Jump to content

Sclerotinia sclerotiorum

From Wikipedia, the free encyclopedia
(Redirected from Sclerotinia libertiana)

Sclerotinia sclerotiorum
Sclerotinia sclerotiorum on Phaseolus
Scientific classification Edit this classification
Domain: Eukaryota
Kingdom: Fungi
Division: Ascomycota
Class: Leotiomycetes
Order: Helotiales
Family: Sclerotiniaceae
Genus: Sclerotinia
Species:
S. sclerotiorum
Binomial name
Sclerotinia sclerotiorum
(Lib.) de Bary (1884)
Synonyms
  • Hymenoscyphus sclerotiorum (Lib.) W.Phillips (1887)
  • Peziza sclerotiorum Lib. (1837)
  • Sclerotinia libertiana Fuckel (1870)
  • Sclerotium varium Pers. (1801)
  • Whetzelinia sclerotiorum (Lib.) Korf & Dumont (1972)

Sclerotinia sclerotiorum is a plant pathogenic fungus and can cause a disease called white mold if conditions are conducive. S. sclerotiorum can also be known as cottony rot, watery soft rot, stem rot, drop, crown rot and blossom blight. A key characteristic of this pathogen is its ability to produce black resting structures known as sclerotia and white fuzzy growths of mycelium on the plant it infects. These sclerotia give rise to a fruiting body in the spring that produces spores in a sac which is why fungi in this class are called sac fungi (Ascomycota). This pathogen can occur on many continents and has a wide host range of plants. When S. sclerotiorum is onset in the field by favorable environmental conditions, losses can be great and control measures should be considered.

Hosts and symptoms

[edit]
Sclerotia from sunflower
Sclerotia from sunflower

S. sclerotiorum is among the most omnivorous of plant pathogens and so would not make a good mycoherbicide. Economically significant hosts include Vicia faba, for which Lithourgidis et al have done extensive work over the years.[1] Common hosts of white mold are herbaceous, succulent plants, particularly flowers and vegetables. Sunflowers are common hosts for white mold. It can also affect woody ornamentals occasionally, usually on juvenile tissue. White mold can affect their hosts at any stage of growth, including seedlings, mature plants, and harvested products. It can usually be found on tissues with high water content and in close proximity to the soil. One of the first symptoms noticed is an obvious area of white, fluffy mycelial growth. Usually this is preceded by pale to dark brown lesions on the stem at the soil line. The mycelium then cover this necrotic area. Once the xylem is affected, other symptoms occur higher up in the plant. These can include chlorosis, wilting, leaf drop, and death quickly follows. On fruits, the initial dark lesions occur on the tissue that comes in contact with the soil. Next, white fungal mycelium covers the fruit and it decays. This can occur when the fruit is in the field or when in storage.[2]

Importance

[edit]

White mold affects a wide range of hosts and causes sclerotinia stem rot. It is known to infect 408 plant species. As a nonspecific plant pathogen,[3] diverse host range and ability to infect plants at any stage of growth makes white mold a very serious disease. The fungus can survive on infected tissues, in the soil, and on living plants. It affects young seedlings, mature plants, and fruit in the field or in storage. White mold can spread quickly in the field from plant to plant. It can also spread in a storage facility throughout the harvested crop. Some crops it affects commonly are soybeans,[4] green beans, sunflowers, canola, and peanuts.[5] White mold is the most common pathogen that affects sunflower and has been found to cause reduction in yield throughout the world including the United States, northern Europe, Great Britain and Russia. [6]

Sclerotinia stem rot (or 'white stem rot',[7] ) causes large yield losses in temperate climates, especially during cool and moist growing seasons. An analysis of soybean yields from 1996 to 2009 in the United States found that sclerotinia stem rot reduced yields by over ten million bushels in half of the studied growing seasons.[8][9] During particularly bad years, these soybean yield reductions caused producers to lose millions of dollars.[10] Compared to 23 common soybean diseases, sclerotinia stem rot was the second most problematic disease in the United States from 1996 to 2009.[8][9] For soybeans, crop yields are inversely correlated with the incidence of Sclerotinia stem rot; an estimated of 0.25 metric ton per ha is lost for each 10% increment of diseased plants.[11]

Environment

[edit]

The pathogenic fungus Sclerotinia sclerotiorum proliferates in moist and cool environments. Under moist field conditions, S. sclerotiorum is capable of completely invading a plant host, colonizing nearly all of the plant's tissues with mycelium. Optimal temperatures for growth range from 15 to 21 degrees Celsius. Under wet conditions, S. sclerotiorum will produce an abundance of mycelium and sclerotia. Like most fungi, S. sclerotiorum prefers darker, shadier conditions as opposed to direct exposure to sunlight. For soybeans specifically, optimal conditions include canopy temperatures less than 28 °C and plant surface wetness for 12–16 h on a daily basis or continuous surface wetness for 42–72 h.[11]

Life cycle

[edit]
This image captures a cluster of apothecia from a downward angle, so that only the tops are visible. The apothecia in this photo are circular, tan, and have a white lining near the edge of the structure. For size reference, a dime is also included.

The lifecycle of Sclerotinia sclerotiorum can be described as monocyclic, as there are no secondary innoculums produced. During late summer to early fall, the fungus will produce a survival structure called a sclerotium either on or inside the tissues of a host plant. S. sclerotiorum sclerotia can remain viable for at least three years[12] and germinate to produce fruiting bodies called apothecia, which are small, thin stalks ending with a cup-like structure about 3–6 mm in diameter.[13] The cup of the apothecium is lined with asci, in which the ascospores are contained. When the ascospores are released from the asci, they are carried by the wind until they land on a suitable host. The ascospores of S. sclerotiorum infect aboveground plant host tissue [14] and begin to invade the host's tissues via mycelium, causing infection. S. sclerotiorum is capable of invading nearly all tissue types including stems, foliage, flowers, fruits, and roots. Eventually white, fluffy mycelium will begin to grow on the surface of the infected tissues. At the end of the growing season, S. sclerotiorum will once again produce sclerotia. The sclerotia will then remain on the surface of the ground or in the soil, on either living or dead plant parts until the next season. The lifecycle will then continue respectively.

There are two theories contending to explain the majority of S. sclerotiorum virulence: The oxalate-dependent theory and the pH-dependent theory. The oxalate theory was very credible because ultraviolet mutants producing knockout of oxalic acid production do have drastically reduced virulence. Similar results have also obtained with Botrytis cinerea, similarly an oxalic acid producing pathogen, with similar knockouts. However Davidson et al 2016 and others have created transgenic hosts for oxalate oxidase and oxalate decarboxylase and charted the results day by day. They find that initial infection is not noticeably dependent on oxalate (although lesion expansion does require it for pH reduction and chelation of calcium). This supports the pH theory, with oxalates being merely a part of pH.[15]

Control

[edit]
Sclerotinia sclerotiorum on bushbean

Control of white mold on crops can depend greatly on cultural, biological, and chemical practices. Cultural practices include planting disease resistant crops,[16] planting at lower densities and higher row spacing to promote air circulation. This would allow for creation of microclimates that are less favorable for disease development.[17][12] Besides that, excessive irrigation should be avoided until flowering (which is the most active period of infection) has ceased.[11] Furthermore, in susceptible areas, crop rotations should include at least two to three years of non-host crops (for example cereals and corn).[12] Good weed control can also limit the amount of host plants in a field and reduce white mold pressure. Fields with heavy disease pressure may also be flooded for a period of four to five weeks so as the sclerotia may lose their viability.[17] Tillage reduction can also reduce the number of viable S. sclerotiorum spores.[18]

Coniothyrium minitans, a coelomycete distributed worldwide, is a pathogen of S. sclerotiorum[19][20] and is a commercial biocontrol agent for sclerotinia stem rot. Application of C. minitans should occur three months before S. sclerotiorum development and be incorporated into the soil.[21] Correct use of C. minitans can reduce S. sclerotiorum by 95% and sclerotinia stem rot 10 to 70%.[22][23]

Systemic and contact fungicides are registered for white models. For instance, in soybeans, there are three classes of fungicides that are labeled for white mold control: methyl benzimidazole carbamates, succinate dehydrogenase inhibitors, and demethylation inhibitors.[12] Additionally, herbicides containing lactofen have also been reported to indirectly control white mold.[24][25][26] However, the use of lactofen herbicides can harm crops in years without high disease potential.[26]

References

[edit]
  1. ^ Saharan, G. S.; Mehta, Naresh (2008). Sclerotinia Diseases of Crop Plants: Biology, Ecology and Disease Management. Dordrecht London: Springer. ISBN 978-1-4020-8407-2. OCLC 288440265. ISBN 978-1-4020-8408-9. ISBN 1402084072. ISBN 2008924858.
  2. ^ "Page 1 : USDA ARS". www.ars.usda.gov. Retrieved 2020-04-29.
  3. ^ Pressete, Carolina Girotto; Giannini, Laila Santos Vieira; de Paula, Daniela Aparecida Chagas; do Carmo, Mariana Araújo Vieira; Assis, Diego Magno; Santos, Mário Ferreira Conceição; Machado, José da Cruz; Marques, Marcos José; Soares, Marisi Gomes; Azevedo, Luciana (December 2019). "Sclerotinia Sclerotiorum (White Mold): Cytotoxic, Mutagenic, and Antimalarial Effects In Vivo and In Vitro". Journal of Food Science. 84 (12): 3866–3875. doi:10.1111/1750-3841.14910. ISSN 0022-1147. PMID 31750949.
  4. ^ Bennett, J. Michael; Rhetoric, Emeritus; Hicks, Dale R.; Naeve, Seth L.; Bennett, Nancy Bush (2014). The Minnesota Soybean Field Book (PDF). St Paul, MN: University of Minnesota Extension. p. 81. Archived from the original (PDF) on 30 September 2013. Retrieved 21 February 2016.
  5. ^ [reference 4]
  6. ^ Harveson, R. M.; Markell, S. G.; Block, C. C.; Gulya, T. J., eds. (January 2016). Compendium of Sunflower Diseases and Pests. The American Phytopathological Society. doi:10.1094/9780890545096. ISBN 978-0-89054-509-6.
  7. ^ McLoughlin, Austein G.; Wytinck, Nick; Walker, Philip L.; Girard, Ian J.; Rashid, Khalid Y.; Kievit, Teresa de; Fernando, W. G. Dilantha; Whyard, Steve; Belmonte, Mark F. (9 May 2018). "Identification and application of exogenous dsRNA confers plant protection against Sclerotinia sclerotiorum and Botrytis cinerea". Sci Rep. 8 (1): 7320. Bibcode:2018NatSR...8.7320M. doi:10.1038/s41598-018-25434-4. PMC 5943259. PMID 29743510.
  8. ^ a b Wrather, Allen; Koenning, Steve (January 2009). "Effects of Diseases on Soybean Yields in the United States 1996 to 2007". Plant Health Progress. 10 (1): 24. doi:10.1094/PHP-2009-0401-01-RS. ISSN 1535-1025.
  9. ^ a b Koenning, Stephen R.; Wrather, J. Allen (January 2010). "Suppression of Soybean Yield Potential in the Continental United States by Plant Diseases from 2006 to 2009". Plant Health Progress. 11 (1): 5. doi:10.1094/PHP-2010-1122-01-RS. ISSN 1535-1025.
  10. ^ "USDA - National Agricultural Statistics Service Homepage". www.nass.usda.gov. Retrieved 2020-04-29.
  11. ^ a b c Hartman, G.L.; Rupe, J.C.; Sikora, E.J.; Domier, L.L.; Davis, J.A.; Steffey, K.L. (2015). Compendium of Soybean Diseases and Pests, Fifth Edition. St. Paul, Minnesota U.S.: The American Phytopathological Society. pp. 285–297. ISBN 978-0-89054-473-0.
  12. ^ a b c d Peltier, Angelique J.; Bradley, Carl A.; Chilvers, Martin I.; Malvick, Dean K.; Mueller, Daren S.; Wise, Kiersten A.; Esker, Paul D. (2012-06-01). "Biology, Yield loss and Control of Sclerotinia Stem Rot of Soybean". Journal of Integrated Pest Management. 3 (2): 1–7. doi:10.1603/IPM11033.
  13. ^ Abawi, G. S. (1979). "Epidemiology of Diseases Caused by Sclerotinia Species". Phytopathology. 69 (8): 899. doi:10.1094/Phyto-69-899.
  14. ^ "White mold (Sclerotinia)". White mold (Sclerotinia). Retrieved 2023-06-20.
  15. ^ Xu, Liangsheng; Li, Guoqing; Jiang, Daohong; Chen, Weidong (2018-08-25). "Sclerotinia sclerotiorum: An Evaluation of Virulence Theories". Annual Review of Phytopathology. 56 (1). Annual Reviews: 311–338. doi:10.1146/annurev-phyto-080417-050052. ISSN 0066-4286. PMID 29958073. S2CID 49615444.
  16. ^ Conrad, Audrey Marie (2022-04-21). Management of Sclerotinia sclerotiorum in soybean using the biofungicides Bacillus amyloliquefaciens and Coniothyrium minitans (thesis thesis). Purdue University Graduate School. doi:10.25394/pgs.19630221.v1.
  17. ^ a b Pohronezny, Ken, 1946- (2003). Compendium of tomato diseases. American phytopathological Society. ISBN 0-89054-300-3. OCLC 451534013.{{cite book}}: CS1 maint: multiple names: authors list (link) CS1 maint: numeric names: authors list (link)
  18. ^ Pethybridge, Sarah J.; Brown, Bryan J.; Kikkert, Julie R.; Ryan, Matthew R. (2019-05-31). "Rolled–crimped cereal rye residue suppresses white mold in no-till soybean and dry bean". Renewable Agriculture and Food Systems. 35 (6): 599–607. doi:10.1017/S174217051900022X. ISSN 1742-1705. S2CID 191660928.
  19. ^ Campbell, W. A. (March 1947). "A New Species of Coniothyrium Parasitic on Sclerotia". Mycologia. 39 (2): 190–195. doi:10.2307/3755006. ISSN 0027-5514. JSTOR 3755006.
  20. ^ Arakere, Udayashankar C.; Konappa, Narasimhamurthy (2022). "12.9 Coniothyrium minitans as biopesticide". Biopesticides.
  21. ^ "CDMS Home". www.cdms.net. Retrieved 2020-04-29.
  22. ^ Boland, G.J. (May 1997). "Stability Analysis for Evaluating the Influence of Environment on Chemical and Biological Control of White Mold (Sclerotinia sclerotiorum) of Bean". Biological Control. 9 (1): 7–14. Bibcode:1997BiolC...9....7B. doi:10.1006/bcon.1997.0515. ISSN 1049-9644.
  23. ^ Zeng, Wenting; Kirk, William; Hao, Jianjun (February 2012). "Field management of Sclerotinia stem rot of soybean using biological control agents". Biological Control. 60 (2): 141–147. Bibcode:2012BiolC..60..141Z. doi:10.1016/j.biocontrol.2011.09.012. ISSN 1049-9644.
  24. ^ Nelson, Kelly A.; Renner, Karen A.; Hammerschmidt, Ray (November 2002). "Cultivar and Herbicide Selection Affects Soybean Development and the Incidence of Sclerotinia Stem Rot". Agronomy Journal. 94 (6): 1270–1281. Bibcode:2002AgrJ...94.1270N. doi:10.2134/agronj2002.1270. ISSN 0002-1962.
  25. ^ Nelson, Kelly A.; Renner, Karen A.; Hammerschmidt, Ray (April 2002). "Effects of Protoporphyrinogen Oxidase Inhibitors on Soybean (Glycine max L.) Response, Sclerotinia sclerotiorum Disease Development, and Phytoalexin Production by Soybean". Weed Technology. 16 (2): 353–359. doi:10.1614/0890-037x(2002)016[0353:eopoio]2.0.co;2. ISSN 0890-037X. S2CID 83664788.
  26. ^ a b Dann, E. K.; Diers, B. W.; Hammerschmidt, R. (July 1999). "Suppression of Sclerotinia Stem Rot of Soybean by Lactofen Herbicide Treatment". Phytopathology. 89 (7): 598–602. doi:10.1094/phyto.1999.89.7.598. ISSN 0031-949X. PMID 18944696.
[edit]
Retrieved from "https://en.wikipedia.org/w/index.php?title=Sclerotinia_sclerotiorum&oldid=1265195952"