Fig. 2.

Expression of novel Schwann cell genes in pou3f1 +/+ and −/− sciatic nerves at P0 and P9. Sections of sciatic nerves are shown after in situhybridization with antisense probes for pou3f1, LacZ, P₀(Mpz), P₂ (P2), dendrin, 18-138, CRP2, and 21-70 mRNA. A, P0 sciatic nerves. Theleft panels show wild-type nerves (+/+); theright panels show knock-out −/− nerves. pou3f1 hybridizes to +/+ but not to −/− nerves, whereas LacZ is the opposite; these results confirm the genotypes of the tissues. Hybridization to mRNA for P₀, whose expression is independent of pou3f1, is observed in both +/+ and −/− sciatic nerves and serves to demarcate them. Myelin P₂ and CRP2 are expressed in +/+ sciatic nerve, but in pou3f1 mutant nerve, little or no signal is observed. Dendrin and 18-138 hybridization produce faint signals in +/+ and no signals in −/−. At this age, 21-70 mRNAs were not detected. These results demonstrate that differences in expression can be detected by in situ hybridization, and that the genes isolated by RDA are misexpressed in pou3f1 mutant nervesin vivo. B, P9 sciatic nerves. The same probes that were hybridized to P0 sciatic nerves were used to assay expression in P9 sciatic nerves. pou3f1 and LacZ expression confirm the genotypes of the tissues, although by P9, pou3f1 expression is declining, whereas LacZ expression in mutants remains high, as has been observed previously (Jaegle and Meijer, 1998). Myelin P₀mRNA expression confirms no significant differences in P₀expression in +/+ and pou3f1 −/− mice. At P9, myelin P₂and 18-138 expression in mutant sciatic nerve is much stronger than at P0 but remains reduced relative to wild type. Dendrin expression is present in +/+ nerves, but there is little or no signal from mutant nerves. CRP2 expression appears equivalent in +/+ and −/−; at this time, expression is declining in +/+ nerves but is probably increasing in −/− nerves. Faint 21-70 expression can be observed in +/+ nerves but not in −/− nerves. Scale bar, 0.5 mm.