Set1-mediated H3K4 methylation is required for Candida albicans virulence by regulating intracellular level of reactive oxygen species

Candida albicans is an opportunistic human fungal pathogen that exists in normal flora but can cause infection in immunocompromised individuals. The transition to pathogenic C. albicans requires a change of various gene expressions. Because histone-modifying enzymes can regulate gene expression, the...

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Autores principales:	Jueun Kim, Shinae Park, So Hee Kwon, Eun-Jin Lee, Jung-Shin Lee
Formato:	article
Lenguaje:	EN
Publicado:	Taylor & Francis Group 2021
Materias:	candida albicans h3k4 methyltransferase set1 cellular ros virulence Infectious and parasitic diseases RC109-216
Acceso en línea:	https://doaj.org/article/665a9202b596483fb1b32a3bcf82ed99
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spelling	oai:doaj.org-article:665a9202b596483fb1b32a3bcf82ed992021-11-04T15:00:45ZSet1-mediated H3K4 methylation is required for Candida albicans virulence by regulating intracellular level of reactive oxygen species2150-55942150-560810.1080/21505594.2021.1980988https://doaj.org/article/665a9202b596483fb1b32a3bcf82ed992021-12-01T00:00:00Zhttp://dx.doi.org/10.1080/21505594.2021.1980988https://doaj.org/toc/2150-5594https://doaj.org/toc/2150-5608Candida albicans is an opportunistic human fungal pathogen that exists in normal flora but can cause infection in immunocompromised individuals. The transition to pathogenic C. albicans requires a change of various gene expressions. Because histone-modifying enzymes can regulate gene expression, they are thought to control the virulence of C. albicans. Indeed, the absence of H3 lysine 4 (H3K4) methyltransferase Set1 has been shown to reduce the virulence of C. albicans; however, Set1-regulated genes responsible for this attenuated virulence phenotype remain unknown. Here, we demonstrated that Set1 positively regulates the expression of mitochondrial protein genes by methylating H3K4. In particular, levels of cellular mitochondrial reactive oxygen species (ROS) were higher in Δset1 than in the wild-type due to the defect of those genes’ expression. Set1 deletion also increases H2O2 sensitivity and prevents proper colony formation when interacting with macrophage in vitro, consistent with its attenuated virulence in vivo. Together, these findings suggest that Set1 is required to regulate proper cellular ROS production by positively regulating the expression of mitochondrial protein genes and subsequently sustaining mitochondrial membrane integrity. Consequently, C. albicans maintains proper ROS levels via Set1-mediated transcriptional regulation, thus establishing a rapid defense against external ROS generated by the host.Jueun KimShinae ParkSo Hee KwonEun-Jin LeeJung-Shin LeeTaylor & Francis Grouparticlecandida albicansh3k4 methyltransferaseset1cellular rosvirulenceInfectious and parasitic diseasesRC109-216ENVirulence, Vol 12, Iss 1, Pp 2648-2658 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	candida albicans h3k4 methyltransferase set1 cellular ros virulence Infectious and parasitic diseases RC109-216
spellingShingle	candida albicans h3k4 methyltransferase set1 cellular ros virulence Infectious and parasitic diseases RC109-216 Jueun Kim Shinae Park So Hee Kwon Eun-Jin Lee Jung-Shin Lee Set1-mediated H3K4 methylation is required for Candida albicans virulence by regulating intracellular level of reactive oxygen species
description	Candida albicans is an opportunistic human fungal pathogen that exists in normal flora but can cause infection in immunocompromised individuals. The transition to pathogenic C. albicans requires a change of various gene expressions. Because histone-modifying enzymes can regulate gene expression, they are thought to control the virulence of C. albicans. Indeed, the absence of H3 lysine 4 (H3K4) methyltransferase Set1 has been shown to reduce the virulence of C. albicans; however, Set1-regulated genes responsible for this attenuated virulence phenotype remain unknown. Here, we demonstrated that Set1 positively regulates the expression of mitochondrial protein genes by methylating H3K4. In particular, levels of cellular mitochondrial reactive oxygen species (ROS) were higher in Δset1 than in the wild-type due to the defect of those genes’ expression. Set1 deletion also increases H2O2 sensitivity and prevents proper colony formation when interacting with macrophage in vitro, consistent with its attenuated virulence in vivo. Together, these findings suggest that Set1 is required to regulate proper cellular ROS production by positively regulating the expression of mitochondrial protein genes and subsequently sustaining mitochondrial membrane integrity. Consequently, C. albicans maintains proper ROS levels via Set1-mediated transcriptional regulation, thus establishing a rapid defense against external ROS generated by the host.
format	article
author	Jueun Kim Shinae Park So Hee Kwon Eun-Jin Lee Jung-Shin Lee
author_facet	Jueun Kim Shinae Park So Hee Kwon Eun-Jin Lee Jung-Shin Lee
author_sort	Jueun Kim
title	Set1-mediated H3K4 methylation is required for Candida albicans virulence by regulating intracellular level of reactive oxygen species
title_short	Set1-mediated H3K4 methylation is required for Candida albicans virulence by regulating intracellular level of reactive oxygen species
title_full	Set1-mediated H3K4 methylation is required for Candida albicans virulence by regulating intracellular level of reactive oxygen species
title_fullStr	Set1-mediated H3K4 methylation is required for Candida albicans virulence by regulating intracellular level of reactive oxygen species
title_full_unstemmed	Set1-mediated H3K4 methylation is required for Candida albicans virulence by regulating intracellular level of reactive oxygen species
title_sort	set1-mediated h3k4 methylation is required for candida albicans virulence by regulating intracellular level of reactive oxygen species
publisher	Taylor & Francis Group
publishDate	2021
url	https://doaj.org/article/665a9202b596483fb1b32a3bcf82ed99
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Set1-mediated H3K4 methylation is required for Candida albicans virulence by regulating intracellular level of reactive oxygen species

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