Essential roles for chromatin protein L3mbtl2 in pluripotent stem cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE38801 | GEO | 2012/07/03
SECONDARY ACCESSION(S): PRJNA168978
REPOSITORIES: GEO
Similar Datasets
Project description:In order to determine the impact of L3mbtl2 on genome wide mRNA expression microarray analysis was carried out in L3mbtl2 knock out ES cells and wild type ES cells. The same analysis was also carried out in knock out cells infected with L3mbtl2-F vector and a control vector. Experiment to study targets of L3mbtl2 in C57bl6/129 hybrid ES cells. 4 samples: wild type, L3mbtl2 knock out, L3mbtl2 knock out rescue and rescue with empty vector
2012-07-02 | E-GEOD-38801 | biostudies-arrayexpress
Project description:To elucidate the (possibly sumo dependent) binding sites of L3MBTL2, wild type L3MBTL2, L3MBTL2-Flag and L3MBTL2-KR-Flag ChIPs from HEK293 cells were analyzed via ChIPseq
2014-01-14 | E-MTAB-1731 | biostudies-arrayexpress
Project description:L3MBTL2 in HEK293 cells - ChIPseq
| PRJEB4205 | ENA
Project description:Polycomb-group complexes are evolutionarily conserved epigenetic machineries that regulate stem cell fate decisions/development and are also implicated in tumorigenesis mainly by histone modification. PRC1 complexes mediates ubiquitylation of histone H2A on lysine 119 and consists of PRC1.1 to PRC1.6 complexes. Here, we studied the functional roles of a PRC1.6 molecule L3MBTL2 in neuroblastoma (NB) cells. L3MBTL2 knockout- and knockdown-experiments elucidated that L3MBTL2 depletion suppressed NB cell proliferation according with cell cycle arrest and gamma-H2A up-regulation. L3MBTL2 knockout profoundly suppressed xenograft tumor formation. Transcriptome analysis detected the suppressed cell cycle-related pathways and the activated the differentiation-related pathways. The remarkable de-repressed genes by the L3MBTL2 knockout were BRME1 and NRIP3. ChIP experiments showed co-localization of the PRC1.6 components PCGF6/E2F6/L3MBTL2 and MYCN at the transcription start sites (TSS) of these genes. L3MBTL2 knockout reduced H2AK119ub marks at the TSS regions but PCGF6 binding was heterogeneously changed. This study clarified the significance of PRC1.6 molecule L3MBTL2 in NB cell homeostasis and the epigenetic mechanism of the L3MBTL2-mediated gene suppression in NB that regulates the PRC1.6 complex localization and H2AK119 mono-ubiquitination in a gene locus-specific manner.
2023-09-26 | GSE201512 | GEO
Project description:Purpose: The goals of this study are to compare Mga-/-, L3mbtl2-/-, Pcgf6-/- and Wild type embryonic stem cells transcriptome profiling (RNA-seq) and compare the target genes of Mga, L3mbtl2 and Pcgf6.
2021-01-21 | GSE144141 | GEO
Project description:Human MBT domain-containing protein L3MBTL2 was found to be an integral component of a protein complex that we termed Polycomb Repressive Complex 1-like 3 (PRC1L3) given the presence of the PcG proteins RING1, RING2 and PCGF6. L3MBTL2 binds chromatin in a histone modification-independent manner and is required for the repressive function of PRC1L3. PRC1L3 also contains E2F6 and CBX3, two factors with wellM-bM-^@M-^Pestablished functions in transcriptional repression. GenomeM-bM-^@M-^Pwide profiling identified several hundred genes that are simultaneously bound by L3MBTL2 and E2F6, preferentially around transcriptional start sites. Importantly, these genes are largely distinct from those targeted by other E2Fs or L3MBTL, another MBTM-bM-^@M-^Pdomain containing protein that interacts with RB1. H3K27 or H3K9 methylation, two chromatin modifications implicated in gene silencing, are not present on all L3MBTL2 target genes. L3MBTL2-specific RNAi results in altered target gene expression patterns and affects the differentiation program of hematopoietic cells. Our data suggest that repression of transcription via chromatin modulation, reflective of PRC1 function, can be achieved by multiple players and does not necessarily require the presence of histone lysine methylation marks. 7 total ChIP-seq datasets; one L3MBTL2 dataset done in duplicate in K562 cells; one E2F6 dataset done in duplicate in K562 cells; one H3K27me3 replicate dataset in K562 cells.
2011-06-07 | E-GEOD-28162 | biostudies-arrayexpress
Project description:Human MBT domain‐containing protein L3MBTL2 was found to be an integral component of a protein complex that we termed Polycomb Repressive Complex 1‐like 3 (PRC1L3) given the presence of the PcG proteins RING1, RING2 and PCGF6. L3MBTL2 binds chromatin in a histone modification‐ independent manner and is required for the repressive function of PRC1L3. PRC1L3 also contains E2F6 and CBX3, two factors with well‐established functions in transcriptional repression. Genome‐wide profiling identified several hundred genes that are simultaneously bound by L3MBTL2 and E2F6, preferentially around transcriptional start sites. Importantly, these genes are largely distinct from those targeted by other E2Fs or L3MBTL, another MBT‐domain containing protein that interacts with RB1. H3K27 or H3K9 methylation, two chromatin modifications implicated in gene silencing, are not present on all L3MBTL2 target genes. L3MBTL2‐specific RNAi results in altered target gene expression patterns and affects the differentiation program of hematopoietic cells. Our data suggest that repression of transcription via chromatin modulation, reflective of PRC1 function, can be achieved by multiple players and does not necessarily require the presence of histone lysine methylation marks. 12 total ChIP-seq datasets; one E2F6 dataset and one Input dataset done from MCF7 cells on Nimblegen ENCODE arrays; one L3MBTL1 dataset and one Input dataset done from MCF7 cells on Nimblegen ENCODE arrays; one L3MBTL2 dataset and one Input dataset done from MCF7 cells on Nimblegen ENCODE arrays; one E2F6 dataset and one Input dataset done from MCF7 cells on Nimblegen 1.5kb promoter arrays; one L3MBTL1 dataset and one Input dataset done from MCF7 cells on Nimblegen 1.5kb promoter arrays; one L3MBTL2 dataset and one Input dataset done from MCF7 cells on Nimblegen 1.5kb promoter arrays.
2011-06-07 | E-GEOD-28161 | biostudies-arrayexpress
Project description:Purpose: Here we report the differential gene expression profile between WT and C3G knock out E14Tg2a cells. The cells were grown in equel seeding density in GMEM Serum +LIF media. RNA was isolated after 48 hr and sequenced Methods: C3G knock out E14Tg2a mouse ES cells were made by CrisprCAS9 mediated knock out strategy. RNA was collected using Trizol method from WT and knock out clone 48 hr after seeding in equel density in a 6 well plate, precoated with gelatin. Results: Using an optimized data analysis workflow, we mapped about 75 million sequence reads per sample to the mouse genome (build mm10) and identified 5797 genes were differentially expressed with adjusted p-value < 0.05(significant) between the WT and C3G-/-. Approximately 17% of the genes showed differential expression between the WT and C3g−/− ESCs, with a fold change ≥1.5 and p value <0.05. Biological pathways and gene ontology enrichment analysis of differentially expressed genes reveals that C3G is required to maintain adhesion of ES cells and for differentiation of mouse ES cells. Conclusions: The study revealed the first transcriptome profile of C3G gene knock out in E14Tg2a mouse embryoinic tem cells. In our study we found that C3G acts as a mediaator of differentiation by activatingERK and integrin signaling and supressing STAT3 and other pluripotency factors like ESRRB and KLF4.
2021-06-21 | GSE159595 | GEO
Project description:Human MBT domain-containing protein L3MBTL2 was found to be an integral component of a protein complex that we termed Polycomb Repressive Complex 1-like 3 (PRC1L3) given the presence of the PcG proteins RING1, RING2 and PCGF6. L3MBTL2 binds chromatin in a histone modification-independent manner and is required for the repressive function of PRC1L3. PRC1L3 also contains E2F6 and CBX3, two factors with well‐established functions in transcriptional repression. Genome‐wide profiling identified several hundred genes that are simultaneously bound by L3MBTL2 and E2F6, preferentially around transcriptional start sites. Importantly, these genes are largely distinct from those targeted by other E2Fs or L3MBTL, another MBT‐domain containing protein that interacts with RB1. H3K27 or H3K9 methylation, two chromatin modifications implicated in gene silencing, are not present on all L3MBTL2 target genes. L3MBTL2-specific RNAi results in altered target gene expression patterns and affects the differentiation program of hematopoietic cells. Our data suggest that repression of transcription via chromatin modulation, reflective of PRC1 function, can be achieved by multiple players and does not necessarily require the presence of histone lysine methylation marks.
2011-06-07 | GSE28162 | GEO
Project description:Human MBT domain‐containing protein L3MBTL2 was found to be an integral component of a protein complex that we termed Polycomb Repressive Complex 1‐like 3 (PRC1L3) given the presence of the PcG proteins RING1, RING2 and PCGF6. L3MBTL2 binds chromatin in a histone modification‐ independent manner and is required for the repressive function of PRC1L3. PRC1L3 also contains E2F6 and CBX3, two factors with well‐established functions in transcriptional repression. Genome‐wide profiling identified several hundred genes that are simultaneously bound by L3MBTL2 and E2F6, preferentially around transcriptional start sites. Importantly, these genes are largely distinct from those targeted by other E2Fs or L3MBTL, another MBT‐domain containing protein that interacts with RB1. H3K27 or H3K9 methylation, two chromatin modifications implicated in gene silencing, are not present on all L3MBTL2 target genes. L3MBTL2‐specific RNAi results in altered target gene expression patterns and affects the differentiation program of hematopoietic cells. Our data suggest that repression of transcription via chromatin modulation, reflective of PRC1 function, can be achieved by multiple players and does not necessarily require the presence of histone lysine methylation marks.
2011-06-07 | GSE28161 | GEO