How the necrotrophic fungus Alternaria brassicicola kills plant cells remains an Enigma

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Title
How the necrotrophic fungus Alternaria brassicicola kills plant cells remains an Enigma
Author(s)
Yang Rae Cho
Bibliographic Citation
Eukaryotic Cell, vol. 14, no. 4, pp. 335-344
Publication Year
2015
Abstract
Alternaria species are mainly saprophytic fungi, but some are plant pathogens. Seven pathotypes of Alternaria alternata use secondary metabolites of host-specific toxins as pathogenicity factors. These toxins kill host cells prior to colonization. Genes associated with toxin synthesis reside on conditionally dispensable chromosomes, supporting the notion that pathogenicity might have been acquired several times by A. alternata. Alternaria brassicicola, however, seems to employ a different mechanism. Evidence on the use of host-specific toxins as pathogenicity factors remains tenuous, even after a diligent search aided by full-genome sequencing and efficient reverse-genetics approaches. Similarly, no individual genes encoding lipases or cell wall-degrading enzymes have been identified as strong virulence factors, although these enzymes have been considered important for fungal pathogenesis. This review describes our current understanding of toxins, lipases, and cell wall-degrading enzymes and their roles in the pathogenesis of A. brassicicola compared to those of other pathogenic fungi. It also describes a set of genes that affect pathogenesis in A. brassicicola. They are involved in various cellular functions that are likely important in most organisms and probably indirectly associated with pathogenesis. Deletion or disruption of these genes results in weakly virulent strains that appear to be sensitive to the defense mechanisms of host plants. Finally, this review discusses the implications of a recent discovery of three important transcription factors associated with pathogenesis and the putative downstream genes that they regulate.
ISSN
1535-9778
Publisher
American Society for Microbiology
DOI
http://dx.doi.org/10.1128/EC.00226-14
Type
Article
Appears in Collections:
1. Journal Articles > Journal Articles
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