IRLnc: a novel functional noncoding RNA contributes to intramuscular fat deposition

BMC Genomics

Hua Yan¹  Ligang Wang¹  Xinhua Hou¹  Lixian Wang¹  Longchao Zhang¹  Tian Zhang²  Zhong-Yin Zhou³ 

[1] Key Laboratory of Farm Animal Genetic Resources and Germplasm Innovation of Ministry of Agriculture of China, Institute of Animal Sciences, Chinese Academy of Agricultural Sciences, 100193, Beijing, China;Key Laboratory of Farm Animal Genetic Resources and Germplasm Innovation of Ministry of Agriculture of China, Institute of Animal Sciences, Chinese Academy of Agricultural Sciences, 100193, Beijing, China;State Key Laboratory Breeding Base of Dao-di Herbs, China Academy of Chinese Medical Sciences National Resource Center for Chinese Materia Medica, 100021, Beijing, China;State Key Laboratory of Genetic Resources and Evolution, Kunming Institute of Zoology, Chinese Academy of Sciences, 650223, Kunming, China;

关键词: Intramuscular fat;    Long non-coding RNA;    Insulin resistance;    Pig;   

DOI  :  10.1186/s12864-020-07349-5

来源: Springer

【 摘 要 】

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 of IRLnc has similar expression pattern with IRLnc. RNAi-mediated loss of function screens identified that IRLnc silencing could inhibit both of the RNA and protein expression of NR4A3. And the in-situ hybridization co-expression experiment indicates that IRLnc may directly binding to NR4A3. As the NR4A3 could regulate the catecholamine catabolism, which could affect insulin sensitivity, we inferred that IRLnc influence IMF decomposition by regulating the expression of NR4A3.ConclusionsIn conclusion, a novel functional noncoding variation named IRLnc has been found contribute to IMF by regulating the expression of NR4A3. These findings suggest novel mechanistic approach for treatment of insulin resistance in human beings and meat quality improvement in animal.

【 授权许可】

CC BY