Jump to content

Cochliobolus victoriae

From Wikipedia, the free encyclopedia

Cochliobolus victoriae
Scientific classification Edit this classification
Domain: Eukaryota
Kingdom: Fungi
Division: Ascomycota
Class: Dothideomycetes
Order: Pleosporales
Family: Pleosporaceae
Genus: Cochliobolus
Species:
C. victoriae
Binomial name
Cochliobolus victoriae
R.R. Nelson, (1960)
Synonyms

Bipolaris victoriae (F. Meehan & H.C. Murphy) Shoemaker, (1959)
Drechslera victoriae (F. Meehan & H.C. Murphy) Subram. & B.L. Jain, (1966)
Helminthosporium sativum var. victoriae (F. Meehan & H.C. Murphy) H.R. Rosen, Wiser & J.O. York, (1953)
Helminthosporium victoriae F. Meehan & H.C. Murphy, (1946)

Cochliobolus victoriae is a fungal plant pathogen. It caused the disease called "Victoria blight" affecting oats and similar grains.

Symptoms

[edit]

Cochliobolus victoriae is a fungus that causes Victoria blight in oats. Symptoms include stem weakening, seedling death, leaf damage, and premature ripening of seeds.[1] Other symptoms include basal necrosis and foliar striping, which begins at the lower leaves and proceeds upwards. Blackened nodes and root rot can also be symptoms.[2] Conidiophores emerge from the stomata or epidermal cells of the diseased oat, usually in groups of two to five, and are a medium-brown color.[2]

Importance

[edit]

Victorian oat varieties have resistance to crown rust, which is considered one of the most important diseases in oats. In the 1940s, Victoria oats were very popular among American oat farmers because of this crown rust resistance. However, the same gene that grants crown rust resistance is also responsible for causing susceptibility to Victoria blight. Victoria blight was first reported in America in 1946. Victoria blight caused huge losses to oat yields, and in 1947 and 1948 it reached epidemic proportions in oat growing regions of America. These huge epidemics caused Victoria oat cultivars to be abandoned by growers[3] Other varieties of oats are not susceptible to Victoria blight, so by switching to these other varieties, further outbreaks of Victoria blight have been prevented. However, this means that growers are unable to take advantage of the crown rust resistance that Victoria oats have.[4] Thus, crown rust remains a serious disease in oats.[5]

Pathogenesis

[edit]

Victoria type oats contain the Pc-2 gene which confers resistance against crown rust caused by the fungus Puccinia coronate. However, the oats that contained this gene are susceptible to Victoria blight. This is because the gene LOV1, which is part of the crown rot resistance, is responsible for susceptibility to Victoria blight.[6] Cochliobolus victoriae produces the toxin victorin. Victorin only effects plants that contain the LOV1 gene, causing these plants to develop Victoria blight.[7]

References

[edit]
  1. ^ "OSU demystifies how oat fungus kills plants". OSU Extension Service. Oregon State University. Retrieved 13 December 2018.
  2. ^ a b Meehan F, Murphy HC (November 1946). "A New Helminthosporium Blight of Oats". Science. 104 (2705): 413–4. doi:10.1126/science.104.2705.413. PMID 17814758.
  3. ^ Ghabrial SA, Dunn SE, Li H, Xie J, Baker TS (2013). "Viruses of Helminthosporium (Cochlioblus) victoriae". Advances in Virus Research. 86: 289–325. doi:10.1016/B978-0-12-394315-6.00011-8. ISBN 9780123943156. PMID 23498911.
  4. ^ Buchenau GW (1960). Etiology and epiphytology of Victoria blight of oats. Retrospective Theses and Dissertations (Ph.D. thesis). Ames Iowa: Iowa State University.
  5. ^ "Oat crown rust : USDA ARS". United States Department of Agriculture (USDA). Retrieved 13 December 2018.
  6. ^ Lorang JM, Sweat TA, Wolpert TJ (September 2007). "Plant disease susceptibility conferred by a "resistance" gene". Proceedings of the National Academy of Sciences of the United States of America. 104 (37): 14861–6. Bibcode:2007PNAS..10414861L. doi:10.1073/pnas.0702572104. PMC 1976202. PMID 17804803.
  7. ^ Wolpert TJ, Lorang JM (July 2016). "Victoria Blight, defense turned upside down". Physiological and Molecular Plant Pathology. 95: 8–13. doi:10.1016/j.pmpp.2016.03.006.
[edit]