{"id":49775,"date":"2022-12-12T12:11:59","date_gmt":"2022-12-12T12:11:59","guid":{"rendered":"https:\/\/dev.metos.global\/?page_id=49775"},"modified":"2026-05-04T10:33:33","modified_gmt":"2026-05-04T10:33:33","slug":"disease-models-rapeseed","status":"publish","type":"page","link":"https:\/\/metos.global\/en\/disease-models-rapeseed\/","title":{"rendered":"Disease models – rapeseed"},"content":{"rendered":"\t\t
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Rapeseed \/ Canola<\/b> disease models\n<\/h2>\t\t\t\t<\/div>\n\t\t\t\t<\/div>\n\t\t\t\t
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The most important oil seed crop of the cool climate regions is affected by two very destructive diseases and three economic important pest insects. Rape seed growing has gained more and more importance in Northern Europe and in Northern America. Due to the growing market of biofuels it will gain more importance in South America and in parts of Asia too. New varieties have increased the yield potential dramatically. To keep these yields economically worthwhile plant protection strategies will gain more importance. FieldClimate.Com is supporting these strategies with disease and pest models for: Sklerotina sclerotina, Phoma lingam and Pollen Beetle (Meligethes aeneus<\/em>).<\/p>\t\t\t\t\t\t\t\t<\/div>\n\t\t\t\t<\/div>\n\t\t\t\t\t<\/div>\n\t\t<\/div>\n\t\t\t\t\t<\/div>\n\t\t<\/section>\n\t\t\t\t

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SCLEROTINIA ROT \u2013<\/br>S. sclerotiorum<\/em><\/a><\/h2>\t\t\t\t<\/div>\n\t\t\t\t<\/div>\n\t\t\t\t\t<\/div>\n\t\t<\/div>\n\t\t\t\t
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BLACK LEG DISEASE \u2013<\/br>Phoma lingam<\/em><\/a><\/h2>\t\t\t\t<\/div>\n\t\t\t\t<\/div>\n\t\t\t\t\t<\/div>\n\t\t<\/div>\n\t\t\t\t
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POLLEN BEETLE \u2013<\/br>Meligethes spp.<\/em><\/a><\/h2>\t\t\t\t<\/div>\n\t\t\t\t<\/div>\n\t\t\t\t\t<\/div>\n\t\t<\/div>\n\t\t\t\t\t<\/div>\n\t\t<\/section>\n\t\t\t\t
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\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\t\t\tRecommended equipment<\/span>\n\t\t\t\t\t<\/span>\n\t\t\t\t\t<\/a>\n\t\t\t\t<\/div>\n\t\t\t\t\t\t\t\t<\/div>\n\t\t\t\t<\/div>\n\t\t\t\t\t<\/div>\n\t\t<\/div>\n\t\t\t\t\t<\/div>\n\t\t<\/section>\n\t\t\t\t
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\n\t\t\t\n\t\t\t\t\t\t<\/span>\n\t\t<\/div>\n\t\t\t\t\t\t<\/div>\n\t\t\t\t<\/div>\n\t\t\t\t\t<\/div>\n\t\t<\/div>\n\t\t\t\t\t<\/div>\n\t\t<\/section>\n\t\t\t\t
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Sclerotinia rot<\/h2>\t\t\t\t<\/div>\n\t\t\t\t<\/div>\n\t\t\t\t
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Sclerotinia rot affects a wide range of plants particularly non-woody species. Sclerotinia rot is caused by S. sclerotiorum<\/em>. Sclerotinia rot can affect plants at any stage of production including seedlings, mature plants and harvested products. Plants with senescing or dead tissue are particularly susceptible to infection.<\/p>

Symptoms<\/h3>

The infected area of a plant initially takes on a dark green or brown water-soaked appearance, then may become paler in color. Dense white cottony mycelium usually develops and the plant begins to wilt and eventually dies. Resting or survival structures (sclerotia) are produced externally on affected plant parts and internally in stem pith cavities. The sclerotia are hard, black, irregular in shape, mostly 2-4 mm in size, and difficult to see once incorporated into the soil.<\/p>

Disease sources and spread<\/h3>

The life-cycle of\u00a0S. sclerotiorum<\/em>\u00a0includes both a\u00a0soil-borne and an air-borne phase. Sclerotia of\u00a0S. sclerotiorum<\/em>\u00a0can survive in the soil for ten years or more. They germinate to produce small funnel-shaped fruiting bodies (apothecia) that are approximately 1 cm in diameter. Apothecia produce air-borne spores, which can cause infection when they land on a susceptible host plant, either via flowers, or by direct germination on leaves. Occasionally, infection of stem bases can occur when fungal strands (mycelium) develop directly from Sclerotia near the surface. New sclerotia develop in infected plant tissue and when the plant dies they remain on the soil surface or may become incorporated during subsequent soil cultivation.<\/p>

Conditions for Infection<\/h3>

After a period of cold conditions in winter, sclerotia, overwintering in the top 5 cm of the soil, germinate from spring onwards to produce apothecia, when\u00a0soil temperatures are 10\u00b0C or higher and the soil is moist. Sclerotia do not germinate in dry soil or when the soil temperature is above 25\u00b0C. Sclerotia buried below 5 cm in the soil are less likely to germinate. Once apothecia are fully formed,\u00a0spore release can occur in the light or dark but is temperature dependent, so tends to peak around midday. Apothecia can last about 20 days at 15 to 20\u00b0C, but shrivel after less than 10 days at 25\u00b0C. For\u00a0flowering herbs, spores landing on petals and stamens germinate rapidly\u00a0(germination within 3-6 hours and infection within 24 hours) in optimum conditions of 15-25\u00b0C, continuous\u00a0leaf wetness and high humidity\u00a0within the crop. Subsequent infection of leaves and stems depends on petals falling and sticking on leaves. The risk of infection is increased if the leaves are wet because this causes more petals to stick. Infected dead or senescing petals provide nutrients for the invasion of the fungus into leaves and stems. For\u00a0non-flowering herbs, infection is mainly by air-borne spores landing directly on leaves. Spores can survive on leaves for several weeks until conditions favorable for leaf infection occur. Spore germination and infection depend on the presence of nutrients on leaves, either from plant wounds or senescing plant material. As for flowering herbs, the optimum spore germination and infection conditions are 15-25\u00b0C with continuous leaf wetness and high humidity. Once plant infection has occurred, rapid disease progress is favoured by warm (15-20\u00b0C) and moist conditions in dense crops.<\/p>

Sclerotinia Infection Model<\/h3>

Carpogenic germination of sclerotia is stimulated by periods of\u00a0continuous soil moisture. Apothecia are formed on the soil surface from which ascospores are released into the air.\u00a0Infection of most crop species is principally associated with ascospores but direct infection of healthy, intact plant tissue from germinating ascospores usually does not occur. Instead, infection of leaf and stem tissue of healthy plants results only when germinating ascospores colonize dead or senescing tissues, usually flower parts such as abscised petals, prior to the formation of infection structures and penetration. Myceliogenic germination of sclerotia at the soil surface can also result in colonization of dead organic matter with subsequent infection of adjacent living plants. However, in some crops, for example\u00a0sunflower myceliogenic germination of sclerotia can directly initiate the infection process of the roots and basal stem resulting in wilt.\u00a0The stimulus for myceliogenic germination and infection in sunflower is not known but likely depends on nutritional signals in the rhizosphere derived from host plants.<\/p>

The infection process
<\/span>Infection of healthy tissue depends on the\u00a0formation of an appressorium, which may be simple or complex in structure depending on the host surface. In most cases, penetration is\u00a0directly through the cuticle\u00a0and not through stomata. Appressoria develop from terminal dichotomous branching of hyphae growing on the host surface and consist of a pad of broad, multi-septate, short hyphae that are orientated perpendicular to the host surface to which they are attached by mucilage. Complex appressoria are often referred to as infection cushions. Although earlier workers considered penetration of the cuticle to be a purely mechanical process there is strong evidence from ultra-structural studies that\u00a0enzymatic digestion of the cuticle also plays a role\u00a0in the penetration process. Little is known about\u00a0S. sclerotiorum<\/em>\u00a0cutinases, however, the genome encodes at least four cutinase-like enzymes (Hegedus unpublished). A large vesicle, formed at the appressorium tip prior to penetration, appears to be released into the host cuticle during penetration. After penetration of the cuticle, a subcuticular vesicle forms from which large hyphae fan out growing over and dissolving the subcuticular wall of the epidermis.<\/p>

Infection by enzymatic degratation of the epidemic cells:<\/span>\u00a0Oxalic acid works in concern with cell wall degrading enzymes, such as polygalacturonase (PG), to bring about the destruction of host tissue by creating an environment conducive for PG attack on pectin in the middle lamella. This in turn releases low molecular weight derivatives that induce the expression of additional PG genes. Indeed, overall PG activity is induced by pectin or pectin-derived monosaccharides, such as galacturonic acid, and is repressed by the presence of glucose. Examination of the expression patterns of individual Sspg genes has revealed that the interplay among PGs and with the host during the various stages of infection is finely co-ordinated. (Dwayne D. Hegedus *, S. Roger Rimmer: Sclerotinia sclerotiorum: When \u2018\u2018to be or not to be\u2019\u2019 a pathogen? FEMS Microbiology Letters 251 (2005) 177\u2013184)<\/p>

Looking for Climate Conditions for Infection of S. sclerotiorum<\/em> has to take consideration of the apothecia formation, the sporulation, the direct infection by apothecia (even if it does not take place very frequent) and the infection from established mycelia by encymatic degradation of the epidemic cells .<\/p>

Apothecia formation and sporulation<\/span>\u00a0takes place if a\u00a0rain of more than 8 mm\u00a0is followed by a period of\u00a0high relative humidity lasting longer than 20 hours at optimum temperature of 21\u00b0C to 26\u00b0C.<\/p>

Direct Infection by Apothecia<\/span>\u00a0can be expected after a\u00a0leaf wetness period followed by 16 hours of relative humidity\u00a0higher than 90% under optimum 21\u00b0C to 26\u00b0C (\u201cappressoria infection\u201d). Wheras saprophytic growth followed by encymatic degratation of the epidermic cells (\u201chydrolytic infection\u201d) can be expected under a slightly lower relative humditiy of 80% lasting for a period of 24 hours under optimum conditions of 21\u00b0C to 26\u00b0C.<\/p>

Literature:<\/em><\/p>