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Identification of MRG15 as barrier to somatic reprogramming

ABSTRACT: Epigenetic reprogramming requires depletion of 4 factors ; Oct4, Sox2, Klf-4 and c-Myc. We have 4 groups of samples. 2 group is collected as fibroblasts and it is referred as Day Zero. The other groups are collected at the sixth day of epigenetic reprogramming referred as Day Six. Day 18 of epigenetic reprogramming, %5- 15 of cell population transformed into pluripotent stem cells. At day six this percentage is lower.Our previous studies have showed that inhibition of H3K36me3 mark thusleading to H3K36me2 mark on chromatin) significantly increased reprogramming efficiency. A CRISPR Knock-Out Library was built to identify which of the H3K36me3 mark reader protein can phenocopy absence of K36me3 loss in terms of reprogramming efficiency. MRG15 Knock Out has showed the most similar increase in reprogramming as loss of K36me3 mark. It has been reported that MRG15 is responsible from alternative splicing of some genes. Our hypothesis is; in the presence of H3K36me3 mark MRG15 can bind this mark on chromatin and recruit proteins related to alternative splicing ( eg. PTBP1)and regulate alternative splicing.

ORGANISM(S): Homo sapiens

PROVIDER: GSE260899 | GEO | 2025/01/01

REPOSITORIES: GEO

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Project description:Epithelial to mesenchymal transition (EMT) is an extreme example of cell plasticity, important for normal development, injury repair, and malignant progression. Widespread epigenetic reprogramming occurs during stem cell differentiation and malignant transformation, but EMT-related epigenetic reprogramming is poorly understood. Here we investigated epigenetic modifications during TGF-β-mediated EMT. While DNA methylation was unchanged during EMT, we found global reduction of the heterochromatin mark H3-lys9 dimethylation (H3K9Me2), increase of the euchromatin mark H3-lys4 trimethylation (H3K4Me3), and increase of the transcriptional mark H3-lys36 trimethylation (H3K36Me3). These changes were largely dependent on lysine-specific deaminase-1 (LSD1), and LSD1 loss-of-function experiments showed marked effects on EMT-driven cell migration and chemoresistance. Genome-scale mapping revealed that chromatin changes were largely specific to large organized heterochromatin K9-modifications (LOCKs), suggesting that EMT is characterized by reprogramming of specific chromatin domains across the genome. Chromatin immunoprecipitation (ChIP) was performed with antibodies against H3K9Me2 (Abcam, ab1220), H3K36Me3 (ab9050), and H3K4Me3 (ab8580) on native (unfixed) chromatin isolated from fully differentiated mouse AML12 cells (confluent, serum starved for 48hrs) either treated with TGF-β for 36hrs to induce EMT or not treated with TGF-β (0hrs, differentiated AML12 cells). DNA purified from these samples was then either whole-genome amplified (H3K36Me3 and H3K4Me3) and hybridized or directly (H3K9Me2) hybridized to NimbleGen 2.1M economy whole-genome tiling arrays #2 (listed below as array 1) and #3 (listed below as array 2), which cover mouse chromosomes 4-14. For each sample, the immunoprecipitated DNA (IP) and the input (control) DNA were hybridized to the arrays, and the IP is normalized to the input. There are 16 total samples listed below. There are 8 sample for H3K9Me2 (TGF-β and no TGF-β for arrays 1 and 2, done in replicate for a total of 8). There are 4 samples for H3K36Me3 (TGF-β and no TGF-β done on array 1 and array 2). There are 4 total samples for H3K4Me3 (TGF-β and no TGF-β done on array 1 and array 2).

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Identification of MRG15 as barrier to somatic reprogramming

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