Functional Analysis of atfA Gene to Stress Response in Pathogenic Thermal Dimorphic Fungus Penicillium marneffei

Penicillium marneffei, the pathogenic thermal dimorphic fungus is a causative agent of a fatal systemic disease, penicilliosis marneffei, in immunocompromised patients especially HIV patients. For growth and survival, this fungus has to adapt to environmental stresses outside and inside host cells...

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Main Authors: Nimmanee, Panjaphorn, Woo, Patrick C. Y., Vanittanakom, Pramote, Youngchim, Sirida, Vanittanakom, Nongnuch
Format: Online
Language:English
Published: Public Library of Science 2014
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4218842/
id pubmed-4218842
recordtype oai_dc
spelling pubmed-42188422014-11-05 Functional Analysis of atfA Gene to Stress Response in Pathogenic Thermal Dimorphic Fungus Penicillium marneffei Nimmanee, Panjaphorn Woo, Patrick C. Y. Vanittanakom, Pramote Youngchim, Sirida Vanittanakom, Nongnuch Research Article Penicillium marneffei, the pathogenic thermal dimorphic fungus is a causative agent of a fatal systemic disease, penicilliosis marneffei, in immunocompromised patients especially HIV patients. For growth and survival, this fungus has to adapt to environmental stresses outside and inside host cells and this adaptation requires stress signaling pathways and regulation of gene expression under various kinds of stresses. In this report, P. marneffei activating transcription factor (atfA) gene encoding bZip-type transcription factor was characterized. To determine functions of this gene, atfA isogenic mutant strain was constructed using the modified split marker recombination method. The phenotypes and susceptibility to varieties of stresses including osmotic, oxidative, heat, UV, cell wall and cell membrane stresses of the mutant strain were compared with the wild type and the atfA complemented strains. Results demonstrated that the mRNA expression level of P. marneffei atfA gene increased under heat stress at 42°C. The atfA mutant was more sensitive to sodium dodecyl sulphate, amphotericin B and tert-butyl hydroperoxide than the wild type and complemented strains but not hydrogen peroxide, menadione, NaCl, sorbitol, calcofluor white, itraconazole, UV stresses and heat stress at 39°C. In addition, recovery of atfA mutant conidia after mouse and human macrophage infections was significantly decreased compared to those of wild type and complemented strains. These results indicated that the atfA gene was required by P. marneffei under specific stress conditions and might be necessary for fighting against host immune cells during the initiation of infection. Public Library of Science 2014-11-03 /pmc/articles/PMC4218842/ /pubmed/25365258 http://dx.doi.org/10.1371/journal.pone.0111200 Text en © 2014 Nimmanee et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Nimmanee, Panjaphorn
Woo, Patrick C. Y.
Vanittanakom, Pramote
Youngchim, Sirida
Vanittanakom, Nongnuch
spellingShingle Nimmanee, Panjaphorn
Woo, Patrick C. Y.
Vanittanakom, Pramote
Youngchim, Sirida
Vanittanakom, Nongnuch
Functional Analysis of atfA Gene to Stress Response in Pathogenic Thermal Dimorphic Fungus Penicillium marneffei
author_facet Nimmanee, Panjaphorn
Woo, Patrick C. Y.
Vanittanakom, Pramote
Youngchim, Sirida
Vanittanakom, Nongnuch
author_sort Nimmanee, Panjaphorn
title Functional Analysis of atfA Gene to Stress Response in Pathogenic Thermal Dimorphic Fungus Penicillium marneffei
title_short Functional Analysis of atfA Gene to Stress Response in Pathogenic Thermal Dimorphic Fungus Penicillium marneffei
title_full Functional Analysis of atfA Gene to Stress Response in Pathogenic Thermal Dimorphic Fungus Penicillium marneffei
title_fullStr Functional Analysis of atfA Gene to Stress Response in Pathogenic Thermal Dimorphic Fungus Penicillium marneffei
title_full_unstemmed Functional Analysis of atfA Gene to Stress Response in Pathogenic Thermal Dimorphic Fungus Penicillium marneffei
title_sort functional analysis of atfa gene to stress response in pathogenic thermal dimorphic fungus penicillium marneffei
description Penicillium marneffei, the pathogenic thermal dimorphic fungus is a causative agent of a fatal systemic disease, penicilliosis marneffei, in immunocompromised patients especially HIV patients. For growth and survival, this fungus has to adapt to environmental stresses outside and inside host cells and this adaptation requires stress signaling pathways and regulation of gene expression under various kinds of stresses. In this report, P. marneffei activating transcription factor (atfA) gene encoding bZip-type transcription factor was characterized. To determine functions of this gene, atfA isogenic mutant strain was constructed using the modified split marker recombination method. The phenotypes and susceptibility to varieties of stresses including osmotic, oxidative, heat, UV, cell wall and cell membrane stresses of the mutant strain were compared with the wild type and the atfA complemented strains. Results demonstrated that the mRNA expression level of P. marneffei atfA gene increased under heat stress at 42°C. The atfA mutant was more sensitive to sodium dodecyl sulphate, amphotericin B and tert-butyl hydroperoxide than the wild type and complemented strains but not hydrogen peroxide, menadione, NaCl, sorbitol, calcofluor white, itraconazole, UV stresses and heat stress at 39°C. In addition, recovery of atfA mutant conidia after mouse and human macrophage infections was significantly decreased compared to those of wild type and complemented strains. These results indicated that the atfA gene was required by P. marneffei under specific stress conditions and might be necessary for fighting against host immune cells during the initiation of infection.
publisher Public Library of Science
publishDate 2014
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4218842/
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