Publication: Cu transporter protein CrpF protects against Cu-induced toxicity in Fusarium oxysporum
Authors
Lorenzo Gutierrez, D. ; Gómez Gil, L. ; Guarro, J. ; Roncero, M. I. G. ; Capilla, J. ; López Fernández, L.
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Publisher
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DOI
https://doi.org/10.1080/21505594.2020.1809324
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info:eu-repo/semantics/article
Description
© <2021>. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/
This document is the Accepted Manuscript version of a Published Work that appeared in final form in VIRULENCE. To access the final edited and published work see DOI 10.1080/21505594.2020.1809324
Abstract
Cu is an essential trace element for cell growth and proliferation. However, excess of Cu
accumulation leads to cellular toxicity. Thus, precise and tight regulation of Cu homeostasis
processes, including transport, delivery, storage, detoxification, and efflux machineries, is required.
Moreover, the maintenance of Cu homeostasis is critical for the survival and virulence of fungal
pathogens. Cu homeostasis has been extensively studied in mammals, bacteria, and yeast, but it
has not yet been well documented in filamentous fungi. In the present work, we investigated Cu
tolerance in the filamentous fungus Fusarium oxysporum by analysing the Cu transporter coding
gene crpF, previously studied in Aspergillus fumigatus. The expression studies demonstrated that
crpF is upregulated in the presence of Cu and its deletion leads to severe sensitivity to low levels
of CuSO4 in F. oxysporum. Targeted deletion of crpF did not significantly alter the resistance of the
fungus to macrophage killing, nor its pathogenic behaviour on the tomato plants. However, the
targeted deletion mutant ΔcrpF showed increased virulence in a murine model of systemic
infection compared to wild-type strain (wt).
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Citation
Virulence, 2020, Vol. 11, Nº. 1, pp.:1108–1121
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Este ítem está sujeto a una licencia Creative Commons. http://creativecommons.org/licenses/by/4.0/