Fig. 9. Regulatory interactions among the Hoxa1, Hoxb1 and Hoxb2 genes. (A-F) Dorsal views of Hoxb1 expression in wild-type (A,C,E) and Hoxb2 mutants (B,D,F) at 8.5 (A,B), 9.5 (C,D) and 10.5 (E,F) dpc. Expression of Hoxb1 is initiated (A,B) but not properly maintained (C-F) in the Hoxb2 mutants. (G-O) Expression of a Hoxb1 lacZ transgene (HL5) in wild type (G,J,M), and Hoxb2 mutants (H,I,K,L,N,O) at 9.5 (G-I), 10.5 (J-L) and 12.5 (M-O) dpc in side views of whole mount embryos (G-I) and dorsal views of flat mounted hindbrains (J-O). Expression of the HL5 transgene is variable in the Hoxb2 mutants (H,I,K,L,N,O). Note also that lacZ expression is maintained in migrating fbms in the wild type (J,M) and in a proportion of migrating fbms in some (K,N), but not all (L,O), Hoxb2 embryos. (P) The regulatory interactions among the three genes. Hoxb1 and Hoxa1 expression is initiated through the action of retinoids (green line). In turn, Hoxa1, Hoxb1 and co-factors Pbx/Meis establish the expression of the latter in the r4 territory (orange line), which is subsequently maintained through Hoxb1 autoregulation (red arrow). Hoxb2 directly or indirectly (broken blue arrow) feedback upon Hoxb1 to maintain its expression in r4. An indirect contribution could be achieved through a requirement for Hoxb2 in the maintenance of the r4 territory. Hoxb1 and Hoxb2 synergise to regulate target genes pertaining to segmental identity and neurogenesis in r4.