Abstract

Botrytis cinerea is a ubiquitous filamentous fungal pathogen of a wide range of plant species. This fungus is able to infect all aerial parts of its host plants; where infection may cause enormous damage both during plant growth and in the post-harvest stage (during cold storage or transport). B. cinerea is a major cause of economic losses in the production chain of cut flowers, bulb flowers and pot plants. Molecular-genetic studies performed over the past decade have provided a wealth of novel insights into the infection mechanisms utilized by this pathogen. Fungal genes important for successful infection by B. cinerea were identified. Such knowledge provided perspectives for designing novel, and rational plant protection strategies that could effectively counteract important pathogen virulence factors. In this study; the infection process will be divided into different stages; moreover, the role of various fungal enzymes and metabolites in the different stages will be discussed. The aim of the current study was to address perspectives for novel control strategies that may reduce and/or delay the damage incited by B. cinerea infection.

Highlights

  • Botrytis cinerea Persoon: Fries is a member of the phylum Ascomycetes, family Sclerotiniaceae

  • One of the important considerations in this strategy was that Polygalacturonase inhibiting proteins (PGIPs) had differential activities towards individual fungal endo-PGs (De Lorenzo et al, 2001). This made it relevant to choose PGIP that were potent against B. cinerea endo-PG isozymes, which in turn were vital for virulence (Ten Have et al, 2002)

  • Microscopic and biochemical observations of the infection strategy of B. cinerea are presently validated by the availability of molecular-genetic tools

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Summary

Introduction

Botrytis cinerea Persoon: Fries (teleomorph Botryotinia fuckeliana, commonly known as grey mold fungus) is a member of the phylum Ascomycetes, family Sclerotiniaceae It causes devastating diseases on about 500 plant species worldwide, such as fresh fruits and vegetables, resulting in great economic losses ranging from $10$100 billion (Hua et al, 2018). Conidia were dispersed by humid air currents, splashing water, tools and clothing to healthy plants where they initiate new infections (Holz et al, 2004). These conidia can infect seedlings, flowers, stems, or leaves (Agrios, 2005). This was attributed to the fact that B. cinerea did not produce toxic compounds or produced such compounds at a low level which might allowed it to continue to grow without being detected by the plant defensive mechanisms

Attachment of conidia
Differentiation of infection structures on the host surface
Oxalic Acid
Induction of Reactive oxygen species
Quiescence
Evasion of chemical defence
Maceration of tissue and disease expansion
Conclusion
Findings
11. References
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