High levels of oxidative stress globally inhibit gene transcription and histone acetylation.
Oxidative stress has been shown to induce ubiquitynation of RNA polymerase II, but direct bearing of that phenomenon on global transcription still remains elusive. In this report, we show that high levels of cellular oxidative stress globally inhibit gene transcription, and that this decrease in transcription is only partly attributable to reduced binding of RNA polymerase II to a model gene promoter. Importantly, we show that this decrease in transcription correlates with a significant decrease in histone H3 and H4 acetylation levels both throughout a model gene, and also globally in the nucleus of cells. Our results suggest that high levels of oxidative stress can inhibit transcription by a mechanism, at least in part, that impedes global histone acetylation levels.
Berthiaume
Maryse
M
Centre de Recherche sur les Mécanismes du Fonctionnement Cellulaire, Département de Biologie, Faculté des Sciences, Université de Sherbrooke, Sherbrooke, Québec, Canada.
Boufaied
Nadia
N
Moisan
Annie
A
Gaudreau
Luc
L
D000107:Acetylation; D045744:Cell Line, Tumor; D006657:Histones / Q000378:metabolism*; D006801:Humans; D006861:Hydrogen Peroxide / Q000633:toxicity; D018384:Oxidative Stress; D011401:Promoter Regions, Genetic; D012319:RNA Polymerase II / Q000378:metabolism; D014158:Transcription, Genetic
D006657:Histones; D006861:Hydrogen Peroxide; D012319:RNA Polymerase II