of researchers monitoring and mapping the evolution of the blackleg pathogen across the Prairies. He spoke to farmers about his latest research at Saskatchewan’s oilseed producer meetings, sponsored by SaskCanola, SaskMustard, SaskFlax and Saskatchewan Agriculture. Peng listed a few reasons for the resurgence of blackleg. One is a change in the makeup of the pathogen that causes blackleg. Another is shortened canola rotations, “in comparison with 10 years ago.” Crop damage from insects or hail also increases the potential for blackleg damage. “With those injuries the disease tends to be much more pronounced,” Peng says.
Since the 90s, farmers have been buying canola seed rated “R” (resistant) for blackleg. “With the resistant cultivars,” Peng says, “the disease was kept in control very well for very many years.”
Now, the resistance built into our seed supply may be breaking down.
To understand how this could happen, it helps to start with some basic information about how canola seed breeders create blackleg resistant canola.
Canola seed breeders have two types of resistance to work with. The first type is quantitative resistance. This type of resistance is thought to be caused by several genes working together, each contributing a small effort to the overall resistance. Although the crop may not be highly resistant at the seedling stage,” Peng says, “(quantitative resistance) somehow slows the infection down a little bit, and that will reduce the infection into the stem and alleviate the disease at a later stage.” As the blackleg pathogen evolves over time, this type of resistance is still effective, but it may not be enough to fully protect canola crops against the blackleg pathogen under the conditions conducive to infection such as hail or insect damage, or a warm, wet spring.
The second type of resistance, qualitative resistance, can be stronger and more effective. It is very specific. The resistance gene in the canola variety must match the specific pathogen avirulence (Avr) gene in the blackleg pathogen population. Where there is a match, the plant will be able to stop the blackleg pathogen at the site of the initial infection — on the cotyledons, leaves and stem. But, if there is no match, the plant is not resistant to blackleg infections.
In developing this qualitative resistance, canola breeders don’t have a lot of genetic material to work with. “We have a limited number of resistance genes for blackleg control,” Peng says. “In order for them to work, you need to have the pathogen population carrying the specific gene, called the Avr gene, in the pathogen.” There are only 16 major resistance genes identified so far. However, most of the blackleg resistant seed available in Western Canada is based on just one or two of these 16 genes: Rlm3 and/or Rlm1. This seed is resistant to the AvrLm3 or AvrLm1 avirulent genes in the blackleg pathogen.
“The diversity is not that high,” Peng says. “We have very limited choices of resistant genes,” Just one gene, Rlm3, is in close to 60 per cent of Canadian canola varieties and breeding lines.
The Rlm3 resistant gene in our canola seed will fight the AvrLm3 gene in the blackleg pathogen. This works well when AvrLm3 is the main gene in the blackleg pathogen in the soil. However, over time, the pathogen population changes.
Peng has had a first-hand look at this evolution. Along with Dr. Dilantha Fernando, plant science professor at the University of Manitoba and Dr. Ralph Lange from Alberta Innovates, Peng is in the middle of a five-year Growing Forward 2 project to map blackleg pathogens in the farmers’ fields.
“Unfortunately, the AvrLm3 gene in the pathogen population has diminished over the years,” Peng says. “That means the major gene resistance is not the major function in our variety performance. That’s the important message to the seed companies.”
When resistant canola plants don’t allow blackleg’s AvrLm3 genes to thrive, the other Avr genes in the pathogen may increase, and can become a larger portion of the pathogen population.
Blackleg can evolve quickly. Some researchers have found that, if the same variety is seeded three years in a row, the blackleg fungus can evolve to overcome the major-gene resistance, especially in areas with a lot of canola production and short crop rotation.
Peng says the blackleg population is evolving, with AvrLm7 reaching a very high level on the prairies. So, the next opportunity to fight blackleg with a major resistance gene is Rlm7.
In language similar to the terms we use to describe weeds that develop resistance to commonly-used herbicides, Peng refers to the ever-changing nature of the fungus and our resistance as an “arms race.”
“It’s going to be an endless battle if we look at it that way.” And, Peng says, “the pathogen always wins, although we beat them back temporarily.”
Just as we need to rotate herbicides to extend their lifespans and fight herbicide resistant weeds, we need to try to keep our canola seed varieties resistant to blackleg. The slower the pathogen changes, Peng says, “the better longevity varieties will have.”
One way to slow down the evolution of the pathogen would be to use seed resistant to different blackleg pathogens. However, in tests that Dr. Dilantha Fernando has conducted in his University of Manitoba lab, Fernando has found that most companies are using “almost the same resistance gene.”
While there are other differences in different corporations’ seed profiles, in tests at his Manitoba lab, Fernando has found that one major gene, the resistance gene Rlm, is present in almost 60 per cent of the Canadian germplasm. This low genetic diversity in our seed supply makes it difficult for farmers to manage the pathogen, and easier for the pathogen to evolve to survive.
Ideally, seed companies will work to find other resistance genes that could be incorporated into the Canadian canola germplasm. Fernando suggests genes from wild species, or other brassica species. “Those might carry different resistance genes,” he says.
Many companies are advertising new canola varieties with “multi-genic” blackleg resistance. These lines have been found to carry two different genes for resistance to the blackleg pathogen. This should lead to better blackleg control, but Fernando says, “In theory, yes, but again, depending on the pathogen population, maybe not.” This is something he’s studying right now.
“The pathogen population is fairly diverse in the farmer’s field. When the pathogen population is fairly diverse putting several different genes together at the same time may be counterproductive.”
With only two resistant genes, one can fight resistance of one strain of pathogen, while the second fights the resistance of another strain. Ultimately, the pathogen may wind up resistant to both of these genes. For example, some of our cultivars carry both Rlm1 and Rlm3. After years of use, however, the AvrLm1 and AvrLm3 are now at almost undetectable levels in the pathogen population. As a result, these two resistance genes are no longer effective against blackleg on the Prairies.
“Even though in theory, on paper, it sounds exciting to have multi-gene resistance, for a few years it might be a little better than having a single gene. But it (the resistance), might be broken fairly quickly.”
In addition to the 16 major genes in canola plants, there are also minor genes present. These minor genes are difficult to identify and work with, but using breeding lines carrying these minor genes could lead to longer-term solutions for blackleg control.
In the field
While there are fungicides registered for control of blackleg on canola, Fernando says using a fungicide to manage blackleg isn’t usually a good economic decision.
What he does recommend will come as no surprise to farmers familiar with herbicide resistant weeds: good rotations.
Fernando recommends limiting canola rotations to one year in three or four. In between, growing crops that are non-hosts to blackleg (like cereals, pulses, or soybeans), will prevent the pathogen from developing and multiplying. Over time the blackleg pathogen population will slowly decline.
Fernando understands that farmers also have to take economics into account; blackleg or not, some will use tighter rotations. “That’s where the R-gene rotation comes into play.”
Fernando would like to see seed companies adopt a system of identifying their seed by resistance “group.” Farmers could rotate canola seed, planting varieties with resistance to different pathogen races. Or, better yet, farmers could choose seed varieties with specific resistance to the inoculum in their area. “We almost have a Prairie map for blackleg pathogen races,” he says. “We now need to come up with the other side,” that is, seed marketed with specific resistance placed by resistance “group.” “That can only be done with the participation of the seed companies.”
In the past few years, environmental conditions have not been terribly conducive to blackleg. Particularly in Saskatchewan, where the incidence has increased only slightly since 2010. However, in southern Manitoba and east-central Alberta, incidence has increased substantially.
“In a year that we have very good environmental conditions for the pathogen, there could be an epidemic. Unfortunately a lot of people do not understand that part.”
Getting an R rating
The Canola Council of Canada organizes and operates co-op trials across the Prairies to evaluate new seed varieties.
To test for blackleg resistance, new varieties are compared to “Westar,” a canola variety that is highly susceptible to blackleg. Researchers examine at least 100 plants of each variety over four replicated plots at each of 10 locations across the prairies. They pull the plants, cut through the stems, then evaluate the severity of blackleg in the plant.
Dr. Dilantha Fernando runs the co-op trials at Carman, Man. Fernando is concerned that the co-op trial locations may not have the same avirulent-gene profile for the pathogen as in farmers’ fields. In fact, he says, the pathogen is changing so rapidly that the pathogens at a co-op site in 2012 might be very different from the population at that same site in 2015. To address this issue, Dr. Peng has initiated a new project to assess the blackleg pathogen avirulent-gene structure at each of the co-op sites commencing in 2015.
So, seed that has been characterized as resistant (“R”) for blackleg will have been resistant to the pathogens in the co-op trial in the year that variety was tested, although that doesn’t necessarily mean the variety will be resistant to the particular pathogen populations in every farmer’s field in future years.
However, Fernando says, most of the inoculum in the soil at the co-op sites is natural inoculum. “It is getting fairly close to what is out there in farmers’ fields.”