IRLnc: a novel functional noncoding RNA contributes to intramuscular fat deposition.
IRLnc: a novel functional noncoding RNA contributes to intramuscular fat deposition.
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IRLnc：一种新型功能性非编码 RNA 有助于肌内脂肪沉积
DOI：
10.1186/s12864-020-07349-5
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发表时间：
2021-02-01
期刊：
影响因子：
4.4
通讯作者：
Wang L
中科院分区：
文献类型：
--
作者：
Wang L;Zhou ZY;Zhang T;Zhang L;Hou X;Yan H;Wang L
动物肌肉脂肪（IMF）与肉质和胰岛素抵抗有关。研究IMF分解的遗传机制对猪肉品质及肥胖、2型糖尿病等疾病的治疗具有积极意义。本研究利用IMF性状分离群体进行RNA测序，分析基因和长基因间非编码RNA （lincRNAs）对IMF的联合或独立作用。结果26个基因，包括6个lincRNA基因在高、低imf猪中表达显著差异。有趣的是，一个名为IMF相关lincRNA （IRLnc）的lincRNA基因不仅在100种脊椎动物中有292bp的保守区，而且在猪和人类中也有保守的上游和下游基因（< 10kb）。实时定量聚合酶链反应（RT-qPCR）验证研究表明，位于irlnc下游的核受体亚家族4组A成员3 （NR4A3）与irlnc具有相似的表达模式。rnai介导的功能缺失筛选发现，atirlncsilencing可以抑制nr4a3的RNA和蛋白表达。原位杂交共表达实验表明，atirlnc可直接结合toNR4A3。由于thenr4a3可以调节儿茶酚胺的分解代谢，从而影响胰岛素敏感性，我们推断atirlc通过调节nr4a3的表达影响IMF的分解。结论发现一种新的功能性非编码变异dirlnchas通过调控nr4a3的表达参与了IMF。这些发现为治疗人类胰岛素抵抗和改善动物肉质提供了新的机制途径。
BackgroundIntramuscular fat (IMF) is associated with meat quality and insulin resistance in animals. Research on genetic mechanism of IMF decomposition has positive meaning to pork quality and diseases such as obesity and type 2 diabetes treatment. In this study, an IMF trait segregation population was used to perform RNA sequencing and to analyze the joint or independent effects of genes and long intergenic non-coding RNAs (lincRNAs) on IMF.ResultsA total of 26 genes including six lincRNA genes show significantly different expression between high- and low-IMF pigs. Interesting, one lincRNA gene, named IMF related lincRNA (IRLnc) not only has a 292-bp conserved region in 100 vertebrates but also has conserved up and down stream genes (< 10 kb) in pig and humans. Real-time quantitative polymerase chain reaction (RT-qPCR) validation study indicated that nuclear receptor subfamily 4 group A member 3 (NR4A3) which located at the downstream ofIRLnchas similar expression pattern withIRLnc. RNAi-mediated loss of function screens identified thatIRLncsilencing could inhibit both of the RNA and protein expression ofNR4A3. And the in-situ hybridization co-expression experiment indicates thatIRLncmay directly binding toNR4A3. As theNR4A3could regulate the catecholamine catabolism, which could affect insulin sensitivity, we inferred thatIRLncinfluence IMF decomposition by regulating the expression ofNR4A3.ConclusionsIn conclusion, a novel functional noncoding variation namedIRLnchas been found contribute to IMF by regulating the expression ofNR4A3. These findings suggest novel mechanistic approach for treatment of insulin resistance in human beings and meat quality improvement in animal.
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