Prmt7 is dispensable in tissue culture models for adipogenic differentiation [v1; ref status: indexed, http://f1000r.es/2im]

Protein arginine methylation is a common posttranslational modification that has been implicated in numerous biological processes including gene expression. The mammalian genome encodes nine protein arginine methyltransferases (Prmts) that catalyze monomethylation, asymmetric dimethylation, and symmetric dimethylation on arginine residues. Protein arginine methyltransferase 7 (Prmt7) is categorized as a type II and type III enzyme that produces symmetric dimethylated arginine and monomethylated arginine, respectively. However, the biological role of Prmt7 is not well characterized. We previously showed that Prmt5, a type II Prmt that associates with Brg1-based SWI/SNF chromatin remodeling complex, is required for adipocyte differentiation. Since Prmt7 also associates with Brg1-based SWI/SNF complex and modifies core histones, we hypothesized that Prmt7 might play a role in transcriptional regulation of adipogenesis. In the present study, we determined that the expression of Prmt7 did not change throughout adipogenic differentiation of C3H10T1/2 mesenchymal cells. Knockdown or over-expression of Prmt7 had no effect on lipid accumulation or adipogenic gene expression in differentiating C3H10T1/2 cells or in C/EBPα-reprogrammed NIH3T3 fibroblasts. Based on these results, we conclude that Prmt7, unlike Prmt5, is dispensable for adipogenic differentiation in tissue culture models. Anthony N. Imbalzano ( ) Corresponding author: [email protected] Hu YJ, Sif S, Imbalzano AN (2013) Prmt7 is dispensable in tissue culture models for adipogenic differentiation [v1; ref How to cite this article: status: indexed, ] 2013, :279 (doi: 10.12688/f1000research.2-279.v1) http://f1000r.es/2im F1000Research 2 © 2013 Hu YJ et al. This is an open access article distributed under the terms of the , which Copyright: Creative Commons Attribution Licence permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Data associated with the article are available under the terms of the (CC0 1.0 Public domain dedication). Creative Commons Zero "No rights reserved" data waiver This work was supported by NIH grants DK084278 to ANI and SS and GM56244 to ANI. ANI is a member of the UMass Grant information: Medical School Diabetes and Endocrine Research Center, supported by the National Institutes of Health grant DK32520. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Competing Interests: No competing interests were disclosed. 18 Dec 2013, :279 (doi: 10.12688/f1000research.2-279.v1) First Published: 2 13 Feb 2014, :279 (doi: 10.12688/f1000research.2-279.v1) First Indexed: 2 Referees