Figure 7: Manipulation of Gα12/13 and RhoA signalling influences CNS mbp expression in gpr56 mutants.
From: The adhesion GPCR Gpr56 regulates oligodendrocyte development via interactions with Gα12/13 and RhoA
(a–d) Injection of morpholinos (3MO) targeting Gα12/13 signalling (gna12-MO, gna13a-MO and gna13b-MO, 1 ng each), constitutively active rhoa synthetic mRNA (10 pg), or phenol-red control yielded embryos with (d) WT, (c) reduced, (b) strongly reduced or (a) nearly absent CNS mbp expression at 65 hpf by WISH (dorsal view shown, anterior is up, white arrows denote CNS mbp expression). We scored mbp expression as follows: 3=WT, 2=reduced, 1=strongly reduced, 0=nearly absent. (e) Phenotypic distribution by genotype and treatment (1 ng 3MO or control-injected). (f) Quantification of CNS mbp score by genotype and treatment (1 ng 3 MO or control-injected). (f) Respective P values: control WT versus control heterozygote: P<0.077; control WT versus control mutant: P<0.0004; 3MO-injected WT versus 3MO-injected heterozygote: P<1.33 × 10−05; 3MO-injected WT versus 3MO-injected mutant: P<2.59 × 10−6). (i) Phenotypic distribution by genotype and treatment (10 pg consitutively active RhoA (rhoV14) or control-injected) (j) Quantification of CNS mbp score by genotype and treatment (10 pg consitutively active RhoA (rhoV14) or control-injected). Respective P-values: control WT versus control mutant: P<0.0009; OE WT versus OE mutant: P<0.343. (g,h,k,l) All analysed injected embryos were morphologically normal. Student’s t-test used to test for statistical significance and error bars are shown as±s.d. Two technical replicates were performed for the 3MO and the OE experiment. NS, not significant.
