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Effect of rhpn2 knowout on gene expression of zebrafish embryos at 72 hpf (hours post fertilization) .

ABSTRACT: Hearing impairment due to hair cell damage has always been a problem for deaf patients，and there are many unknown genes for deafness.Presently, we have established a zebrafish model that exhibits significant hearing loss induced by hair cell damged with rhpn2 was knockouted. Utilizing this model, we analyzed and compared the differentially expressed genes of wild type and rhpn2 mutant embryos. The results revealed that 631 genes were down-regulated significantly in rhpn2 mutant embryos, respectively, compared with control.

ORGANISM(S): Danio rerio

PROVIDER: GSE283253 | GEO | 2024/12/31

REPOSITORIES: GEO

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Project description:Li-Fraumeni syndrome (LFS) is a disorder due to inherited mutations in the TP53 gene resulting in an increased risk of developing several types of cancer. MicroRNA miR-34a has been implicated downstream of p53 on the basis of being a direct transcriptional target and, when over-expressed, having pro-apoptotic phenotypes in cell lines. Moreover, miR-34a has been shown to be a modifier gene in the context of LFS, since its epigenetic silencing increases the likelihood of tumour development in patients with mutant TP53. However, the in vivo consequences of miR-34 loss are still unclear. For example, mice lacking all three (a,b,c) miR-34 homologs show no detectable abnormalities in p53 responses. The relative expression of different miR-34 genes in zebrafish was studied using qRT-PCR with specific assays. The miR-34a, miR-34b and miR-34c display unique onset of developmental expression and expression levels, with miR-34a being the most abundant and constant in expression. All of the miR-34 genes also showed clear induction by p53 when DNA-damaging treatments are performed. Using CRISPR-Cas9 technology, we generated a zebrafish miR-34a deletion mutant to further investigate the roles of miR-34a on its own and its association with the p53 pathway. Predictably, a miR-34a deletion mutant demonstrated absence of miR-34a, though without miR-34b and miR-34c compensation beyond baseline expression levels. Mutants survive to adulthood, show no overt phenotypes and have normal apoptotic responses to DNA-damaging irradiation or camptothecin treatments. To further explore the effects of miR-34a, we performed gene expression profiling using RNA-seq of wild-type and miR-34a deletion mutant zebrafish embryos at 72 hpf. We wanted to explore how miR-34a loss affects differentiated organs in larval zebrafish. This resulted in 389 genes UP and 374 genes DOWN at 1.5-fold change and FDR < 0.05. There was no significant enrichment of predicted miR-34a target genes among the differentially regulated genes but some interesting biological trends were found and will be described in the paper associated with this dataset.

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Effect of rhpn2 knowout on gene expression of zebrafish embryos at 72 hpf (hours post fertilization) .

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