Rapeseed infection occurs primarily during the flowering period via falling petals that adhere to the vegetative parts of the plant and serve as a substrate for ascospore germination. Water-soaked lesions form at the points of contact, which become covered with a white, cottony fungal growth under high humidity conditions. As these lesions expand, they girdle the stems, causing nutrient disruption, premature senescence, brittleness, and lodging of the crop. Black sclerotia of the pathogen develop inside the infected tissues.
Breeding for resistance to Sclerotinia stem rot is hindered by the lack of fully resistant cultivars and clearly defined fungal pathotypes. Rapeseed resistance is quantitative and controlled by a complex polygenic system. In scientific practice, candidate genes such as BnHIR2.7 or MPK3 modules are identified; however, there are no generally accepted markers for commercial cultivars, and the breeding process is aimed at achieving partial field resistance through the accumulation of a gene complex.
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White mold.