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Mesendoderm differentiation of WT and PHD2 knockout mESCs (scRNA-seq)

ABSTRACT: mesendoderm differentiation of WT and PHD2 knockout mESCs (scRNA-seq)

PROVIDER: PRJNA1028512 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26394382_1.fastq.gz	Fastqsanger.gz
	SRR26394382_2.fastq.gz	Fastqsanger.gz
	SRR26394383_1.fastq.gz	Fastqsanger.gz
	SRR26394383_2.fastq.gz	Fastqsanger.gz
	SRR26394384_1.fastq.gz	Fastqsanger.gz

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mesendoderm differentiation of WT and PHD2 knockout mESCs (scRNA-seq)

Project description:To study the cell composition and gene expression profile in the mesendoderm differentiation of WT and PHD2 knockout, we performed scRNA-seq on the cells collected from the differentiation of WT and PHD2 knockout AB2.2 mESCs at differentiation day 4. PHD2 knockoutout mESCs were constructed by CRISPR/Cas9. The differentiation was performed using a non-lineage tendency differentiation protocol.

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Project description:To study the gene expression profile in the mesendoderm differerntiation of control and Hif-1a overexpression, we performed RNA-seq on the total RNA samples collected from the differentiation of control and Hif-1a overexpression AB2.2 mESCs at differentiation day 4.In addition, to study the gene expression profile in the mesendoderm differerntiation of Hif-1a knockdown under normoxia and hypoxia, we performed RNA-seq on the total RNA samples collected from the differentiation of Hif-1a knockdown AB2.2 mESCs under normoxia or hypoxia at differentiation day 4. Cell lines were built by infecting AB2.2 cells with lentiviruses. Each group contained three biological replicates. The expression matrix was obtained by Hisat2 followed by Stringtie.

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Project description:Purpose: This study aimed at exploring the deregulated genes in setd2 knockout mESCs compared with wt, more particularly to find the mechanism controlled by setd2,which was required for endoderm differentiation. Methods: Setd2 wt and ko mESCs were generated by deep sequencing, using Illumina GAIIx. Using Avadis NGS (version:1.3) software to analyze the sequence reads that passed quality filter to acquire the expression level of all genes. qRT–PCR validation was performed usingSYBR Green assays. Results: Using an optimized data analysis workflow, we mapped about 80 million sequence reads per sample to the mouse genome (build mm9) and identified 17,827 transcripts in the sted2 wt and ko mESCs. About 2,516 genes were deregulated in setd2 ko mESCs, more than 10 genes were validated using qRT-PCR. Conclusions: Through RNA-seq,we noticed that a subset of genes that related to MAPK signaling pathways were down-regulated in ko mESCs. This provided a bridge to connect setd2 and mESCs endoderm differentiation. One wt and one ko mESCs were generated by deep sequencing, using Illumina GAIIx.

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Quantitative Analysis of Wild Type(wt) and Setd2 knockout(ko) mESCs Transcriptomes [RNA-Seq]

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Project description:Prolyl hydroxylase domain protein 2 (PHD2) is one of the intracellular oxygen sensors that mediates proteasomal degradation of hypoxia-inducible factor (HIF)-α via hydroxylation under normoxia. Because of its canonical function in the hypoxia signaling pathway, PHD2 is generally regarded as a tumor suppressor. However, the effects of PHD2 in tumorigenesis are not entirely dependent on HIF-α. Based on the data obtained from The Cancer Genome Atlas (TCGA) database, we found that the expression of PHD2 is upregulated in non-small cell lung cancer (NSCLC), which accounts for approximately 80-85% of lung cancers, suggesting that PHD2 may play an important role in NSCLC. However, the function of PHD2 in NSCLC remains largely unknown. In this study, we established PHD2-deficient H1299 cells to investigate the function of PHD2 in NSCLC, and found that PHD2 suppressed cell proliferation and metabolism, but induced ROS levels in human NSCLC cells. Further results indicated that the function of PHD2 in NSCLC is dependent on its enzymatic activity and partially independent of HIF. Moreover, we performed RNA-seq and transcriptomics analysis to explore the underlying mechanisms, and identified some potential targets and pathways regulated by PHD2, apart from the canonical HIF-mediated hypoxia signaling pathway. These results provide some clues to uncover novel roles of PHD2 in lung cancer progression.

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