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NFIC overexpression perturbs normal haematopoeisis by promoting myeloid differentiaon

ABSTRACT: NFIC overexpression perturbs normal haematopoeisis by promoting myeloid differentiaon

PROVIDER: PRJNA824534 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18680432.fastq.gz	Fastqsanger.gz
	SRR18680433.fastq.gz	Fastqsanger.gz
	SRR18680434.fastq.gz	Fastqsanger.gz
	SRR18680435.fastq.gz	Fastqsanger.gz
	SRR18680436.fastq.gz	Fastqsanger.gz

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NFIC overexpression perturbs normal haematopoeisis by promoting myeloid differentiaon

Project description:Nuclear factor I-C belongs to a family of CTF binding transcription factor which is known for its role cellular differentiation. In our recent study we identified increased expression of NFIC in. AML samples as compared to normal haematpoitic stem and progenitor cells (HSPCs). We also found that overexpression of NFIC in cord blood derived HSPCs perturbed normal haematopoiesis by increasing monocyte production. Therefore in this analysis we aimed to identify the effect of NFIC overexpression in normal HSPCs at single cell level using single cell RNA (scRNA) sequencing. Cluster analysis based on the cellular and functional identities, identified eight clusters according to their terminal differentiation as monocytes, erythrocytes, dendritic cells (DC), megakaryocytes, neutrophils, megakaryocyte-erythroid progenitor cells, basophil/mast progenitor cells and eosinophils. We found that NFIC overexpressing CD34+ HSPCs had increased percentage of monocytes as compared to control. To understand the molecular basis of this, we focussed our analysis on monocytes to determine changes in mRNA expression following NFIC overexpression. We identified 164 and 88 significantly up-regulated and down-regulated genes, respectively (p<0.05, FDR<0.05) in NFIC overexpressing monocytes as compared to control. Pathway analysis identified enrichment in genes involved in mTOR signalling, cancer cell death and survival, energy metabolism pathways and oxidative phosphorylation. Therefore our scRNA suggested that NFIC play a role in monocytic growth development and its overexpression may lead to monocytic bias in normal haematopoiesis.

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An Nfic-Hedgehog Signaling Cascade Regulates Tooth Root Development

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IGF2BP2-regulated alternative splicing of NFIC causes excessive granulosa cell proliferation in PCOS [IRIP-seq]

Project description:The expression of IGF2BP2 in GCs from PCOS patients was detected using RT-qPCR and western blot. We captured IGF2BP2-interacting transcripts, global transcriptome together with alternative splicing by RNA immunoprecipitation sequencing (RIP-seq) and RNA sequencing (RNA-seq). KGN cells transfected with IGF2BP2 overexpressing plasmids and nuclear factor 1 C-type (NFIC) siRNAs, were applied to CCK-8, EdU and TUNEL assays. IGF2BP2 was highly expressed in GCs from PCOS patients. As a RBP, it preferentially bound to the 3’and 5’UTRs of mRNAs with GGAC motif and a newly found GAAG motif. The overexpression of IGF2BP2 changed the transcriptome profile of KGN cells. IGF2BP2 functioned to regulate alternative splicing events (ASEs) and promote cell proliferation through inhibiting exon skipping events of NFIC. In conclusion, we demonstrated that IGF2BP2 promotes granulosa cell proliferation via regulating alternative splicing of NFIC in PCOS. The findings help to better understand the roles of IGF2BP2 in the pathogenesis of PCOS.

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