Expression profiling of lncRNAs and mRNAs reveals regulation of muscle growth in the Pacific abalone, Haliotis discus hannai

• Published in: Scientific reports Vol. 8; no. 1; pp. 16839 - 9
• Main Authors: Huang, Jianfang, Luo, Xuan, Zeng, Liting, Huang, Zekun, Huang, Miaoqin, You, Weiwei, Ke, Caihuan
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 15.11.2018; Nature Publishing Group
• Subjects: 1-Phosphatidylinositol 3-kinase; 631/61/514/1949; 704/829/826; AKT protein; Antisense RNA; Bioinformatics; Haliotis discus hannai; Humanities and Social Sciences; Insulin; MAP kinase; multidisciplinary; Physical growth; Ribonucleic acid; RNA; Science; Science (multidisciplinary); Signal transduction; Adductor Muscle Samples; Muscle Growth; Discus Hannai; Pacific Abalone; Extracellular Regulated Kinases 1 And 2 (ERK1/2)
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/s41598-018-35202-z

Long non-coding RNAs (lncRNAs) are known to play a major role in the epigenetic regulation of muscle development. Unfortunately there is little understanding of the mechanisms with which they regulate muscle growth in abalone. Therefore, we used RNA-seq to study the muscle transcriptomes of six Haliotis discus hannai specimens: three large (L_HD group) and three small (S_HD group). We identified 2463 lncRNAs in abalone muscle belonging to two subtypes: 160 anti-sense lncRNAs and 2303 intergenic lncRNAs (lincRNAs). In the L_HD group, we identified 204 significantly differentially expressed lncRNAs (55 upregulated and 149 downregulated), and 2268 significantly differentially expressed mRNAs (994 upregulated and 1274 downregulated), as compared to the S_HD group. The bioinformatics analysis indicated that lncRNAs were relate to cell growth, regulation of growth, MAPK signaling pathway, TGF-β signaling pathway, PI3K-Akt and insulin signaling pathway, which involved in regulating muscle growth. These findings contribute to understanding the possible regulatory mechanisms of muscle growth in Pacific abalone.