How to diagnose Cercospora blight in soybeans

Necrotrophic pathogens, recurrent in soybean crops, do not They rarely end up classified as end-of-cycle disease (CLD). It is the case brown spot and especially cercospora blight, easily confused with other diseases leaves. Its evolution occurs through the phytotoxin Cercosporin, which helps directly in the assertiveness of the diagnosis of the leaf symptom.

The geographic location of Brazil confers specific agroclimatic privileges of a macro-region located in around the tropics. These conditions allow the survival, development and reproduction of the vast majority of species on the planet, are of interest agricultural or not. In this particular, living beings that use agricultural cultivation as a substrate for its perpetuation, it has a vast horizon to survive, due to the monoculture system. This environment allows a wide range of pathogens find excellent conditions to survive for a few months of the year, even with the absence of culture. Necrotrophic pathogens have the ability to survive without a living host, through resistance structures in the soil or in saprophytic activities, nourishing themselves from organic matter.

Some of the necrotrophic pathogens, recurring in soybean cultivation, were formerly and incorrectly called of end-of-cycle diseases (CLD). They received this name due to their lack of knowledge of its epidemiology, only through its symptomatic observation, present at the end of the soybean crop cycle. Among the pathogens with these characteristics, meet the brown spot (septoria wisteria) and cercospora blight (cercospora kikuchii). Especially the latter, it has very specific characteristics of infection and presents symptoms that can be confused with other foliar diseases in soy. The evolution of the disease occurs through a phytotoxin produced by C. kikuchii, which directly assists in assertiveness of the diagnosis of the leaf symptom.

Cercosporin

The phytotoxin called Cercosporin had the first report in Japan, around the 70s, where researchers described the route of biosynthesis of this compound (Okubo et al., 1975). They concluded that the route begins with the condensation of acetate and malate molecules, establishing the polyketide pathway, a large class of secondary metabolites present in bacteria, fungi, plants and some animals.

A fundamental factor for your production and virulence, is the presence of light (Ehrenshaft et al., 1991). The molecule of cercosporin absorbs wavelengths in the visible range, between 400nm and 600nm, that is, from purple to yellow. Therefore, the trigger for the production of this phytotoxin is triggered immediately by the presence of light, being suppressed with the dark. Furthermore, temperatures above 30°C inhibit the production of cercosporin. This helps to understand that in warmer regions, the presence of cercospora blight symptoms becomes visible in years milder or very late in the crop cycle.

With the absorption of light, cercosporin is produced, energizes quickly and is converted into a triplet state Fence* (enzymatically generated triplet species capable of transferring energy to multiple acceptors). In this form, the Fence* transfers energy to chlorophyll, making it triplet (Chl*), which in turn will transfer the energy to the acceptor most greedy for electrons, oxygen. With unpaired electrons, production begins cascade of Reactive Oxygen Species (ROS) in the plant cell, such as singlet oxygen (1O2), superoxide radical (-O2), peroxyl radical (HO2), hydrogen peroxide (H2O2) and hydroxyl radical (OH-). ROS cause lipid peroxidation (Scheme 1), destroying cellular integrity, inducing extravasation of the cytoplasmic content (Scheme 2), causing cell death (Daub & Ehrenshaft, 2000). Some hypotheses suggest that the extravasation of Nutrients from the cytoplasm to the intercellular spaces facilitate growth and sporulation of the fungus (Daub et al., 1983).

Cercosporin in disease process

The production of Cercosporin is carried out by C. kikuchii for assist in the process of infection and virulence on the susceptible host. O The first report of this association was made by Upchurch et al. (1991), observing that mutants of the pathogen, which did not produce cercosporin, were not capable of causing infection in soybean leaves. In other works, Almeida et al. (2005) found a relationship of 83% between the pathogens that produce cercosporin and the severity of the disease in the plant. They also discussed that, isolated that presented more purple to red halos in culture medium, were also those that produced the most cercosporin and were therefore the most virulent. Furthermore, isolates that produced low levels of the phytotoxin caused very small lesions with a low rate of progress.

Another important factor in this relationship and expression of symptoms is the presence of light. Several studies have proven that in the dark or shaded, the penetration and evolution of symptoms was lower, when compared with the condition under direct light. This characteristic elucidates the diagnosis, sometimes confused, with the symptomatic expression of the disease.

Symptoms of blight cercospora are seen on the top leaves of the crop and hardly in the lower third, where brown spot is prevalent.

From the formation stage of the grain until it is filled, the moment of greatest expression of the symptoms of blight. On the top leaves, the process of symptomatic expression begins, through a light tanning in the inter-vein region of the leaflet, easily confused with adjuvant phytotoxicity. As the cycle of culture, provided with leaf wetness for hydration of conidia and production of cercosporin, symptoms progress, quickly progressing to chlorosis, followed by necrosis and torsion of the leaflet edge. In In some cases, it is still possible to see a purplish appearance of the veins, stems and vegetables, ending the pathogen cycle in the host, with the grain.

Article published in issue 215 of Cultivar Grandes Culturas, April 2017.