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Posttranscriptional Control of Neural Progenitors Temporal Dynamics During Neocortical Development by Syncrip

ABSTRACT: Posttranscriptional Control of Neural Progenitors Temporal Dynamics During Neocortical Development by Syncrip

PROVIDER: PRJNA1204921 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31861800_1.fastq.gz	Fastqsanger.gz
	SRR31861800_2.fastq.gz	Fastqsanger.gz
	SRR31861801_1.fastq.gz	Fastqsanger.gz
	SRR31861801_2.fastq.gz	Fastqsanger.gz
	SRR31861802_1.fastq.gz	Fastqsanger.gz

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Posttranscriptional Control of Neural Progenitors Temporal Dynamics During Neocortical Development by Syncrip

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

Posttranscriptional Control of Neural Progenitors Temporal Dynamics During Neocortical Development by Syncrip.

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.

| S-EPMC11848603 | biostudies-literature

The cytoplasmic SYNCRIP mRNA interactome of mammalian neurons

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

Conserved transcriptional regulation by BRN1 and BRN2 in neocortical progenitors drives mammalian neural specification and neocortical expansion

Project description:Conserved transcriptional regulation by BRN1 and BRN2 in neocortical progenitors drives mammalian neural specification and neocortical expansion

| PRJNA953007 | ENA

HyperTRIBE uncovers SYNCRIP RNA binding activity in hematopoietic stem cells (HSCs) and multipotent progenitors (MPPs)

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

single cell RNA-seq in transplanted bone marrow cells from SYNCRIP conditional mouse model

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

Conserved transcriptional regulation by BRN1 and BRN2 in neocortical progenitors drives mammalian neural specification and neocortical expansion

Project description:To investigate BRN1/2 function in neocortical development, we knockout BRN1/2 in the dorsal telencephalon (BRN1/2 cKO) We then performed gene expression profiling analysis using data obtained from scRNA-seq of 13 different mice at E12.5 and E14.5

2024-07-05 | GSE229129 | GEO

Proteomic analysis of SYNCRIP deficient HSPCs

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

Gene expression profiles between mtROShigh and mtROSlow cells dissociated from E14.5 neocortical cells were compared by microarray

Project description:sample collection protocol:We used FACS to separate the E14.5 neocortical cells into high mitochondrial reactive oxygen species (mtROS) and low mitochondrial ROS cell populations and compared their expression profiles. Transition of progenitors through progressive stages of differentiation probably involves dynamic changes in mtROS levels, depending on the needs of the cell. We found that the progenitors had higher levels of mtROS, but these levels significantly decreased with differentiation.

2017-03-30 | E-MTAB-5438 | biostudies-arrayexpress

Transcriptome of ovarian cancer cells overexpressing SYNCRIP or SNU13

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

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