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Proper Sterol Distribution Is Required for Candida albicans Hyphal Formation and Virulence

P. McCourt, H.-Y. Liu, J. E. Parker, C. Gallo-Ebert, M. Donigan, A. Bata, C. Giordano, Steven Kelly Orcid Logo, J. T. Nickels, Josie Parker

G3 Genes|Genomes|Genetics, Volume: 6, Issue: 11

Swansea University Authors: Steven Kelly Orcid Logo, Josie Parker

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DOI (Published version): 10.1534/g3.116.033969

Abstract

Candida albicans is an opportunistic fungus responsible for the majority of systemic fungal infections. Multiple factors contribute to C. albicans pathogenicity. C. albicans strains lacking CaArv1 are avirulent. Arv1 has a conserved Arv1 homology domain (AHD) that has a zinc-binding domain containin...

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Published in: G3 Genes|Genomes|Genetics
ISSN: 2160-1836
Published: 2016
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URI: https://cronfa.swan.ac.uk/Record/cronfa31346
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spelling 2021-10-26T16:37:40.6065454 v2 31346 2016-12-01 Proper Sterol Distribution Is Required for Candida albicans Hyphal Formation and Virulence b17cebaf09b4d737b9378a3581e3de93 0000-0001-7991-5040 Steven Kelly Steven Kelly true false e563ed4e1c7db8d1e131fb78a5f8d0d5 Josie Parker Josie Parker true false 2016-12-01 BMS Candida albicans is an opportunistic fungus responsible for the majority of systemic fungal infections. Multiple factors contribute to C. albicans pathogenicity. C. albicans strains lacking CaArv1 are avirulent. Arv1 has a conserved Arv1 homology domain (AHD) that has a zinc-binding domain containing two cysteine clusters. Here, we explored the role of the CaAHD and zinc-binding motif in CaArv1-dependent virulence. Overall, we found that the CaAHD was necessary but not sufficient for cells to be virulent, whereas the zinc-binding domain was essential, as Caarv1/Caarv1 cells expressing the full-length zinc-binding domain mutants, Caarv1C3S and Caarv1C28S, were avirulent. Phenotypically, we found a direct correlation between the avirulence of Caarv1/Caarv1, Caarrv1AHD, Caarv1C3S, and Caarv1C28S cells and defects in bud site selection, septa formation and localization, and hyphal formation and elongation. Importantly, all avirulent mutant strains lacked the ability to maintain proper sterol distribution. Overall, our results have established the importance of the AHD and zinc-binding domain in fungal invasion, and have correlated an avirulent phenotype with the inability to maintain proper sterol distribution. Journal Article G3 Genes|Genomes|Genetics 6 11 2160-1836 virulence, Candida, sterol, hyphae, lipid 31 12 2016 2016-12-31 10.1534/g3.116.033969 COLLEGE NANME Biomedical Sciences COLLEGE CODE BMS Swansea University 2021-10-26T16:37:40.6065454 2016-12-01T13:43:58.3577507 Faculty of Medicine, Health and Life Sciences Swansea University Medical School - Medicine P. McCourt 1 H.-Y. Liu 2 J. E. Parker 3 C. Gallo-Ebert 4 M. Donigan 5 A. Bata 6 C. Giordano 7 Steven Kelly 0000-0001-7991-5040 8 J. T. Nickels 9 Josie Parker 10 0031346-10012017160636.pdf kelly3455.full.pdf 2017-01-10T16:06:36.3230000 Output 1412423 application/pdf Version of Record true 2017-01-10T00:00:00.0000000 This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International License true
title Proper Sterol Distribution Is Required for Candida albicans Hyphal Formation and Virulence
spellingShingle Proper Sterol Distribution Is Required for Candida albicans Hyphal Formation and Virulence
Steven Kelly
Josie Parker
title_short Proper Sterol Distribution Is Required for Candida albicans Hyphal Formation and Virulence
title_full Proper Sterol Distribution Is Required for Candida albicans Hyphal Formation and Virulence
title_fullStr Proper Sterol Distribution Is Required for Candida albicans Hyphal Formation and Virulence
title_full_unstemmed Proper Sterol Distribution Is Required for Candida albicans Hyphal Formation and Virulence
title_sort Proper Sterol Distribution Is Required for Candida albicans Hyphal Formation and Virulence
author_id_str_mv b17cebaf09b4d737b9378a3581e3de93
e563ed4e1c7db8d1e131fb78a5f8d0d5
author_id_fullname_str_mv b17cebaf09b4d737b9378a3581e3de93_***_Steven Kelly
e563ed4e1c7db8d1e131fb78a5f8d0d5_***_Josie Parker
author Steven Kelly
Josie Parker
author2 P. McCourt
H.-Y. Liu
J. E. Parker
C. Gallo-Ebert
M. Donigan
A. Bata
C. Giordano
Steven Kelly
J. T. Nickels
Josie Parker
format Journal article
container_title G3 Genes|Genomes|Genetics
container_volume 6
container_issue 11
publishDate 2016
institution Swansea University
issn 2160-1836
doi_str_mv 10.1534/g3.116.033969
college_str Faculty of Medicine, Health and Life Sciences
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hierarchy_top_id facultyofmedicinehealthandlifesciences
hierarchy_top_title Faculty of Medicine, Health and Life Sciences
hierarchy_parent_id facultyofmedicinehealthandlifesciences
hierarchy_parent_title Faculty of Medicine, Health and Life Sciences
department_str Swansea University Medical School - Medicine{{{_:::_}}}Faculty of Medicine, Health and Life Sciences{{{_:::_}}}Swansea University Medical School - Medicine
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description Candida albicans is an opportunistic fungus responsible for the majority of systemic fungal infections. Multiple factors contribute to C. albicans pathogenicity. C. albicans strains lacking CaArv1 are avirulent. Arv1 has a conserved Arv1 homology domain (AHD) that has a zinc-binding domain containing two cysteine clusters. Here, we explored the role of the CaAHD and zinc-binding motif in CaArv1-dependent virulence. Overall, we found that the CaAHD was necessary but not sufficient for cells to be virulent, whereas the zinc-binding domain was essential, as Caarv1/Caarv1 cells expressing the full-length zinc-binding domain mutants, Caarv1C3S and Caarv1C28S, were avirulent. Phenotypically, we found a direct correlation between the avirulence of Caarv1/Caarv1, Caarrv1AHD, Caarv1C3S, and Caarv1C28S cells and defects in bud site selection, septa formation and localization, and hyphal formation and elongation. Importantly, all avirulent mutant strains lacked the ability to maintain proper sterol distribution. Overall, our results have established the importance of the AHD and zinc-binding domain in fungal invasion, and have correlated an avirulent phenotype with the inability to maintain proper sterol distribution.
published_date 2016-12-31T03:38:18Z
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score 11.012678

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