Table_2_Nutrient-Driven O-GlcNAcylation at Promoters Impacts Genome-Wide RNA Pol II Distribution.XLSX Michael W. Krause Dona C. Love Salil K. Ghosh Peng Wang Sijung Yun Tetsunari Fukushige John A. Hanover 10.3389/fendo.2018.00521.s004 https://frontiersin.figshare.com/articles/dataset/Table_2_Nutrient-Driven_O-GlcNAcylation_at_Promoters_Impacts_Genome-Wide_RNA_Pol_II_Distribution_XLSX/7067006 <p>Nutrient-driven O-GlcNAcylation has been linked to epigenetic regulation of gene expression in metazoans. In C. elegans, O-GlcNAc marks the promoters of over 800 developmental, metabolic, and stress-related genes; these O-GlcNAc marked genes show a strong 5′, promoter-proximal bias in the distribution of RNA Polymerase II (Pol II). In response to starvation or feeding, the steady state distribution of O-GlcNAc at promoters remain nearly constant presumably due to dynamic cycling mediated by the transferase OGT-1 and the O-GlcNAcase OGA-1. However, in viable mutants lacking either of these enzymes of O-GlcNAc metabolism, the nutrient-responsive GlcNAcylation of promoters is dramatically altered. Blocked O-GlcNAc cycling leads to a striking nutrient-dependent accumulation of O-GlcNAc on RNA Pol II. O-GlcNAc cycling mutants also show an exaggerated, nutrient-responsive redistribution of promoter-proximal RNA Pol II isoforms and extensive transcriptional deregulation. Our findings suggest a complex interplay between the O-GlcNAc modification at promoters, the kinase-dependent “CTD-code,” and co-factors regulating RNA Pol II dynamics. Nutrient-responsive O-GlcNAc cycling may buffer the transcriptional apparatus from dramatic swings in nutrient availability by modulating promoter activity to meet metabolic and developmental needs.</p> 2018-09-10 04:19:11 O-GlcNAc RNA-polymerase II CTD transcription genetic nutrients polymerase dynamics glycobiology