Interference With ACSL1 Gene in Bovine Adipocytes: Transcriptome Profiling of mRNA and lncRNA Related to Unsaturated Fatty Acid Synthesis.

Yanbin Bai,Yuzhu Luo,Zhidong Zhao,Yong Ma,Xiu Liu,Xiangmin Han,Jingsheng Li,Jiqing Wang,Jiang Hu,Shaobin Li,Xupeng Li,Bingang Shi,Zongchang Chen,Sayed Haidar Abbas Raza,Hongshan Tian

doi:10.3389/fvets.2021.788316

Abstract

The enzyme long-chain acyl-CoA synthetase 1 (ACSL1) is essential for lipid metabolism. The ACSL1 gene controls unsaturated fatty acid (UFA) synthesis as well as the formation of lipid droplets in bovine adipocytes. Here, we used RNA-Seq to determine lncRNA and mRNA that regulate UFA synthesis in bovine adipocytes using RNA interference and non-interference with ACSL1. The corresponding target genes of differentially expressed (DE) lncRNAs and the DE mRNAs were found to be enriched in lipid and FA metabolism-related pathways, according to GO and KEGG analyses. The differentially expressed lncRNA- differentially expressed mRNA (DEL-DEM) interaction network indicated that some DELs, such as TCONS_00069661, TCONS_00040771, TCONS_ 00035606, TCONS_00048301, TCONS_001309018, and TCONS_00122946, were critical for UFA synthesis. These findings assist our understanding of the regulation of UFA synthesis by lncRNAs and mRNAs in bovine adipocytes.

Highlights

As a member of the ACSL family (ACSL1, 3, 4, 5, and 6), long-chain acyl-CoA synthase 1 (ACSL1) is needed for the activation, transportation, and degradation of fatty acids (FAs), as well as lipid synthesis [1, 2]
The cultured F3 generation bovine pre-adipocytes were collected on differentiation days 0, 2, 4, 6, and 8, and qRTPCR was performed to determine the relative expression of ACSL1
We transfected three pairs of siRNAs into the bovine adipocytes and determined their expression after 48 h to screen the most efficient siRNA fragments for silencing ACSL1

Summary

Introduction

As a member of the ACSL family (ACSL1, 3, 4, 5, and 6), long-chain acyl-CoA synthase 1 (ACSL1) is needed for the activation, transportation, and degradation of fatty acids (FAs), as well as lipid synthesis [1, 2]. ACSL1 is found on the outer mitochondrial membrane [2] and converts longchain FAs into fatty acyl-CoA to synthesize triglycerides [3], stimulate FA deposition, activate FAs [1], and to enter the β-oxidation pathway [4]. Overexpression of ACSL1 activates and transports FA for the synthesis of diglycerides and phospholipids rather than cholesterol esters [10]. The arachidonic acid levels were further stimulated by the overexpression of ACSL1 [11].

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Discussion

Conclusion