Ontology highlight
ABSTRACT:
PROVIDER: PRJNA847369 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:'Mitogen-Induced Defective Mitosis Transforms Neural Progenitor Cells
| PRJNA854043 | ENA
Project description:Impaired control of the G1/S checkpoint allows initiation of DNA replication under non-permissive conditions. Unscheduled S-phase entry is associated with DNA replication stress, demanding for other checkpoints or cellular pathways to maintain proliferation. Here, we uncovered a requirement for ADARp150 to sustain proliferation of G1/S-checkpoint-defective cells under growth-restricting conditions. Besides its well-established mRNA editing function in inversely oriented short interspersed nuclear elements (SINEs), we found ADARp150 to exert a critical function in mitosis. ADARp150 depletion resulted in tetraploidization, impeding cell proliferation in mitogen-deprived conditions. Mechanistically we show that ADAR1 depletion induced aberrant expression of Cyclin B3, which was causative for mitotic failure and whole-genome duplication. Finally, we find that also in vivo ADAR1-depletion-provoked tetraploidization hampers tumor outgrowth.
2024-10-10 | GSE262277 | GEO
Project description:The male germline transcriptome changes dramatically during the mitosis-to-meiosis transition to activate late spermatogenesis genes and to transiently suppress genes commonly expressed in somatic lineages and spermatogenesis progenitor cells, termed somatic/progenitor genes. These changes reflect epigenetic regulation. Induction of late spermatogenesis genes during spermatogenesis is facilitated by poised chromatin established in the stem cell phases of spermatogonia, whereas silencing of somatic/progenitor genes during meiosis and postmeiosis is associated with formation of bivalent domains which also allows the recovery of the somatic/progenitor program after fertilization. Importantly, during spermatogenesis mechanisms of epigenetic regulation on sex chromosomes are different from autosomes: X-linked somatic/progenitor genes are suppressed by meiotic sex chromosome inactivation without deposition of H3K27me3. Our results suggest that bivalent H3K27me3 and H3K4me2/3 domains are not limited to developmental promoters (which maintain bivalent domains that are silent throughout the reproductive cycle), but also underlie reversible silencing of somatic/progenitor genes during the mitosis-to-meiosis transition in late spermatogenesis. 29 samples analyzed by ChIP-Seq
2015-06-18 | E-GEOD-69946 | biostudies-arrayexpress
Project description:Mitosis deregulation is a key event during carcinogenesis. Alternative splicing spectrum alteration plays a critical role during mitosis shift. However, the molecules responsible for dysregulated alternative splicing driving carcinogenetic mitosis remain poorly defined. Here, we demonstrate that cancer metastasis-associated antigen 1 (MTA1), a well-known oncogenic chromatin modifier, broadly interacts and co-expresses with RBPs across cancers, contributes to cancerous mitosis-related alternative splicing. Using developed fCLIP-seq technology, we show that MTA1 binds abundant transcripts, preferentially at splicing-responsible motifs, influencing both the abundance and alternative splicing (AS) of target transcripts. MTA1 is cytoplasmic and extrachromosomal at mitosis. Through the RNA-association activity, MTA1 regulates the mRNA level and guides the AS of a serious of mitosis regulators to control the mitosis. MTA1 deletion abrogated the dynamic AS switches of variants for ATRX and MYBL2 at mitotic stage, which are relevant to mitosis and tumorigenesis. MTA1 dysfunction causes a defective mitotic arrest, leading to aberrant chromosome segregation, and resultantly chromosomal instability (CIN) in cancer cells and tissues, which eventually contributes to tumorigenesis. Currently, little is known about the RNA splicing during mitosis, here, we present MTA1 as a pivotal RNA-binding protein, functioning to orchestrate the dynamic splicing of mitosis regulators linked to mitosis control in tumorigenesis.
2020-03-30 | PXD018242 |
Project description:Induced muscle progenitor cells
| PRJNA716685 | ENA
Project description:Induced muscle progenitor cells
| PRJNA648431 | ENA
Project description:<p>Pilocytic astrocytoma (PA), the most common childhood brain tumor, is a low-grade glioma with a single driver BRAF rearrangement. Here, we perform scRNAseq in six PAs using methods that enabled detection of the rearrangement. When compared to higher-grade gliomas, a strikingly higher proportion of the PA cancer cells exhibit a differentiated, astrocyte-like phenotype. A smaller proportion of cells exhibit a progenitor-like phenotype with evidence of proliferation. These express a mitogen-activated protein kinase (MAPK) program that was absent from higher-grade gliomas. Immune cells, especially microglia, comprise 40% of all cells in the PAs and account for differences in bulk expression profiles between tumor locations and subtypes. These data indicate that MAPK signaling is restricted to relatively undifferentiated cancer cells in PA, with implications for investigational therapies directed at this pathway.</p> <p>Note that 931 out of 1234 samples in the Sequence Read Archive (SRA) passed QC and have transcript count data available from the Broad Institute Single Cell Portal. The transcript count data can be found at <a href="https://singlecell.broadinstitute.org/single_cell/study/SCP271/pilocytic-astrocytoma-single-cell-rna-seq#study-download" target="_blank">https://singlecell.broadinstitute.org/single_cell/study/SCP271/pilocytic-astrocytoma-single-cell-rna-seq#study-download</a></p>
| phs001854 | dbGaP
Project description:The processing of RNAs by chromatin-associated proteins (CAPs) is highlighted by the latest findings. However, whether and how CAP-RNA interactions regulate cancer biology remain underdefined. Using modified fCLIP-seq technology, we show that, cancer metastasis-associated antigen 1 (MTA1), a well-known oncogenic chromatin modifier, binds bulk transcripts, preferentially at splicing-responsible motifs, influencing the abundance and alternative splicing (AS) of target transcripts, preferentially those encoding mitosis regulators. MTA1 orchestrates the fluctuant pre-mRNA AS kinetics of mitosis regulators, such as ATRX and MYBL2, during mitosis. MTA1 overexpression causes a defective mitotic arrest, leading to aberrant chromosome segregation, and CIN occurrence in cancer cells and clinical tumors, which eventually contributes to tumorigenesis. Hence, we present MTA1 as a pivotal RNA-binding CAP linked to mitosis control in tumorigenesis.
2020-07-17 | GSE123955 | GEO
Project description:TLDA miRNA profiling on purified rat cardiomyocytes (Myo) (Ctl) and myocyte-derived progenitor cells (MDCs) demonstrated significant dedifferentiation of myocytes and identity of stemness, cell cycle progression and proliferation in MDCs after continuous culture in mitogen-rich medium for about 2 weeks.
2010-09-22 | GSE24252 | GEO
Project description:Sister chromatid exchanges (SCEs) are a product of joint DNA molecules resolution, and are considered to require homologous recombination (HR). Canonical HR factors BRCA1, BRCA2 and RAD51 were indeed essential for SCE induction in response to irradiation-induced DNA breaks. By contrast, replication-blocking agents, including PARP inhibitors, induced SCEs independently of BRCA1, BRCA2 or RAD51. HR-independent SCEs were associated with incomplete DNA replication, as evidenced by post-replicative single-stranded DNA (ssDNA) accumulation and enrichment of PARP inhibitor-induced SCEs at common fragile sites (CFSs). Importantly, PARP-induced DNA lesions were transmitted into mitosis, pointing towards SCEs originating from mitotic processing of underreplicated DNA. We found polymerase theta to be associated to mitotic DNA lesions, to be required for SCE formation and to prevent chromosome fragmentation upon PARP inhibition in HR-defective cells. Combined, our data show that replication-blocking agents lead to underreplicated DNA in mitosis, which is processed into SCEs independently of canonical HR factors.
2023-03-11 | PXD028670 | Pride