| Added by | standudu |
|---|---|
| Group name | EquipeCTCS |
| Item Type | Journal Article |
| Title | The Wnt-target gene Dlk-1 is regulated by the Prmt5-associated factor Copr5 during adipogenic conversion |
| Creator | Paul et al. |
| Author | Conception Paul |
| Author | Claude Sardet |
| Author | Eric Fabbrizio |
| Abstract | Protein arginine methyl transferase 5 (Prmt5) regulates various differentiation processes, including adipogenesis. Here, we investigated adipogenic conversion in cells and mice in which Copr5, a Prmt5- and histone-binding protein, was genetically invalidated. Compared to control littermates, the retroperitoneal white adipose tissue (WAT) of Copr5 KO mice was slightly but significantly reduced between 8 and 16 week/old and contained fewer and larger adipocytes. Moreover, the adipogenic conversion of Copr5 KO embryoid bodies (EB) and of primary embryo fibroblasts (Mefs) was markedly delayed. Differential transcriptomic analysis identified Copr5 as a negative regulator of the Dlk-1 gene, a Wnt target gene involved in the control of adipocyte progenitors cell fate. Dlk-1 expression was upregulated in Copr5 KO Mefs and the Vascular Stromal Fraction (VSF) of Copr5 KO WAT. Chromatin immunoprecipitation (ChIP) show that the ablation of Copr5 has impaired both the recruitment of Prmt5 and ?-catenin at the Dlk-1 promoter. Overall, our data suggest that Copr5 is involved in the transcriptional control exerted by the Wnt pathway on early steps of adipogenesis. |
| Publication | Biology Open |
| Volume | 4 |
| Issue | 3 |
| Pages | 312-316 |
| Date | Feb 13, 2015 |
| Journal Abbr | Biol Open |
| Language | eng |
| DOI | 10.1242/bio.201411247 |
| ISSN | 2046-6390 |
| Library Catalog | PubMed |
| Extra | PMID: 25681392 PMCID: PMC4359737 |
| Tags | ?-catenin, Adipocyte, co-senior/ corresponding authors, Copr5, corresponding, Differentiation, Dlk-1, first, first-last-corresponding, original, Prmt5 |
| Date Added | 2019/05/31 - 12:02:23 |
| Date Modified | 2022/08/01 - 16:12:37 |
| Notes and Attachments | PubMed entry (Attachment) Texte intégral (Attachment) |
Institut de Recherche en Cancérologie de
