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Genomic characterisation of mushroom pathogenic pseudomonads and their interaction with bacteriophages

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Storey, N., Rabiey, M., Neuman, B. W., Jackson, R. W. and Mulley, G. orcid id iconORCID: https://orcid.org/0000-0003-0650-478X (2020) Genomic characterisation of mushroom pathogenic pseudomonads and their interaction with bacteriophages. Viruses, 12 (11). ISSN 1999-4915 doi: 10.3390/v12111286

Abstract/Summary

Bacterial diseases of the edible white button mushroom Agaricus bisporus caused by Pseudomonas species cause a reduction in crop yield, resulting in considerable economic loss. We examined bacterial pathogens of mushrooms and bacteriophages that target them to understand the disease and opportunities for control. The Pseudomonas tolaasii genome encoded a single type III protein secretion system (T3SS), but contained the largest number of non-ribosomal peptide synthase (NRPS) genes, multimodular enzymes that can play a role in pathogenicity, including a putative tolaasin-producing gene cluster, a toxin causing blotch disease symptom. However, Pseudomonas agarici encoded the lowest number of NRPS and three putative T3SS while non-pathogenic Pseudomonas sp. NS1 had intermediate numbers. Potential bacteriophage resistance mechanisms were identified in all three strains, but only P. agarici NCPPB 2472 was observed to have a single Type I-F CRISPR/Cas system predicted to be involved in phage resistance. Three novel bacteriophages, NV1, ϕNV3, and NV6, were isolated from environmental samples. Bacteriophage NV1 and ϕNV3 had a narrow host range for specific mushroom pathogens, whereas phage NV6 was able to infect both mushroom pathogens. ϕNV3 and NV6 genomes were almost identical and differentiated within their T7-like tail fiber protein, indicating this is likely the major host specificity determinant. Our findings provide the foundations for future comparative analyses to study mushroom disease and phage resistance.

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Item Type Article
URI https://reading-clone.eprints-hosting.org/id/eprint/111717
Item Type Article
Refereed Yes
Divisions Life Sciences > School of Biological Sciences > Biomedical Sciences
Publisher MDPI
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