Blackleg and canola can get along… until

Keys to restoring a healthy relationship between blackleg and canola include wider rotations of both crops and canola varieties with different resistance genes

This clipped stem shows how blackleg damages the crown of a canola plant.

After hearing many presentations on blackleg in canola, I was confused. I heard that disease pathogens usually harm their host plant, but blackleg doesn’t necessarily. In fact, blackleg and brassica species such as canola usually get along.

On the other hand, we know that blackleg is now a major problem. Why?

University of Manitoba professor and plant pathologist Dilantha Fernando, a blackleg specialist, patiently walked me through the plant and pathogen relationship earlier this fall.

Fernando explained, starting with a little background…

We have 14 known blackleg pathotypes on the Prairies. Fernando and his colleagues have been digging around for them for years and keep finding more pathotypes and even sub-races. In the let’s-keep-it-simple naming scheme, the pathotypes are named avirulence Leptosphaeria maculans 1, 2, 3 and so on. AvrLm for short.

Interestingly, blackleg pathotypes are picky about how they interact with host plants. If the single-gene resistance in a canola hybrid matches the AvrLm pathotype, the pathogen will not cause disease.

Single-gene resistance to L. maculans (Rlm) is numbered using the same scheme. A canola plant with the gene named Rlm3 will not get blackleg if the pathotype present in a field is AvrLm3. The two recognize each other — they have a “good relationship,” Fernando says.

He added that if the gene and pathotype do not match — Rlm4 and AvrLm3, for example — the pathogen is “confused” and can’t get into the plant at all.

Now I was confused, too, so I interrupted to ask: If Rlm3 and AvrLm3 go together happily like a “lock and key,” as Fernando added for analogy, and all other combinations have no connection — no infection — when does the “disease” part occur?

Put another way, if this relationship between AvrLm3 and Rlm3 is so “good” — which means no dead plants — what does the pathogen get out of this?

Live and let live

Fernando tried a new tack. Back where brassica plants originated, they may have “co-evolved” with L. maculans, he says. The pathogen takes the nutrients it needs from the plants but is happy to let its host live. Blackleg still forms lesions on leaves and stems, but it doesn’t spread through the stem or create its deadly necrosis of the crown. Then it uses the dead stem’s pieces to host its resting spores, and the cycle moves along in a healthy husband-and-wife existence. Both get to live and do their thing.

Which they did until a few years ago when there was a massive collapse of Westar’s resistance to blackleg. When looking for resistance genes to clean up the mess, researchers looked at other germplasm sources and found a dynamite gene that worked wonders — Rlm3, which is now the backbone of most blackleg resistance in Western Canada. This single-gene resistance source, though backed up by a few minor genes that have — in many cases — prevented full-scale wipeouts like Westar’s, is now failing in some fields.

Another tight rotation concern

That’s because when you bombard the blackleg population with Rlm3 in a tight rotation, you eventually select for mutations of the matching AvrLm3. By letting these mutations into the mix, the lock-and-key, husband-and-wife good relationship falls apart and becomes virulent. Instead of coming home to hug and kiss its canola family, the pathogen eats them. When this happens, pathologists rename the pathotype “avrLm” with a lowercase “a.”

Blackleg becomes an issue only when the matching population goes virulent — “avrLm” versus “AvrLm.” This is a classic case of familiarity breeding contempt. Too much of the same old, same old and the relationship goes sour. But there is help!

A grower can fix the relationship two ways: One, extend the canola rotation. This gives the avrLm3-infested residue time to break down and disintegrate, lowering the blackleg spore load across the board — virulent and avirulent. This works better when neighbouring fields are not in canola.

Two, grow a variety that has a resistance package different from the avrLm pathotype. If the field is full of avrLm3, grow a variety that doesn’t have the Rlm3 gene, although this requires identification of the dominant pathotypes in a field and knowledge of the Rlm genes in each canola variety.

The Australian solution

Australia has adopted this solution. Fernando is part of the charge to bring it to Canada. He and other leading blackleg pathologists in Western Canada are working on studies right now to identify AvrLm species present across the Prairies. As part of his research, he will head to Australia this fall to understand first-hand how the Australian system works for farmers and seed companies.

Blackleg prefers to be in a good relationship with canola, Fernando adds. It will not stay in the avrLm3 stage for long — as long as it doesn’t have canola with the Rlm3 gene to feed its fury. After a few years’ break, the population will hopefully shift back to AvrLm3, Fernando says.

A system of canola gene rotation can be very effective at keeping blackleg virulence and, therefore, blackleg infection rates low. This would be, as described in Fernando’s research objective, the solution to “durable blackleg resistance stewardship.”

The key to “durability” is to keep the crop and farmers happy and, importantly, L. maculans happy, too. I now understand how that can work. Finally.

Jay Whetter is a communications manager with the Canola Council of Canada. Email him at [email protected].

About the author


Jay Whetter is communications manager for the Canola Council of Canada.



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