Fig. 6. fgf8-/-; OtxH embryos have a total lack of
Fgf activity and show both a proliferation decrease and a cell death
increase. (A-D) Lateral view of 20-somite stage live embryos
stained with Acridine Orange and cell quantification (n, numbers of
quantified embryos). No change in cell death is observed in
fgf8-/- mutant embryos (compare A with C), while OtxH
shows an increase in dying cells (B), which is enhanced in
fgf8-/-; OtxH (D). These differences are more drastic at
prim-22 stage (wild type: 18±4, n=3; OtxH 26±2,
n=3; fgf8-/-: 12±2, n=3;
fgf8-/-; OtxH: 44.33±6.03, n=3).
(E-H) Dorsal views of prim-22 stage posterior brain immunostained with
the H3 reveal a decrease in proliferation rate in fgf8-/-
mutant (G), while lack of Otx in this context does not worsen the phenotype
(H), see also quantifications. (I-P) erm expression pattern in
the mid/hindbrain region of the genetic context studied at bud stage (dorsal
view, I-L) and at prim-5 stage (lateral view, M-P). This Fgf transcriptional
target is never induced in the presumptive mes/met (arrow) in
fgf8-/- (K,O) or fgf8-/-; OtxH (L,P)
embryos.