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Transcriptomes of control and JAG1-deficient cochlea

ABSTRACT: Transcriptomes of control and JAG1-deficient cochlea

PROVIDER: PRJNA795159 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17467435.fastq.gz	Fastqsanger.gz
	SRR17467436.fastq.gz	Fastqsanger.gz
	SRR17467437.fastq.gz	Fastqsanger.gz
	SRR17467438.fastq.gz	Fastqsanger.gz
	SRR17467439.fastq.gz	Fastqsanger.gz

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Transcriptomes of control and JAG1-deficient cochlea

Project description:The aim of this study is to identify the gene targets of the Notch ligand JAG1 in the postnatal cochlea. JAG1 was conditionally deleted in mice carrying both an inducible Cre allele (Sox2CreER) and a floxed (fl) Jag1 allele. Tamoxifen was administered to P0/P1 pups. Cochlear tissues from 6 Sox2CreER/+Jag1fl/fl and wildtype littermate controls were dissected under the dissecting microscope in ice-cold DEPC-treated PBS and stored in RNAlater (Invitrogen) at 4C. The RNAs were purified by RNeasy Micro Kit (QIAGEN). The quality and quantity of RNAs were measured by a 2100 bioanalyzer (Agilent). Illumina compatible sequencing libraries were generated by the University of Rochester Genomics Research Center. Libraries were hybridized to the Illumina flow cell and single-end reads of 100nts were generated. Identification of significantly differentially expressed genes was determined using DeSeq2. We found 548 differentially expressed genes with an adjusted p-value of <0.05, 411 of those genes were significantly upregulated while 137 were significantly downregulated. Analysis of pathways revealed novel genes involved downstream of JAG1-Notch signaling in the postnatal cochlea.

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Project description:We analyzed the transcriptomes of 30 isolated apical OHCs and basal OHCs from rat cochlea, and the results showed that more than 50 genes were differentially expressed and 20 genes were uniquely expressed among these populations. We analyzed these genes with a focus on their functions related to cellular structure and transmembrane channels and their vulnerability to and involvement in hereditary deafness caused by OHC defects. Our results could serve as a guideline for exploring the molecular mechanisms underlying the biological properties of OHCs.

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Project description:Endothelial cell (EC) sensing of fluid shear stress regulates atherosclerosis, a disease of arteries that causes heart attack and stroke. Atherosclerosis preferentially develops at regions of arteries exposed to low oscillatory shear stress (LOSS), whereas high shear regions are protected. We show using inducible EC-specific genetic deletion in hyperlipidaemic mice that the Notch ligands JAG1 and DLL4 have opposing roles in atherosclerosis. While endothelial Jag1 promoted atherosclerosis at sites of LOSS, endothelial Dll4 was atheroprotective. Analysis of porcine and murine arteries and cultured human coronary artery EC exposed to experimental flow revealed that JAG1 and its receptor NOTCH4 are strongly upregulated by LOSS. Functional studies in cultured cells and in mice with EC-specific deletion of Jag1 show that JAG1-NOTCH4 signalling drives vascular dysfunction by repressing endothelial repair. These data demonstrate a fundamental role for JAG1-NOTCH4 in sensing LOSS during disease, and suggest therapeutic targeting of this pathway to treat atherosclerosis.

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