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Sclerotinia sclerotiorum causes white mold disease, resulting in losses of up to 50% in several host plants worldwide. It is a harmful fungus as it infects plants at any stage of development, in the field, or in storage; this includes young seedlings, mature plants, and fruits. The accessibility of molecular and biological methods has contributed significantly to our understanding of S. sclerotiorum etiology and progression. The present research aimed to characterize S. sclerotiorum causing white mold disease in eggplant (S. melobgena), evaluate the potentiality of some bio-agents for inhibiting the fungus growth and develop a strategy for dealing with the disease challenge. Eggplants grown in open fields and greenhouses showed cottony growth on their stems, followed by the emergence of sclerotia. A fungal growth with fluffy mycelium and considerable sclerotia was isolated from the infected tissues. Polyphasic characterization and phytopathological analysis identified the fungus as S. sclerotiorum. The symptoms previously seen in the field were reproduced by inoculating healthy eggplant roots, stems, and leaves with the fungus. The ITS rDNA sequencing (564 bp) homology and phylogenetic analysis showed 99% sequence similarity of the isolate with multiple S. sclerotiorum. A wide range of strategies are required for disease management. S. sclerotiorum is sensitive to competition from other bacteria. Such a technique might act as an initial basis for effective biological control of white mold. The results demonstrated that eight isolates have very strong antagonistic activity against S. sclerotiorum. Reduced rates ranged from 63.1% (65 D) to 39.0.1% (75 A1). At the same time, the effect of the Trichoderma harzianum fungus against the pathogen S. sclerotium was apparent in restricting mycelium growth and inhibiting the fungus growth. ITS sequencing identified the mycopathogen. The interaction of seven Bacillus spp isolates with S. sclerotiorum on PDA culture media highlighted these isolates' capacity to limit the pathogen's mycelial growth. Furthermore, the antimicrobial agent must remain in the same environment for an extended period while also being active against the pathogen.
Alsalamah et al. (Sat,) studied this question.
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