Abstract
There is growing evidences indicating that long intergenic non-coding RNAs (lincRNAs) play key roles as regulatory molecules in a variety of cellular processes, including gene expression, splicing, apoptosis, and inflammatory regulation. It has garnered significant attention in recent years that lincRNAs could regulate the immune responses to pathogen infections in teleost. Here, we identified a lincRNA linc009 that significantly responded to the Vibrio anguillarum infection in turbot (Scophthalmus maximus). The length of linc009 was 1774 bp and located on turbot chromosome 19. Specifically, we found that linc009 was mainly localized in the nucleus, where it may repress the expression of the target genes by recruiting DNA methyltransferases (DNMTs) to specific gene promoters. In turbot, linc009 was constitutively expressed in the examined tissues, with the highest expression level in kidney and the lowest expression level in muscle. Furthermore, the expression of linc009 was significantly up-regulated after V. anguillarum infection and LPS stimulation. At the same time, the upregulation of linc009 expression inhibited the expression of proinflammatory cytokines (TNF-α and IL-1β), NF-κB, and IKKβ. Finally, apoptosis was analysed in turbot SMK cells. The apoptosis rate of SMK cells increased rapidly following linc009 overexpression. The results of apoptotic analyses suggested that the lncRNA linc009 played a negative role in regulating cell apoptosis. To sum up, our study showed that linc009 could play a negative regulatory role in the innate immunity of turbot by down-regulating the expression of pro-inflammatory factors, which strongly demonstrated that lincRNAs are involved in the antibacterial immune response of turbot. This study provided valuable insights into the function and regulatory mechanism of lncRNAs in teleost.