Phialophora gregata

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Phialophora gregata
Scientific classification OOjs UI icon edit-ltr.svg
Domain: Eukaryota
Kingdom: Fungi
Division: Ascomycota
Class: Eurotiomycetes
Order: Chaetothyriales
Family: Herpotrichiellaceae
Genus: Phialophora
Species:
P. gregata
Binomial name
Phialophora gregata
(Allington & D.W. Chamb.) W. Gams, (1971)
Synonyms

Cadophora gregata
Cephalosporium gregatum

Phialophora gregata is a Deuteromycete [1] fungus that is a plant pathogen which causes the disease commonly known as brown stem rot of soybean. P. gregata does not produce survival structures, but has the ability to overwinter as mycelium in decaying soybean residue. [2]

Contents

Two strains of the fungus exist; [2] genotype A causes both foliar and stem symptoms, while genotype B causes only stem symptoms. [2] Common leaf symptoms are browning, chlorosis, and necrosis [2] Foliar symptoms which are often seen with genotype A are chlorosis, defoliation, and wilting. [2] [3]

Brown Stem Rot of soybeans is a common fungal disease in soybeans grown in the upper Midwest and Canada. Brown Stem Rot (BSR) may commonly reduce yield of soybeans by 10-30% on susceptible varieties, [4] up to 10 bu./acre in severe cases. BSR decreases both the number of beans per pod as well as bean size as a result of wilting, premature defoliation and lodging. [5] In addition to decreasing yield, plants infected by BSR can be difficult to harvest due to lodging of soybean plants. University of Wisconsin Extension Field Crop Pathologist, Damon Smith ranks Brown Stem Rot as the third most important soybean disease in Wisconsin. [4] Brown Stem Rot can impact most susceptible soybean beans in the north central states, especially during cooler late summer months. [5]

There are many ways to manage Phialophora gregata. The most effective form of management is disease resistance, [2] but crop rotation, tillage, SCN management, and changing the pH of the soil can also be effective [2] [6]

Symptoms and signs

Phialophora gregata’s infection of a soybean plant is accompanied by browning of the plant’s vascular and pith tissues. [2] The plant often exhibits chlorosis and necrosis, as well as leaf browning. [2] Wilting and defoliation are also known to occur. [2] Signs of infection often go unnoticed until reproductive stages of a plant’s life cycle. They can be diagnosed earlier on by opening the stem and visualizing the pathogen. One can visualize signs by cutting open the stem in early stages of infection, [2] but symptoms do not become apparent until after the soybean pod formation. [7]

Depending on which strain infects the plant, and what the environmental conditions are, [8] the effect is more or less potent. Genotype A causes browning of stems as well as foliar symptoms such as interveinal chlorosis, defoliation and wilting. [2] [3] Symptomatic leaves have a shriveled appearance, but remain attached to the stem. [3] Genotype B causes only browning of stems. [3]

Secondary symptoms of brown stem rot are stunting, premature death, decrease in seed number, reduced pod set, and decrease in seed size. [3]

Disease from P. gregata is easily confused with Fusarium wilt, due to the similar vascular symptoms observed in both. [9] The diseases could be differentiated through growth on isolation media. [9] The two diseases can be further distinguished by splitting the stems. A split stem with Fusarium infection would have tan or light brown discoloration in the cortex and a normal white pith, while a split stem with P. gregata would have a discolored, reddish brown pith. [7] Root rot and blue masses of spores are symptoms only caused by Fusarium. [7]

Environment

The fungal pathogen, Phialophora gregata, that causes Brown Stem Rot (BSR) of soybeans prefers conditions that are also optimal to soybean plant growth. Later planted soybeans are more susceptible to BSR as cooler temperatures during early pod forming stages make the plant most vulnerable. [10] Early season wet conditions can also favor early season pathogen growth, often causing more dramatic affects later in season. [8] Foliar symptoms of BSR are favored when conditions are cool during flowering and pod formation. [10] The Phialophora gregata pathogen proliferates in stem tissues when soil has high moisture content and air temperatures remain near 60-75 degrees Fahrenheit. [3] Fungal growth of Phialophora gregata shuts down above 80 degrees Fahrenheit. [8] Low water available to the plant, late in season can also dramatically increase disease severity. [10] As the disease is soilborne, it is not uncommon to find clusters of diseased plants together. [3] Additionally, the prevalence of Soybean Cyst Nematodes (SCN) can affect the growth of Phialophora gregata, the BSR pathogen. Greater populations of SCN, can greatly increase the likelihood and impact of Brown Stem Rot. [11]

Disease cycle

The Phialophora gregata fungus is a deuteromycete with a monocyclic life cycle. There are two strains of Phialophora gregata, referred to as genotype A and genotype B. [6] Genotype A causes both foliar and stem symptoms, while genotype B causes only stem symptoms. [2]

The Phialophora gregata fungus produces no survival structures, but can overwinter as mycelium [12] in decaying soybean residue. During overwintering, conidia are produced; these conidia are the inoculum for new plants in the spring. [12] The amount of asexual reproduction that occurs during the winter affects the spring inoculum levels. [12] Infection initially occurs in the roots of young soybean plants, and then spreads to the stem (and foliage, depending on the strain). [2] Generally, early and severe foliar symptoms indicate that the yield losses will be heavier. [6]

Economic significance

Brown Stem Rot of soybeans is a source of major crop loss. It is not uncommon for soybeans grown in management systems prone for brown stem rot to have yield losses between 10%, with a maximum potential loss of 30%. [2] [13] It has been listed as the 3rd most important disease to soybeans in Wisconsin. [2] [13] A recent study showed that nearly half the counties in Iowa, from 2006 and 2007, had brown stem rot of soybean. [6]

Management

Brown Stem Rot can be easily managed using several techniques employed by the grower. Common techniques include crop rotation, tillage, selection and Soybean Cyst Nematode management. There are currently no available seed treatments or fungicides to prevent or protect against BSR.

Crop rotation

The easiest and most effective way to protect against Brown Stem Rot in soybeans is crop rotation. Phialophora gregata has no overwintering structures but instead lives in plant debris. Due to this, waiting until plant debris has decomposed (at least one full growing season) is the most effective way to control this disease [5] . In cases of severe infection 2–3 years without planting soybeans in infected fields may be necessary. [10]

Disease resistance

Given the presence of Phialophora gregata on much of the nation’s soybean acres, research and development have gone into selecting soybean varieties that have greater resistance to BSR, although not immunity. Brown stem rot has the uncanny ability to produce yield loss even without obvious symptoms. [13] Higher rated BSR tolerance in beans can be selected for when choosing a variety to be grown. Genetic Resistance should not be relied upon when expected BSR pressure is high. [10] Additionally, choosing varieties higher rated for tolerance against soybean Cyst nematode can be effective. [14]

Tillage

More decomposition of soybean residue results in less pathogen, as the fungus can only survive on soybean residue. [10] Therefore, tillage can be effective. Once the soybean residue has decomposed, the survival of P. gregata is drastically decreased. It is common for farmers to practice both crop rotations and tillage in a cyclic fashion. [15] This is done by conducting little to no tillage when a soybean crop is planted after corn, followed by intensive tillage when a corn crop is planted after soybean. [15]

Management of soybean cyst nematode (Heterodera glycines)

P. gregata is often found to be more severe in the presence of SCN; [2] soybean plants showing resistance to SCN have been found to produce greater yields. [2] Soybean plants with resistance to both SCN and genotype A of P. gregata can grow normally, even when both pathogens are present. [6] Given the correlation between SCN populations and disease impact of BSR it is important to control SCN. SCN can be controlled using rotation to non-susceptible crops, seed treatments, variety selection and nematicides. [11]

Monitoring soil pH

Maintaining a soil pH near 6.5-7.5 can also help protect against BSR. There is evidence of significantly lower disease severity [2] with a near neutral soil pH, although there is no evidence to suggest a neutral pH prevents BSR. [14]

Related Research Articles

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Fusarium wilt is a common vascular wilt fungal disease, exhibiting symptoms similar to Verticillium wilt. This disease has been investigated extensively since the early years of this century. The pathogen that causes Fusarium wilt is Fusarium oxysporum. The species is further divided into formae speciales based on host plant.

<span class="mw-page-title-main">Soybean cyst nematode</span> Species of roundworm

The soybean cyst nematode (SCN), Heterodera glycines, is the most devastating pest to soybean crop yields in the U.S., targeting the roots of soybean and other legume plants. When infection is severe SCNs cause stunting, yellowing, impaired canopy development, and yield loss. The symptoms caused by SCNs can go easily unrecognized by farmers—in some cases there are no warning symptoms before a loss of 40% of the yield. Due to the slight stunting and yellowing, many farmers may mistake these symptoms as environmental problems when in fact they are SCNs. Another symptom of SCNs that may affect farmers' yields is stunted roots with fewer nitrogen-fixing nodules. Due to the fact that soybean cyst nematodes can only move a few centimeters in the soil by themselves, they mostly are spread via tillage or plant transplants. This area of infection will look patchy and nonuniform making diagnosis more difficult for farmers. They can be seen in the roots of summer soybean plants if the roots are taken out very carefully and gently washed with water. The egg masses should be seen as bright white or yellow "pearls" on the roots. The later the roots are pulled the harder it will be to diagnose due to the SCNs female dying and turning a much darker color, forming a "cyst". The best way to know if a field is infected by soybean cyst nematodes is to take a soil sample to a nematologist.

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<i>Pyrenophora tritici-repentis</i> Species of fungus

Pyrenophora tritici-repentis (teleomorph) and Drechslera tritici-repentis (anamorph) is a necrotrophic plant pathogen of fungal origin, phylum Ascomycota. The pathogen causes a disease originally named yellow spot but now commonly called tan spot, yellow leaf spot, yellow leaf blotch or helminthosporiosis. At least eight races of the pathogen are known to occur based on their virulence on a wheat differential set.

<i>Gibberella zeae</i> Species of fungus

Gibberella zeae, also known by the name of its anamorph Fusarium graminearum, is a fungal plant pathogen which causes fusarium head blight (FHB), a devastating disease on wheat and barley. The pathogen is responsible for billions of dollars in economic losses worldwide each year. Infection causes shifts in the amino acid composition of wheat, resulting in shriveled kernels and contaminating the remaining grain with mycotoxins, mainly deoxynivalenol (DON), which inhibits protein biosynthesis; and zearalenone, an estrogenic mycotoxin. These toxins cause vomiting, liver damage, and reproductive defects in livestock, and are harmful to humans through contaminated food. Despite great efforts to find resistance genes against F. graminearum, no completely resistant variety is currently available. Research on the biology of F. graminearum is directed towards gaining insight into more details about the infection process and reveal weak spots in the life cycle of this pathogen to develop fungicides that can protect wheat from scab infection.

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References

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