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Modulation of gene expression dynamics by co-transcriptional histone methylations
- Modulation of gene expression dynamics by co-transcriptional histone methylations
- Woo, Hyeonju; Ha, So Dam; Lee, Sung Bae; Buratowski, Stephen; Kim, TaeSoo
- DGIST Authors
- Lee, Sung Bae
- Issue Date
- Experimental and Molecular Medicine, 49
- Article Type
- Acetyltransferase Complex; Antisense Transcription; Coding Regions; Deacetylase Complex; H2B Ubiquitylation; H3K4 Methylation; K 36 Methylation; RNA Polymerase II; Saccharomyces Cerevisiae; SET2 Methylation
- Co-transcriptional methylations of histone H3 at lysines 4 and 36, highly conserved methyl marks from yeast to humans, have profound roles in regulation of histone acetylation. These modifications function to recruit and/or activate distinct histone acetyltransferases (HATs) or histone deacetylases (HDACs). Whereas H3K4me3 increases acetylation at promoters via multiple HATs, H3K4me2 targets Set3 HDAC to deacetylate histones in 5' transcribed regions. In 3' regions of genes, H3K36me2/3 facilitates deacetylation by Rpd3S HDAC and slows elongation. Despite their important functions in deacetylation, no strong effects on global gene expression have been seen under optimized or laboratory growth conditions. Instead, H3K4me2-Set3 HDAC and Set2-Rpd3S pathways primarily delay the kinetics of messenger RNA (mRNA) and long noncoding RNA (lncRNA) induction upon environmental changes. A majority of mRNA genes regulated by these pathways have an overlapping lncRNA transcription either from an upstream or an antisense promoter. Surprisingly, the distance between mRNA and lncRNA promoters seems to specify the repressive effects of the two pathways. Given that co-transcriptional methylations and acetylation have been linked to many cancers, studying their functions in a dynamic condition or during cancer progression will be much more important and help identify novel genes associated with cancers.
- NATURE PUBLISHING GROUP
- Related Researcher
Lee, Sung Bae
SB LAB(Lab of Neurodegenerative diseases and Aging)
Cellular mechanism of neurodegenerative diseases; Neuronal maintenance and remodeling; 퇴행성 뇌질환의 세포기전; 신경계 유지 및 리모델링 연구
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- Brain and Cognitive SciencesETC1. Journal Articles
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