GONUTS has been updated to MW1.31 Most things seem to be working but be sure to report problems.
You don't have sufficient rights on this wiki to edit tables. Perhaps you need to log in. Changes you make in the Table editor will not be saved back to the wiki
Tanaka, SS, Nakane, A, Yamaguchi, YL, Terabayashi, T, Abe, T, Nakao, K, Asashima, M, Steiner, KA, Tam, PP and Nishinakamura, R (2013) Dullard/Ctdnep1 modulates WNT signalling activity for the formation of primordial germ cells in the mouse embryo. PLoS ONE 8:e57428
Dullard/Ctdnep1 is a member of the serine/threonine phosphatase family of the C-terminal domain of eukaryotic RNA polymerase II. Embryos lacking Dullard activity fail to form primordial germ cells (PGCs). In the mouse, the formation of PGCs is influenced by BMP4 and WNT3 activity. Although Dullard is reputed to negatively regulate BMP receptor function, in this study we found mutations in Dullard had no detectable effect on BMP4 and p-Smad activity. Furthermore Dullard mutations did not influence the dosage-dependent inductive effect of Bmp4 in PGC formation. However, Dullard may function as a positive regulator of WNT signalling. Combined loss of one copy each of Dullard and Wnt3 had a synergistic effect on the reduction of PGC numbers in the compound heterozygous embryo. In addition, loss of Dullard function was accompanied by down-regulation of WNT/β-catenin signalling activity and a reduction in the level of Dishevelled 2 (Dvl2). Therefore, Dullard may play a role in the fine-tuning of WNT signalling activity by modulating the expression of ligands/antagonists and the availability of Dvl2 protein during specification of the germ cell lineage.
Adaptor Proteins, Signal Transducing/genetics; Adaptor Proteins, Signal Transducing/metabolism; Animals; Bone Morphogenetic Protein 4/genetics; Bone Morphogenetic Protein 4/metabolism; Cell Lineage/genetics; Embryo, Mammalian; Gene Expression Regulation, Developmental; Germ Cells/cytology; Germ Cells/metabolism; Heterozygote; Homozygote; Mice; Morphogenesis/genetics; Mutation; Phosphoprotein Phosphatases/deficiency; Phosphoprotein Phosphatases/genetics; Phosphoproteins/genetics; Phosphoproteins/metabolism; Signal Transduction/genetics; Smad Proteins/genetics; Smad Proteins/metabolism; Wnt3 Protein/genetics; Wnt3 Protein/metabolism; beta Catenin/genetics; beta Catenin/metabolism