Lnc9141 a and b play a different role in bovine myoblast proliferation, apoptosis and differentiation

Abstract Previously, our transcriptome sequencing revealed that lnc9141 was differentially expressed in muscles of fetal bovine, calf and adult bovine, which is considered provide the basis for raising the muscle mass. In this study, we identified lnc9141 characters. lnc9141 has different transcription start sites and 3’ alternative splicing sites of exon 1, producing lnc9141-a and lnc9141-b transcripts that were highly expressed in the heart and lung. Moreover, neither lnc9141-a nor lnc9141-b did have the ability to encode proteins. The functions of lnc9141-a and lnc9141-b were explored by cell cycle, EdU and MTT assay. The results showed that lnc9141-a or lnc9141-b overexpression decreased the number of myoblasts in the S phase, and increased the proportion of cells in the G0/G1 phase. Furthermore, overexpressing lnc9141-a and lnc9141-b respectively down-regulated the expression of Cyclin D1. However, lnc9141-a or lnc9141-b interference was found to increase the number of S-phase myoblasts, and up-regulate Cyclin D1 and Cyclin E expression. Through Annexin V-FITC/PI double staining and the expression of apoptosis marker genes (Bax, Bcl2 and Caspase 3), it was found that lnc9141-b could regulate the expression of Bax gene. Meantime, high expression of lnc9141-b could decrease MyHC expression. In addition, the intergenic region between lnc9141 and IRX5 was 2.3 kb, with a head-to-head orientation. The study also revealed that the core regions of the lnc9141 and IRX5 promoter. Our study demonstrated both lnc9141 a and b expression inhibited bovine myoblast proliferation. However, lnc9141-b regulated Bax and MyHC expression. The regulatory mechanism of lnc9141-a and lnc9141-b needs to be further explored.