Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2023 Dec;14(1):2174294.
doi: 10.1080/21505594.2023.2174294.

The defective gut colonization of Candida albicans hog1 MAPK mutants is restored by overexpressing the transcriptional regulator of the white opaque transition WOR1

Elvira Román  1 , Daniel Prieto  1 , Susana Hidalgo-Vico  1 , Rebeca Alonso-Monge  1 , Jesús Pla  1
Affiliations

The defective gut colonization of Candida albicans hog1 MAPK mutants is restored by overexpressing the transcriptional regulator of the white opaque transition WOR1

Elvira Román et al. Virulence. 2023 Dec.

Abstract

The transcriptional master regulator of the white opaque transition of Candida albicans WOR1 is important for the adaptation to the commensal lifestyle in the mammalian gut, a major source of invasive candidiasis. We have generated cells that overproduce Wor1 in mutants defective in the Hog1 MAP kinase, defective in several stress responses and unable to colonize the mice gut. WOR1 overexpression allows hog1 to be established as a commensal in the murine gut in a commensalism model and even compete with wild-type C. albicans cells for establishment. This increased fitness correlates with an enhanced ability to adhere to biotic surfaces as well as increased proteinase and phospholipase production and a decrease in filamentation in vitro. We also show that hog1 WOR1OE are avirulent in a systemic candidiasis model in mice.

Keywords: Candida albicans; Hog1; MAPK; Wor1; commensalism; gut colonization.

PubMed Disclaimer

Conflict of interest statement

No potential conflict of interest was reported by the authors.

Figures

Figure 1.
Figure 1.
WOR1 overexpression suppresses fitness defects of hog1 mutants.
Figure 2.
Figure 2.
Competition of hog1-WOR1OE cells with wild-type cells.
Figure 3.
Figure 3.
Effect of overexpression of WOR1 in hog1 cells adhesion.
Figure 4.
Figure 4.
Role of Als3 in fitness.
Figure 5.
Figure 5.
Effect of Wor1 overproduction in hog1 morphogenesis.
Figure 6.
Figure 6.
Determination of phospholipase and protease activity in WOR1OE cells.
Figure 7.
Figure 7.
Effect of Wor1 overproduction in mouse viability (in a systemic candidiasis model).
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

References

    1. Pfaller MA, Diekema DJ.. Epidemiology of invasive candidiasis: a persistent public health problem. Clin Microbiol Rev. 2007;20(1):133–16. - PMC - PubMed
    1. Pfaller MA, Diekema DJ. Epidemiology of invasive mycoses in North America. Crit Rev Microbiol. 2010;36(1):1–53. - PubMed
    1. Gudlaugsson O, Gillespie S, Lee K, et al. Attributable mortality of nosocomial candidemia. Revisited Clin Infect Dis. 2003;37(9):1172–1177. DOI:10.1086/378745 - DOI - PubMed
    1. Brown GD, Denning DW, Gow NA, et al. Hidden killers: human fungal infections. Sci Transl Med. 2012;4(165):165rv13. - PubMed
    1. Magill SS, Swoboda SM, Johnson EA, et al. The association between anatomic site of Candida colonization, invasive candidiasis, and mortality in critically ill surgical patients. Diagn Microbiol Infect Dis. 2006;55(4):293–301. DOI:10.1016/j.diagmicrobio.2006.03.013 - DOI - PubMed

Publication types

Substances

Supplementary concepts