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Triazole Phytotoxicity in Soybeans

By Kyle Broderick

A number of soybean samples have been coming into the Plant & Pest Diagnostic Clinic showing interveinal chlorosis and necrosis that is commonly associated with either Sudden Death Syndrome or Brown Stem Rot (Figures 1 and 2). However, when splitting the stems and crown tissue, the pith and vascular tissue is still white and not showing discoloration that is generally caused by a fungal infection (Figure 3). In many cases, these symptoms are occurring field-wide and symptoms are not always evident on the newest leaves. These symptoms are not caused by a pathogen, but likely phytotoxicity due to the application of a triazole (DMI) fungicide.

Figure 1. Interveinal chlorosis and necrosis on soybean leave

Figure 1. Interveinal chlorosis and necrosis on soybean leaves caused by Sudden Death Syndrome. Photos by Kyle Broderick

Figure 2. Interveinal chlorosis and necrosis

Figure 2. Interveinal chlorosis and necrosis caused by triazole phytotoxicity.


Figure 3. Lower stem and crown tissue of soybean

Figure 3. Lower stem and crown tissue of soybean with symptoms of triazole phytotoxicity. Note the lack of internal vascular discoloration that is commonly associated with Sudden Death Syndrome or Brown Stem Rot.
 

The prevalence of Group 11 (QoI a.k.a. Strobulurin) fungicide-resistant Frogeye Leaf Spot across Nebraska has led to more farmers using other fungicides and tank mixes with multiple modes of action to achieve control. One of the main groups of fungicides being utilized to control QoI-resistant frogeye leaf spot are triazoles (Group 3/DMI) fungicides

Triazoles can vary in their effects resulting in phytotoxicity and the level of injury depends on fungicide rate, adjuvants used, soybean genetics and environmental conditions at the time of application. Symptoms have been appearing 2-3 weeks after fungicide application and follow a spray pattern or have a field-wide distribution. Triazoles are xylem-mobile, so their movement through the plant is dependent on the moisture. Symptoms can be amplified when the fields are under drought stress due to the xylem-mobile nature of triazole fungicides. If the plants are drought-stressed, the fungicide remains in the leaf tissue longer, resulting in greater injury. Note that this injury will be on the leaves in the upper canopy that are expanding at the time of application.

Figure 4. Vascular discoloration of lower stem and crown

Figure 4. Vascular discoloration of lower stem and crown commonly associated with Sudden Death Syndrome.

fig 5

Figure 5. Internal browning and “stacking” of pith associated with Brown Stem Rot.

Sudden death syndrome (SDS) is caused by the soilborne fungus Fusarium virguliforme. Foliar symptoms of SDS typically appear at R3 and later and consist of chlorotic (yellow) spots between the veins of the upper leaves. The chlorotic spots eventually turn brown (necrotic) as the tissue dies. Leaves may drop, but the petioles remain attached. The taproot of SDS-infected plants typically rots away, otherwise below-ground symptoms of SDS are difficult to distinguish from other root rot pathogens. When splitting the stems, the vascular tissue of the lower stem/crown will be brown and discolored, but the upper portion of the stem pith remains white (Figure 4). 

Brown stem rot (BSR) is caused by the soilborne fungus Cadophora gregata. Similar to SDS, this fungal pathogen causes interveinal chlorosis and necrosis of the upper leaves; however, foliar symptoms are not always present depending on the soybean variety, fungal strain and environmental conditions in the field. Splitting the stem lengthwise reveals internal browning of the vascular tissue and pith, especially at nodes and in the lower stem (Figure 5). BSR is favored by cool, wet soils and symptoms may be suppressed during periods of low soil moisture and high temperatures.

Source : unl.edu

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The 15-Year Bet Behind Every New Variety

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Canada is trying to decide how much agricultural research capacity it can afford to lose. Brian Rossnagel believes the better question is whether the country can afford to rebuild it.

The longtime barley and oat breeder makes the case with a simple fact about his profession: the consequences of today’s decisions may not become visible for 10 or 15 years.

“Pick the right parents. That’s the biggest thing,” Rossnagel says. “If you pick the wrong parents, you’re not going to get anywhere—and you don’t know that until 10 years, 15 years later.”

That warning carries particular weight as Agriculture and Agri-Food Canada moves to reduce spending and streamline parts of its science operations. The department’s 2026–27 plan anticipates the loss of approximately 665 positions by 2028–29 and says some research will be reduced where capacity exists in academia or industry. AAFC says the changes will make its science operations more cost-effective over the long term.

For Canada’s seed industry, Rossnagel’s career illustrates what is at stake.

This fall, the retired University of Saskatchewan breeder will be inducted into the Canadian Agricultural Hall of Fame. During his 35-year career at the Crop Development Centre, he helped develop more than 100 barley and oat varieties, including CDC Austenson—one of Western Canada’s most widely grown feed barleys. His induction recognizes not only those varieties, but the collaboration and research system that made them possible.

Rossnagel is quick to emphasize that none of it was the work of one person.

“The first thing I thought about was all the other people who contributed to whatever success I and my program had over the years,” he says. “We know that it’s not an individual who does this. It’s a group—a team.”

That team extends well beyond the breeder whose name appears beside a variety. It includes technicians, pathologists, quality specialists, statisticians, regional testing sites, seed growers and industry partners. It also includes the breeders who came before and those who will carry the germplasm forward.

CDC Fraser barley, for example, moved through three breeding careers. Its parents came from Brian Harvey’s program. Rossnagel advanced the material after Harvey retired, and Aaron Beattie later guided it through registration and release.

That kind of handoff is normal in plant breeding. The person who makes the original cross may never see the resulting variety reach farmers.

It also explains why lost research capacity cannot simply be switched back on when budgets improve.

“If you shut it off, it’s very, very difficult—and particularly costly—to start it up again,” Rossnagel says. “If you have to start from scratch, it’s going to be at least 10 years before anybody notices whether you’re getting anything done or not.”

The concern is not simply how many experimental lines Canada can process. Modern equipment, statistical tools and genetic technologies allow today’s breeding programs to evaluate tens of thousands of lines—far more than Rossnagel could handle when he entered the field in the early 1970s.

But efficiency and automation do not generate every idea.

“If you pare back down, and instead of having six or seven individual scientists concentrating on wheat breeding, you go down and say three people could handle all this, well, that’s half the ideas gone,” he says. “Particularly if you happen to lose the three people who had the really neat and innovative ideas, boy, that’s a problem.”

It is a timely distinction for Canadian agriculture. Consolidating programs may preserve the volume of material moving through a system, at least initially. It may not preserve the diversity of thinking, regional knowledge or willingness to pursue unconventional crosses.

That regional knowledge matters because Canadian agriculture is not one uniform production environment. A variety suited to southern Alberta may face different disease, moisture and maturity pressures than one grown in Manitoba, Ontario or Atlantic Canada.

“Agriculture is applied biology,” Rossnagel says. “Biology, all around the Earth, moves from the poles to the equator. It does not move from Newfoundland to B.C. like politics do.”