lncSAMM50 Enhances Adipogenic Differentiation of Buffalo Adipocytes With No Effect on Its Host Gene

Author:

Zhu Ruirui,Feng Xue,Wei Yutong,Guo Duo,Li Jiaojiao,Liu Qingyou,Jiang Jianrong,Shi Deshun,Huang Jieping

Abstract

Fat deposition is one of the most important traits that are mediated by a set of complex regulatory factors in meat animals. Several researches have revealed the significant role of long non-coding RNAs (lncRNAs) in fat deposition while the precise regulatory mechanism is still largely elusive. In this study, we investigated the lncRNA profiles of adipose and muscle tissues in buffalo by using the Illumina HiSeq 3000 platform. In total, 43,809 lncRNAs were finally identified based on the computer algorithm. A comparison analysis revealed 241 lncRNAs that are differentially expressed (DE) in adipose and muscle tissues. We focused on lncSAMM50, a DE lncRNA that has a high expression in adipose tissue. Sequence alignment showed that lncSAMM50 is transcribed from the antisense strand of the upstream region of sorting and assembly machinery component 50 homolog (SAMM50), a gene involved in the function of mitochondrion and is subsequently demonstrated to inhibit the adipogenic differentiation of 3T3-L1 adipocyte cells in this study. lncSAMM50 is highly expressed in adipose tissue and upregulated in the mature adipocytes and mainly exists in the nucleus. Gain-of-function experiments demonstrated that lncSAMM50 promotes the adipogenic differentiation by upregulating adipogenic markers but with no effect on its host gene SAMM50 in buffalo adipocytes. These results indicate that lncSAMM50 enhances fat deposition in buffalo and provide a new factor for the regulatory network of adipogenesis.

Funder

National Natural Science Foundation of China

Publisher

Frontiers Media SA

Subject

Genetics(clinical),Genetics,Molecular Medicine

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