LncPLAAT3-AS Regulates PLAAT3-Mediated Adipocyte Differentiation and Lipogenesis in Pigs through miR-503-5p

Abstract

Animal fat deposition has a significant impact on meat flavor and texture. However, the molecular mechanisms of fat deposition are not well understood. LncPLAAT3-AS is a naturally occurring transcript that is abundant in porcine adipose tissue. Here, we focus on the regulatory role of lncPLAAT3-AS in promoting preadipocyte proliferation and adipocyte differentiation. By overexpressing or repressing lncPLAAT3 expression, we found that lncPLAAT3-AS promoted the transcription of its host gene PLAAT3, a regulator of adipocyte differentiation. In addition, we predicted the region of lncPLAAT3-AS that binds to miR-503-5p and showed by dual luciferase assay that lncPLAAT3-AS acts as a sponge to absorb miR-503-5p. Interestingly, miR-503-5p also targets and represses PLAAT3 expression and helps regulate porcine preadipocyte proliferation and differentiation. Taken together, these results show that lncPLAAT3-AS upregulates PLAAT3 expression by absorbing miR-503-5p, suggesting a potential regulatory mechanism based on competing endogenous RNAs. Finally, we explored lncPLAAT3-AS and PLAAT3 expression in adipose tissue and found that both molecules were expressed at significantly higher levels in fatty pig breeds compared to lean pig breeds. In summary, we identified the mechanism by which lncPLAAT3-AS regulates porcine preadipocyte proliferation and differentiation, contributing to our understanding of the molecular mechanisms of lipid deposition in pigs.

Gene loss and relaxed selection of plaat1 in vertebrates adapted to low-light environments

“…Plaat3's absence or divergence outside of mammals is also noteworthy, as it plays vital roles in obesity, cancer invasion and vitamin-A storage [57][58][59]. Remarkably, in the course of this work, we observed the venomous mammal Sorex araneus had more than 30 duplications of plaat3, which is also present in the salivary transcriptome of another venomous shrew, Blarina brevicauda, which suggests that plaat3 might have been recruited into the venom proteome in shrews.…”

Loss of phospholipase PLAAT3 causes a mixed lipodystrophic and neurological syndrome due to impaired PPARγ signaling

“…(41,(45)(46)(47) Furthermore, our data are in line with earlier studies suggesting a central role for PLAAT3 in adipocyte differentiation in several species. (19)(20)(21) A close link between PLAAT3 and PPARγ is supported by a murine adipocyte differentiation study demonstrating that Plaat3 mRNA levels started to increase between 6 and 12h after Pparγ-mediated initiation of differentiation. (19) A similar observation was made for human PLAAT3 transcripts whose expression began to rise 6h after induction of human pre-adipocyte differentiation and continued to increase during adipogenesis, like PPARγ, whose expression started a few hours earlier.…”

“…(5) Other studies have suggested an important role of PLAAT3 in adipocyte differentiation. (19)(20)(21) We used Plaat3 -/mice-derived inguinal WAT samples (7) for morphological and multiomics studies to further clarify the pathogenic mechanism of PLAAT3-related LS. In total, we collected 12 inguinal Plaat3 -/-WAT biopsy specimens and 12 Plaat3 +/inguinal WAT control specimens.…”

Identification of a Novel Long Non-Coding RNA G8110 That Modulates Porcine Adipogenic Differentiation and Inflammatory Responses

“…Meanwhile, in pigs, for instance, PU.1 antisense lncRNA transcribed from porcine PU.1 inhibits the translation of PU.1 mRNA and promotes adipose production [33]. The lncRNA PLA2G16-AS regulates the expression of PLA2G16 by complementing the host gene, which plays an important role in porcine fat deposition [34,35]. In this paper, we explore the potential molecular mechanism of lncRNA G8110 in regulating adipocyte differentiation.…”