Project description:Mta1 gene expression reveals new targets and functions. Mta1 functions in p53 dependent and independent manner. Genes regulated by Mta1 in the presence and absence of p53 were indetified This expression data contains 5 different samples (MEFs) 1.wild type 2. Mta1 knockout 3. Mta1 re-expression in the knock out MEFs 4. P53 knockout and 5. Mta1 over expression in P53 knock out MEFs. Various sample comparisons were done and genes with p-value< 0.05 and fold change M-bM-^IM-% 2.0 were considered statistically significant 5 samples (triplicates of each, total 15) were analyzed. We generated pairwise comparisons between the WT vs Mta1-KO; Mta1-KO vs Mta1-KO/Mta1; P53-KO vs P53-KO/Mta1.
Project description:Chromatin modifier metastatic tumor protein 1 (MTA1), closely correlated with the development and progression in breast cancer, has a fantastic role in multiple cellular processes, including gene expression and cell homeostasis. Although MTA1 is a stress-responsive gene, its role in genotoxic adaptation remains unexplored. Here, we demonstrate that O-GlcNAc modification promotes MTA1 to interact with chromatin and regulates target gene expression, contributing to breast cancer cell genotoxic adaptation. MTA1 is modified with O-GlcNAc residues at serine 237/241/246 in adriamycin adaptive breast cancer cells and that modification improves the genome-wide interactions of MTA1 with gene promotor regions by enhancing its association with nucleosome remodeling and histone deacetylation (NuRD) complex. Further, O-GlcNAc-modulated MTA1 chromatin-binding influences the specific transcriptional regulation of genes involved in the adaptation of breast cancer cells to genotoxic stress. We performed chromatin immunoprecipitation followed by sequencing (ChIP-seq) using anti-HA magnetic beads in HA-MTA1-WT or HA-MTA1-3A stably expressed MCF-7 cells. Next-generation sequencing libraries were generated and amplified for 15 cycles with BGISEQ kit. 100-300 bp DNA fragments were gel-purified and sequenced with BGISEQ-500 (BGI). Two biological replicates of the ChIP-seq were performed. We also analyzed gene expression in MTA1-WT and MTA1-3A expressed cells by RNA-seq.