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MRNAseq in control (WT) and Nes:Cre_Qk cKO

ABSTRACT: mRNAseq in control (WT) and Nes:Cre_Qk cKO

PROVIDER: PRJNA510335 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8327930_1.fastq.gz	Fastqsanger.gz
	SRR8327930_2.fastq.gz	Fastqsanger.gz
	SRR8327931_1.fastq.gz	Fastqsanger.gz
	SRR8327931_2.fastq.gz	Fastqsanger.gz
	SRR8327932_1.fastq.gz	Fastqsanger.gz

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mRNAseq in control (WT) and Nes:Cre_Qk cKO

Project description:We sequenced mRNA from mouse E14.5 embryonic cortex to compare gene expression level and alternative splicing events between 2 control (WT) and 2 Qk cKO. A set of tissue specific splicing factors are thought to govern alternative splicing events during neural progenitors (NPC) to neuron transition by regulating neuron specific exons. Here we proposed one such a factor, RNA-binding protein Qki5, which is specifically expressed in neural stem cells. We performed mRNAseq analysis by using mRNAs obtained from developing cerebral cortices in Qk conditional knockout (cKO) mice. Expectedly, we found huge numbers of alternative splicing changes between control and conditional knock-out relative to that of transcripts level changes. Furthermore, DAVID and Meta-scape analysis revealed that affected spliced genes are involved in axon-development and microtubule-based process. Among these, Ninein protein coding mRNA is listed as a Qk protein dependent alternative splicing targets. Interestingly, this exon encodes very long poly-peptides (2,121 nt) and is known as a previously defined dynamic RNA switch during NPC-to-neuron transition. In addition, we validated that the regulation of this large exon is consistent with Qki5 dependent alternative exon inclusion mode obtained from our previous Qki5 HITS-CLIP analysis. Together Qki5 will add to a list factor of alternative splicing in NPC-to-neuron transition.

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Project description:Purpose: The goals of this study are to compare the transcriptomic profile (mRNA-seq) of HD and control patient iPSC-derived neural cells to identify alterations in gene expression Methods: RNA were isolated from HD and control iPSC-derived neural cells. mRNAseq using Illumina Truseq mRNA PolyA+ v2 lib prep and Hiseq 2000. Statistical difference in mRNA levels were calculated with subsequent GO and pathway analysis Results: mRNAseq and statistical analysis revealed 1869 differentially expressed genes between HD and control iPSC-derived neural cells. Conclusions: Our study shows 1869 differentially expressed genes between HD and control iPSC-derived neural cells, and reveals gene networks that relevant to the mechanism of HD pathogenesis.

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