Cryphonectria parasitica
Classification
Higher order taxa
Domain: Fungus, Kingdom: Fungus, Phylum: Ascomycetes, Class: Sordariomycete, Order: Diaporthales, Family: Cryphonectriaceae, Genus: Cryphonectria, Species: Cryphonectria parasitica
Species
Cryphonectria parasitica
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NCBI: Taxonomy |
Description and significance
Cryphonectria parasitica is a deadly fungus originally found on American chestnut trees outside the chestnut's native range. Cryphonectria parasitica was first observed in the New York City Zoo in 1904 and became known as the "chestnut blight." Originally taxonomically known as Diaporthe parasitica, the fungus was later reclassified into the genus Endothia and finally named Cryphonectria parasitic. This foreign pathogen brings deadly disaster. Its emergence has resulted in the American chestnut becoming the dominant species in the forest canopy of North America, while in Europe, some special chestnut populations such as Castanea sativa Mill. have brought near-extinction hazards. This pattern of introduced fungal pathogens wreaking havoc on tree species has persisted, with ash dieback (caused by Hymenoscyphus fraxineus) in Europe being the most recent example (Gross et al. 2014). It is worth noting that chestnut wilt has attracted attention due to its hypovirulence phenomenon, in which viral infection weakens the virulence of the pathogen, providing a basis for biological control of the disease. In addition, conservation breeding efforts aim to restore the American chestnut to its status as an important forest species.
Genome structure
Both Cryphonectria parasitica mycoreoviruses (CpMYRV-1 and CpMYRV-2) consist of 11 genome segments categorized under Group 1. Despite sharing this structural similarity, they exhibit only around 29% amino acid sequence identity in the capping enzyme, affirming their classification as distinct species.
The complete genome of Cryphonectria parasitica mycoreovirus-1 (CpMRV-1) spans 23,436 base pairs (bp), with the length of individual segments varying between 732 bp and 4,127 bp. This results in a distinctive electrophoretic profile, exhibiting a pattern of 3, 3, 2, 3 segments when analyzed using either 11% polyacrylamide gel electrophoresis (PAGE) or 1% agarose gel electrophoresis (AGE).
Cryphonectria parasitica strain EP155
Cryphonectria parasitica strain EP155, one of the strains causing damage to American chestnut trees, was originally isolated from chestnut canker. The genome sequencing and assembly process involved the use of Sanger sequencing protocols, resulting in a high-quality assembly of 26 scaffolds containing 33 contigs, spanning 43.9 Mb. The assembly was further refined using genetic linkage data, providing valuable insights into the organization of the genome at the chromosome level. Functional annotations of the genome revealed a total of 11,609 genes, with over 85% showing similarities to proteins from the NCBI nonredundant protein database. The genome also contains a significant number of genes involved in pathogenicity, secondary metabolite production, and cytochrome P450s.
Host range
Cryphonectria parasitica primarily infects various species within the genus Castanea, including the American chestnut, European chestnut, Chinese chestnut (C. mollissima Blume), and Japanese chestnut (C. crenata Siebold & Zucc.), all of which belong to the family Fagaceae.
Life Cycle
Cryphonectria parasitica is the causative agent of chestnut blight. They use damage to tree trunks or branches to enter trees and become parasitic. Furthermore, recent studies have shown that Cryphonectria parasitica can infect abandoned galls of chestnut gall wasps, providing new pathways for pathogens to invade host tissues. Both sexual and asexual spores of Cryphonectria parasitica can cause infection. When the spores germinate, ulcers form. Later, Cryphonectria parasitica may produce spores on infected bark and recently dead chestnut wood. The fruiting body, called a stroma, is composed of sexual (ascotheca) and asexual (pycnidia) structures and develops in numerous yellow-orange to reddish-brown pustules. These structures range from 0.5 to 4 mm in diameter and up to 2.5 mm in height and are embedded in the bark, with both types of fruiting bodies often coexisting closely.
The complex life cycle and diverse reproductive structures of Cryphonectria parasitica facilitate its successful colonization and spread in chestnut populations. By exploiting a variety of entry points and employing sexual and asexual reproduction methods, Cryphonectria parasitica exhibits remarkable adaptability and resilience, posing an ongoing challenge to the management and conservation of chestnut trees. The emergence of Cryphonectria parasitica has had a great impact on different chestnut trees and even oak species in various regions, and even led to the extinction of chestnut trees in the United States for a certain period of time. It has had a very negative impact on agriculture and the economy.
Disease Symptoms
Cryphonectria parasitica mainly infects the branches of trees, so Cryphonectria parasitica is classified as a bark pathogen. Symptom expression on susceptible hosts, including European and American chestnuts, varies depending on the virulence of the Cryphonectria parasitica strain and the age of the infected tree part. Virulent strains of Cryphonectria parasitica form necrotic lesions on the bark, known as cankers, that can rapidly kill smaller branches or twigs within months. But on thicker branches, it usually takes several years for the cankers to develop before death occurs. While red and orange colors form on young stems and branches, the color is less noticeable on thicker branches, making it more difficult to judge.
Within the bark and cambium, the characteristic light brown fans of Cryphonectria parasitica mycelium will appear, a telltale sign of chestnut wilt infection. If the cambium is killed, the bark will sink inward, making the canker look sunken. Afterwards the tree dies and the leaves wilt and turn yellow or brown.
Unlike cankers caused by virulent strains, cankers caused by less virulent strains are usually non-fatal. Stromata harboring the fruiting bodies of Cryphonectria parasitica may develop on the surface of cankers, while symptoms on oaks consist of slowly developing, calling using cankers that typically do not lead to stem or branch death.
Epidemiology
New populations of Cryphonectria parasitica usually result from the introduction of one or more genotypes. It is likely that new Cryphonectria parasitica populations in North America were accidentally introduced with infected plant material. North American Cryphonectria parasitica has the fastest growth rate at 20°C, while European chestnut Cryphonectria parasitica has the fastest growth rate at 27°C and is significantly slower below 20°C. Adequate moisture provided by humid air, rain or dew is also critical for the survival, development and spread of Cryphonectria parasitica, for example, moist conditions trigger spore release. There is a seasonal pattern in European chestnut susceptibility to C. parasitica, with a peak in spring and summer and a decrease in autumn and winter, possibly due to changes in bark nutritional value and moisture content.
History
Cryphonectria parasitica was first discovered in East Asia, specifically China, Japan, and Korea. However, in the 20th century it was inadvertently introduced to North America and Europe via infected chestnut plants. After its discovery in 1904, it spread rapidly throughout the American chestnut's native distribution range at a rate of more than 30 kilometers per year, covering approximately 3.6 million hectares in eastern North America. This resulted in the endangered chestnut tree in North America and it has a great impact on the economy and environment. In Europe, the pathogen was officially detected in 1938 near Genoa, Italy's main international port. Genetic studies suggest that North America may have been the original source of introduction to Italy. By 1950, chestnut wilt had become widespread in Italy's main chestnut-growing areas and quickly spread to neighboring France. Between the 1920s and 1950s, Europe imported large quantities of chestnut trees from Asia and the United States, which may have facilitated the spread of C. parasitica. Ironically, the purpose of many of these imports was to obtain chestnut trees that were resistant to ink disease, the most serious chestnut disease before the arrival of chestnut wilt.
