57 research outputs found

    Timing of fungal invasion using host's ripening hormone as a signal.

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    Cutinase gene disruption in Fusarium solani f sp pisi decreases its virulence on pea.

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    Fusarium solani f sp pisi (Nectria haematococca) isolate 77-2-3 with one cutinase gene produced 10 to 20% of the cutinase produced by isolate T-8 that has multiple cutinase genes, whereas cutinase gene-disrupted mutant 77-102 of isolate 77-2-3 did not produce cutinase. On the surface of pea stem segments, lesion formation was most frequent and most severe with T-8, less frequent and less severe with 77-2-3, and much less frequent and much milder with the gene-disrupted mutant. Microscopic examination of the lesions caused by the mutant strongly suggest that it penetrated the host mostly via the stomata. In seedling assays, 77-2-3 caused severe lesions on every seedling and stunted growth, whereas the mutant showed very mild lesions on one-third of the seedlings with no stunting. Thus, cutinase gene disruption resulted in a significant decrease in the pathogenicity of F. s. pisi on pea

    Cloning of a gene expressed during appressorium formation by Colletotrichum gloeosporioides and a marked decrease in virulence by disruption of this gene.

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    Appressorium formation in germinating Colletotrichum gloeosporioides is induced by the surface wax of its host. One of the genes expressed uniquely in C. gloeosporioides during appressorium formation induced by the host signal has been designated cap20, and this gene and its cDNA were cloned and sequenced. Nucleotide sequences of both revealed an open reading frame that could encode a 183-amino acid polypeptide that did not have significant homology with any known proteins. Reverse transcriptase-polymerase chain reaction detected cap20 gene transcripts at the infection front on the surface and within tomato fruits infected by C. gloeosporioides. Gene-disrupted mutants incapable of expressing cap20 showed a drastically decreased virulence on avocado and tomato fruits. These results suggest that cap20 plays a significant role in the infection of the host

    Surface signaling in pathogenesis.

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