Genome wide mapping of NFI and SMAD2/3 binding in senescence
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ABSTRACT:
PROVIDER: PRJNA610870 | ENA |
REPOSITORIES: ENA
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Project description:The Nuclear Factor I (NFI) family of DNA binding proteins (also called CAAT box transcription factors or CTF) is involved both in replication of adenoviral DNA and in regulation of gene expression. Using chromatin immuno-precipitation and high throughput sequencing (method termed ChIP-Seq) we performed genome-wide mapping of Nuclear Factor I DNA binding sites in mouse embryonic fibroblasts. We found that in vivo and in vitro NFI binding specificities are identical, since previously established position weight matrix was found to accurately predict binding sites for NFI group of proteins. Positional correlation between + and - strand ChIP-Seq tags revealed that NFI is a nucleosome-binding protein, unlike some other transcription factors. We further found that NFI binding correlates with the specific histone modification H3K4me3, the marker of transcribed promoters. Combining ChIP-Seq with the microarray expression data, we found that NFI associates with promoters with higher transcription level. We estimate that transcribed promoters may be more accessible to transcription factor binding than their nearby regions since NFI preferentially bind their DNA target sites located around transcription start sites. Knocking-out one of the NFI proteins (NFI-C), reduced the occupancy of predicted sites, however at the same time indicating that cells could compensate the missing protein with the other members of the family. Keywords: ChIP-Seq (chromatin immunoprecipitation and high throughput sequencing) ChIP-Seq (chromatin immunoprecipitation and high throughput sequencing) using antibody against NFI family of transcription factors in two cell types (wild type and NFI-C knock-out mouse embryonic fibroblasts MEFs)
2010-04-24 | E-GEOD-15844 | biostudies-arrayexpress
Project description:The Nuclear Factor I (NFI) family of DNA binding proteins (also called CAAT box transcription factors or CTF) is involved both in replication of adenoviral DNA and in regulation of gene expression. Using chromatin immuno-precipitation and high throughput sequencing (method termed ChIP-Seq) we performed genome-wide mapping of Nuclear Factor I DNA binding sites in mouse embryonic fibroblasts. We found that in vivo and in vitro NFI binding specificities are identical, since previously established position weight matrix was found to accurately predict binding sites for NFI group of proteins. Positional correlation between + and - strand ChIP-Seq tags revealed that NFI is a nucleosome-binding protein, unlike some other transcription factors. We further found that NFI binding correlates with the specific histone modification H3K4me3, the marker of transcribed promoters. Combining ChIP-Seq with the microarray expression data, we found that NFI associates with promoters with higher transcription level. We estimate that transcribed promoters may be more accessible to transcription factor binding than their nearby regions since NFI preferentially bind their DNA target sites located around transcription start sites. Knocking-out one of the NFI proteins (NFI-C), reduced the occupancy of predicted sites, however at the same time indicating that cells could compensate the missing protein with the other members of the family. Keywords: ChIP-Seq (chromatin immunoprecipitation and high throughput sequencing)
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Project description:The conserved Nuclear Factor I (NFI) family of transcription factors is unique to animals and essential for mammalian development. The C. elegans genome encodes a single NFI family member, whereas vertebrate genomes encode four distinct NFI protein subtypes (A, B, C, and X). NFI-1 deficient worms exhibit abnormalities including reduced lifespan, defects in movement and pharyngeal pumping, and delayed egg-laying. To explore the functional basis of these phenotypes, we sought to comprehensively identify NFI-1 binding targets in C. elegans. We first established NFI-1 DNA-binding specificity using an in vitro DNA-selection strategy. Analysis yielded a consensus motif of TTGGCA(N3)TGCCAA, which occurs 586 times in the genome, a 100-fold higher frequency than expected. We next asked which sites were occupied by NFI-1 in vivo by performing chromatin immunoprecipitation of NFI-1 followed by microarray hybridization (ChIP-chip). Only 55 genomic locations were identified, an unexpectedly small target set. In vivo NFI-1 binding sites tend to be upstream of genes involved in core cellular processes such as chromatin remodeling, mRNA splicing, and translation. Remarkably, 67/80 (84%) of the C. briggsae homologs of the identified targets contain conserved NFI binding sites in their promoters. These experiments provide a foundation for understanding how NFI-1 is recruited to unexpectedly few in vivo sites to perform its developmental functions, despite a vast over-representation of its binding site. To our knowledge, this represents the first genome-wide location study of any transcription factor in C. elegans, and the first genome-wide analysis in any species of an NFI transcription factor. 4 biological replicates of NFI-1 ChIP-chip (including 1 dye-swap) were performed with 2 pre-immune Mock ChIP-chip controls from corresponding extracts.
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Project description:Inhibitors for cyclin-dependent kinase (CDK) 4 and CDK6 have been established as effective therapeutic options for hormone receptor (HR)-positive, HER2-negative advanced breast cancer. Although the CDK4/6 inhibitors mainly target the cyclin D-CDK4/6-retinoblastoma tumor suppressor protein (RB) axis, little is known about clinical impact of inhibiting phosphorylation of other CDK4/6 target proteins. Here, we have focused on other CDK4/6 targets, SMAD proteins. We showed that a CDK4/6 inhibitor Palbociclib and Activin-SMAD2 signaling cooperatively inhibited cell cycle progression of a luminal-type breast cancer cell line T47D. Mechanistically, Palbociclib enhanced SMAD2 binding to the genome through inhibiting linker phosphorylation of the SMAD2 protein by CDK4/6. Comparison of the SMAD2 ChIP-seq data of T47D with those of a triple-negative breast cancer cell line Hs578T indicated that Palbociclib augments different SMAD2-mediated program defined based on types of cells, and enhances SMAD2 binding to the target regions on the genome without affecting its binding pattern. Collectively, the CDK4/6 inhibitor facilitates the cytostatic effects of Activin-SMAD2, while it also enhances its tumor promoting effects depending on types of breast cancer.
2018-10-23 | GSE117496 | GEO