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FocSge1 in Fusarium oxysporum f. sp. cubense race 1 is essential for full virulence
BACKGROUND: Fusarium wilt disease of banana is one of the most devastating diseases and was responsible for destroying banana plantations in the late nineteenth century. Fusarium oxysporum f. sp. cubense is the causative agent. Presently, both race 1 and 4 strains of Foc are creating havoc in the ma...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7427899/ https://www.ncbi.nlm.nih.gov/pubmed/32795268 http://dx.doi.org/10.1186/s12866-020-01936-y |
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author | Gurdaswani, Vartika Ghag, Siddhesh B. Ganapathi, Thumballi R. |
author_facet | Gurdaswani, Vartika Ghag, Siddhesh B. Ganapathi, Thumballi R. |
author_sort | Gurdaswani, Vartika |
collection | PubMed |
description | BACKGROUND: Fusarium wilt disease of banana is one of the most devastating diseases and was responsible for destroying banana plantations in the late nineteenth century. Fusarium oxysporum f. sp. cubense is the causative agent. Presently, both race 1 and 4 strains of Foc are creating havoc in the major banana-growing regions of the world. There is an urgent need to devise strategies to control this disease; that is possible only after a thorough understanding of the molecular basis of this disease. RESULTS: There are a few regulators of Foc pathogenicity which are triggered during this infection, among which Sge1 (Six Gene Expression 1) regulates the expression of effector genes. The protein sequence is conserved in both race 1 and 4 strains of Foc indicating that this gene is vital for pathogenesis. The deletion mutant, FocSge1 displayed poor conidial count, loss of hydrophobicity, reduced pigmentation, decrease in fusaric acid production and pathogenicity as compared to the wild-type and genetically complemented strain. Furthermore, the C-terminal domain of FocSge1 protein is crucial for its activity as deletion of this region results in a knockout-like phenotype. CONCLUSION: These results indicated that FocSge1 plays a critical role in normal growth and pathogenicity with the C-terminal domain being crucial for its activity. |
format | Online Article Text |
id | pubmed-7427899 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-74278992020-08-17 FocSge1 in Fusarium oxysporum f. sp. cubense race 1 is essential for full virulence Gurdaswani, Vartika Ghag, Siddhesh B. Ganapathi, Thumballi R. BMC Microbiol Research Article BACKGROUND: Fusarium wilt disease of banana is one of the most devastating diseases and was responsible for destroying banana plantations in the late nineteenth century. Fusarium oxysporum f. sp. cubense is the causative agent. Presently, both race 1 and 4 strains of Foc are creating havoc in the major banana-growing regions of the world. There is an urgent need to devise strategies to control this disease; that is possible only after a thorough understanding of the molecular basis of this disease. RESULTS: There are a few regulators of Foc pathogenicity which are triggered during this infection, among which Sge1 (Six Gene Expression 1) regulates the expression of effector genes. The protein sequence is conserved in both race 1 and 4 strains of Foc indicating that this gene is vital for pathogenesis. The deletion mutant, FocSge1 displayed poor conidial count, loss of hydrophobicity, reduced pigmentation, decrease in fusaric acid production and pathogenicity as compared to the wild-type and genetically complemented strain. Furthermore, the C-terminal domain of FocSge1 protein is crucial for its activity as deletion of this region results in a knockout-like phenotype. CONCLUSION: These results indicated that FocSge1 plays a critical role in normal growth and pathogenicity with the C-terminal domain being crucial for its activity. BioMed Central 2020-08-14 /pmc/articles/PMC7427899/ /pubmed/32795268 http://dx.doi.org/10.1186/s12866-020-01936-y Text en © The Author(s) 2020 Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Research Article Gurdaswani, Vartika Ghag, Siddhesh B. Ganapathi, Thumballi R. FocSge1 in Fusarium oxysporum f. sp. cubense race 1 is essential for full virulence |
title | FocSge1 in Fusarium oxysporum f. sp. cubense race 1 is essential for full virulence |
title_full | FocSge1 in Fusarium oxysporum f. sp. cubense race 1 is essential for full virulence |
title_fullStr | FocSge1 in Fusarium oxysporum f. sp. cubense race 1 is essential for full virulence |
title_full_unstemmed | FocSge1 in Fusarium oxysporum f. sp. cubense race 1 is essential for full virulence |
title_short | FocSge1 in Fusarium oxysporum f. sp. cubense race 1 is essential for full virulence |
title_sort | focsge1 in fusarium oxysporum f. sp. cubense race 1 is essential for full virulence |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7427899/ https://www.ncbi.nlm.nih.gov/pubmed/32795268 http://dx.doi.org/10.1186/s12866-020-01936-y |
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