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Long non‐coding RNA NEAT 1 & 2 regulates phosphorylation of SR proteins and PKCβII splicing during 3T3 L1 adipogenesis
Author(s) -
Cooper Denise R,
Carter Gay,
Li Pengfei,
Watson James,
Patel Niketa A
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.941.2
Subject(s) - adipogenesis , sr protein , microbiology and biotechnology , phosphorylation , rna splicing , glut4 , alternative splicing , chemistry , lipid droplet , protein kinase b , biology , rna , glucose uptake , biochemistry , messenger rna , insulin , gene , endocrinology , mesenchymal stem cell
The alternative splicing (AS) of PKCβII on day (D)6 of adipogenesis allows for 3T3‐L1 cells to develop full insulin responsive glucose transport and accumulate lipid droplets. PKCβII activates Akt via mTORC2 and increases glucose transport via membrane fusion of GLUT4 vesicles (BBRC 388 (2009) 554). The regulation of AS is poorly understood during this process. Long non‐coding (lnc) RNAs are key regulatory molecules in differentiating cells. They can organize splicing proteins in the nucleus for phosphorylation. Here we demonstrated the highly regulated expression of NEAT1 & 2 during adipogenesis by RT‐PCR. On D6, NEAT1 & 2 were elevated 2‐ fold vs D0 in union with increased Clk1 kinase and PKCβII expression. Cells were treated with siRNA for NEAT1. On D0, phosphorylation of SR proteins, SRp40 and 55, by Clk1 kinase decreased. Remarkably, PKCβII AS was dysregulated (elevated) by D2. This suggests that lncRNAs may organize serine/arginine rich “SR” splicing proteins via their RRM domains for Clk phosphorylation in AS during differentiation. Regulation of lncRNA levels during adipogenesis may further determine the level of AS activity in combination with Clk1 expression.