The RNA binding protein SYNCRIP is a component of the exosomal machinery controlling microRNAs sorting
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB12915 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR1299070.fastq.gz | Fastqsanger.gz | |||
| ERR1299080.fastq.gz | Fastqsanger.gz | |||
| ERR1299090.fastq.gz | Fastqsanger.gz | |||
| ERR1299071.fastq.gz | Fastqsanger.gz | |||
| ERR1299081.fastq.gz | Fastqsanger.gz |
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Project description:Despite clear evidence that exosomal microRNAs (miRNAs) are able to modulate the cellular microenvironment and that exosomal RNA cargo selection is often deregulated in pathological conditions, the mechanisms controlling specific RNA sorting into extracellular vescicles are still poorly understood. We identified here the RNA binding protein SYNCRIP (Synaptotagmin-binding Cytoplasmic RNA-Interacting Protein, also known as hnRNP-Q or NSAP1) as a component of the hepatocyte exosomal miRNA sorting machinery. SYNCRIP was found to bind directly a subset of miRNAs enriched in exosomes, sharing a common extra-seed sequence that we named hEXO motif. In vivo knock-down of SYNCRIP impaired microRNA sorting in exosomes and the hEXO motif was proven to play a role in the regulation of miRNA localization, as its embedment into a poorly exported miRNA enhanced its loading into exosomes. These results provide a new insight in the mechanisms of miRNA exosomal sorting process, that ca be exploited to further understand the role of these extracellular vescicles in cell-to-cell communications and the control of tissue micoenvironments.
2016-09-02 | E-MTAB-4502 | biostudies-arrayexpress
Project description:SYNCRIP, a member of the cellular heterogeneous nuclear ribonucleoprotein (hnRNP) family of RNA binding proteins, regulates various aspects of neuronal development and plasticity. Although SYNCRIP has been identified as a component of cytoplasmic RNA granules in dendrites of mammalian neurons, only little is known about the specific SYNCRIP target mRNAs that mediate its effect on neuronal morphogenesis and function. Here, we present a comprehensive characterization of the cytoplasmic SYNCRIP mRNA interactome using iCLIP in primary rat cortical neurons. We identify hundreds of bona fide SYNCRIP target mRNAs, many of which encode for proteins involved in neurogenesis, neuronal migration and neurite outgrowth. From our analysis, the stabilization of mRNAs encoding for components of the microtubule network, such as doublecortin (Dcx), emerges as a novel mechanism of SYNCRIP function in addition to the previously reported control of actin dynamics. Furthermore, we found that SYNCRIP interacts with miRISC and synergizes with pro-neural miRNAs, such as miR-9. Based on our findings, we propose a model whereby SYNCRIP promotes early neuronal differentiation by a two-tier mechanism involving the stabilization of pro-neural mRNAs by direct 3’UTR interaction and the repression of anti-neural mRNAs in a complex with neuronal miRISC. Together, our findings provide a rationale for future studies investigating the function of SYNCRIP in mammalian brain development and disease.
2021-05-05 | GSE149561 | GEO
Project description:Shutdown is a component of the Drosophila piRNA biogenesis machinery
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Project description:SYNCRIP depletion results in HSCs losing their self renewal abilities. Single cell sequencing was conducted in SYNCRIP WT and KO bone marrow LK (lineage -, cKit+) cells to decipher the effect of Syncrip deletion on cellular identities along the hematopoietic hierarchy, and to gain an in-depth assessment of the transcriptomic changes in different cell types upon SYNCRIP loss.
2023-03-01 | GSE202421 | GEO
Project description:Alterations in SYNCRIP activity were found to alter gene transcription in leukemia cells. The effects of transcription alterations on expression of the corresponding proteins were investigated by LC/MSMS
2023-05-10 | PXD019779 | Pride
Project description:The development of the mammalian neocortex is precisely regulated by temporal gene expression, yet the temporal regulatory mechanisms of cortical neurogenesis, particularly how radial glial cells (RGCs) sequentially generate deep to superficial neurons, remain unclear. Here, the hnRNP family member Syncrip (hnRNP Q) is identified as a key modulator of superficial neuronal differentiation in neocortical neurogenesis. Syncrip knockout in RGCs disrupts differentiation and abnormal neuronal localization, ultimately resulting in superficial cortical layer defects as well as learning and memory impairments in mice. Single‐cell RNA sequencing analysis demonstrated that the knockout of Syncrip disrupts the late‐stage neurogenesis, stalling transcriptional progression in RGCs. Mechanistically, Syncrip maintains the transcription of temporal process‐related transcription factors by recruiting stabilization complexes through phase separation, crucially regulating the Notch signaling pathway that determines the fate of RGCs. Furthermore, pathogenic human mutations in Syncrip weaken its phase‐separation capability, failing to form stable complexes normally. Thus, Syncrip acts as a mediator of posttranscriptional regulatory mechanisms, governing the fate progression of RGCs and the advancement of intrinsic temporal programs. This study establishes an intracellular mechanism for posttranscriptional regulation of progressive fate determination in cortical neurogenesis.
2025-01-02 | GSE285581 | GEO
Project description:Sorting nitrifying microorganism with targeted cell sorting
| PRJEB81149 | ENA
Project description:We showed that in response to chemotherapy, dying cancer cells can secrete spliceosomal components into the extracellular space. These therapy-induced secretomes enriched with spliceosomal components promote the chemoresistance of recipient tumor cells. We demonstrated that spliceosomal proteins SNU13 and SYNCRIP can relocalize from dying tumor cells to recipient tumor cells via extracellular vesicles. To investigate whether the increased abundance of splicing factors could be the reason for the acquisition of a more aggressive phenotype by tumor cells, we got SKOV3 cell lines stably overexpressing SYNCRIP or SNU13. These cell lines were more resistant to cisplatin compared to control cell line expressing empty vector. Next, to investigate how the therapy response is formed in tumor cells with and without overexpression of spliceosomal proteins SNU13 or SYNCRIP, we performed RNAseq analysis of these cells before and 24 hours after cisplatin treatment. Enrichement analyses showed that in response to cisplatin, genes associated with DNA repair and cell cycle regulation were upregulated in cancer cell lines overexpressing SYNCRIP or SNU13 compared with control cells. This study revealed previously unknown signaling molecules in the microenvironment of ovarian cancer that have potential clinical significance.
2024-04-24 | GSE241913 | GEO
Project description:RNA binding proteins (RBPs) tightly control mRNA abundance, stability and translation while mutations or altered expression of specific factors can drive malignancy1,2. However, the identity of the RBPs that govern cancer stem cell self-renewal remains poorly characterized. The MSI2 RBP is a central regulator of translation of the cancer stem cell program3-5,6. Here we report, through proteomics analysis of the MSI2 interacting RBP network and functional shRNA screening, 24 genes required for in vivo leukemia, 20 of which are direct MSI2 protein interactors. Seven of these shRNA screen hits were retested in vitro and found to be required for myeloid colony formation. SYNCRIP (also known as HNRP-Q or NSAP1) was the most differentially required gene between normal (c-kit enriched cells) and myeloid leukemia cells. SYNCRIP is highly expressed in mouse and human leukemia cells and its depletion increases apoptosis, differentiation and delays leukemogenesis. Gene expression profiling of SYNCRIP depleted cells demonstrates a loss of the MLL-AF9 and HOXA9 leukemia stem cell gene associated program. SYNCRIP interacts with MSI2 indirectly through shared mRNA targets (such as Hoxa9, Myc and Ikzf2) and MSI2 or HOXA9 overexpression rescues the effects of SYNCRIP depletion. Strikingly, the shRNA-SYNCRIP gene expression signature can predict survival in AML patients. Overall, we uncovered a functionally dysregulated riboproteome in cancer that can be further distinguished from normal cells and propose that targeting this network could result in a novel therapeutic strategy in eradicating cancer stem cells.
2017-04-24 | GSE74178 | GEO
Project description:Identifying SYNCRIP RNA-binding targets in HSC and MPP populations, in order to uncover which direct targets influence SYNCRIP's role in maintaining HSCs self renewal capacity.
2023-03-01 | GSE202464 | GEO