Project description:We determined DNA-binding sites of the yeast transcription factor Yfl052w by ChIP-exo. Cells were grown in the YP media containing palatinose. Yfl052w was tagged with HA tag and anti-HA antibody was used for the immunoprecipitation. Examination of Yfl052 trancription factor in HA-tagged and wt cells (as a control)
Project description:We determined DNA-binding sites of the yeast transcription factor Yfl052w by ChIP-exo. Cells were grown in the YP media containing palatinose. Yfl052w was tagged with HA tag and anti-HA antibody was used for the immunoprecipitation. Examination of Yfl052 trancription factor in HA-tagged and wt cells (as a control)
Project description:These ChIP-exo data were used to validate the predictions from our live-cell single-molecule imaging experiment The ChIP-exo mapping of ultra-fine localization of endogenous Sox2, halo-Sox2, and two halo-Sox2 mutants (halo-Sox2M and halo-Sox2D) in embryonic stem cells.
Project description:Mapping ultra-high resolution of Sp1:DNA interaction would provide us with valuable new mechanistic insights into Sp1-mediated gene regulatory network in Huntington Disease cell culture model. STHdh Q7/Q7 cells were directly fixed and used for the ChIP-exo experiment.
Project description:Mapping ultra high resolution of Brachyury:DNA interaction would provide us with valuable new mechanistic insights into complex molecular transactions at Brachyury-bound enhancers. Embryonic stem cells were differentiated into Brachyury-positive mesoendoderm cells. And, ChIP-exo experiment was then performed to identify detailed Brachyury-DNA binding profiles.
Project description:This study involves the role of yeast mRNA decay factors in transcription. The experiment included here are the ChIP-exo results of three decay factors: Xrn1, Dcp2 & Lsm1. Four experiments were made: Xrn1, Dcp2, Lsm1 and control (no-TAP tag), in two replicates.
Project description:To investigate enhancer activity in OE19 cells, we performed ATAC_STARR-seq and CUT&Tag_STARR-seq using antibodies against H3K27ac, BRD4 and MED1 .
Project description:Circadian and metabolic physiology are intricately intertwined, as illustrated by Rev-erb , a transcription factor (TF) that functions both as a core repressive component of the cell autonomous clock and as a regulator of metabolic genes. Here we show that Rev-erb modulates the clock and metabolism by different genomic mechanisms. Clock control requires Rev-erb to bind directly to the genome at its cognate sites, where it competes with activating ROR TFs. By contrast, Rev-erb regulates metabolic genes primarily by recruiting the HDAC3 corepressor to sites to which it is tethered by cell type-specific transcription factors. Thus, direct competition between Rev-erb and ROR TFs provides a universal mechanism for self-sustained control of molecular clock across all tissues, whereas Rev-erb utilizes lineage-determining factors to convey a tissue-specific epigenomic rhythm that regulates metabolism tailored to the specific need of that tissue. Biological replicates were uploaded in separated files and indicated in the file names.