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首页> 外文期刊>BMC Genomics >Whole-genome regulation analysis of histone H3 lysin 27 trimethylation in subclinical mastitis cows infected by Staphylococcus aureus
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Whole-genome regulation analysis of histone H3 lysin 27 trimethylation in subclinical mastitis cows infected by Staphylococcus aureus

机译:金黄色葡萄球菌感染的亚临床乳腺炎奶牛组蛋白H3溶素27三甲基化的全基因组调控分析

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Background S. aureus is one of the major etiological agents causing bovine subclinical mastitis. The regulatory effects of H3K27me3 on gene expression in subclinical S. aureus mastitis cows are unknown. This study aimed to profile genome-wide transcriptional changes regulated by H3K27me3 in bovine lymphocytes applied in subclinical S. aureus mastitis cows and healthy controls. Results A total of 61 differentially expressed genes (DEGs) were detected in subclinical S. aureus mastitis cows compared to the healthy controls, of which 25 DEGs are up-regulated and the rest are down-regulated genes in subclinical S.aureus mastitis cows. The up-regulated genes are mainly involved in the Jak-STAT signaling pathway, cytokine-cytokine receptor interaction, and T cell receptor-signaling pathway, while the down-regulated genes are related to metabolism pathways. Combination analysis of histone methylation and gene expression revealed that H3K27 trimethylation levels in silent genes were higher in subclinical S. aureus mastitis cattle than in healthy cows. The key regions of H3K27me3 target genes related to subclinical S. aureus mastitis were the upstream 2?kb regions of the DEGs relative to transcription start site (TSS). Conclusions The current study provides a novel insight into the interaction between S. aureus and lymphocytes in lactating cows by histone H3 methylation regulation. The differentially expressed genes in bovine lymphocytes regulated by H3K27me3 on upstream 2?kb regions ( IL10, PTX3 and etc.) may relate to S. aureus mastitis susceptibility and could be considered as key candidate genes for anti- S. aureus mastitis study and breeding.
机译:背景金黄色葡萄球菌是引起牛亚临床乳腺炎的主要病因之一。 H3K27me3对亚临床金黄色葡萄球菌乳腺炎母牛基因表达的调节作用尚不清楚。这项研究的目的是分析在亚临床金黄色葡萄球菌乳腺炎母牛和健康对照中使用的牛淋巴细胞中,H3K27me3调节的全基因组转录变化。结果与健康对照相比,在亚临床金黄色葡萄球菌乳牛中共检测到61个差异表达基因(DEG),其中在亚临床金黄色葡萄球菌乳腺牛中检测到25个DEGs上调,其余基因被下调。上调的基因主要参与Jak-STAT信号通路,细胞因子-细胞因子受体的相互作用和T细胞受体的信号通路,而下调的基因与代谢途径有关。组蛋白甲基化和基因表达的组合分析表明,亚临床金黄色葡萄球菌乳腺炎牛的沉默基因中,H3K27三甲基化水平高于健康牛。与亚临床金黄色葡萄球菌乳腺炎有关的H3K27me3靶基因的关键区域是相对于转录起始位点(TSS)的DEGs的上游2?kb区。结论本研究为通过组蛋白H3甲基化调节对金黄色葡萄球菌与泌乳母牛淋巴细胞之间的相互作用提供了新的见解。 H3K27me3在上游2?kb区(IL10,PTX3等)调控的牛淋巴细胞中差异表达的基因可能与金黄色葡萄球菌乳腺炎易感性有关,可以被认为是抗金黄色葡萄球菌乳腺炎研究和繁殖的关键候选基因。 。

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