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Fig. 3
β-arrestins control the level of Cxcl12a in the tissue and can direct PGC migration. (A) In embryos depleted for endogenous Cxcl12a and provided with uniform Cxcl12a (injection of MO-resistant cxcl12a mRNA), germ cells accumulate in regions depleted of β-arrestin (red). Such primordial germ cell (PGC) localization is not observed in clones in which β-arrestin was not affected and depends on Cxcl12a and Cxcr7b function. The percentage of PGCs located in each domain in 11-hpf embryos was determined and an average among the embryos (N) for each treatment was calculated. Error bars indicate s.e.m. A significant difference (P<0.001, Student’s t-test) was observed for the experiment shown on the left. (B) A typical result for the experiments shown in A, in which β-arrestin activity is similar in regions A and B (control MO) or is knocked down in region B (β-arrestin MOs). (C) Generation of clones depleted of β-arrestin (or control clones) in embryos uniformly expressing CyPet (a cyan fluorescent protein derivative), Cxcr7b and Cxcl12-Venus. (D) Intensity profiles of Cxcl12a-Venus in control chimera (top) and β-arrestin morphant chimera (bottom) measured from the embryos presented in C at 11 hpf. a.u., arbitrary units.