|
|
|
|
|
|
|
||||
| Home Help Feedback Subscriptions Archive Search Table of Contents | ||||
|
Fig. 7. Hindbrain and spinal cord defects associated with loss of Cdx function
are not rescued by posterior Hox gene overexpression. (A-I)
Branchial motor neuron distribution (A-C, GFP-positive cells), hindbrain
markers krx20 (D-I, red) and val (D-F, purple), and spinal
cord oligodendtrocyte marker olig2 (G-I, purple staining), in
cdx1a/cdx4-deficient zebrafish embryos injected with 25 pg of
hoxc6a and hoxa9a mRNA. (A-C) At 50 hpf, control and
hoxc6a and hoxa9a mRNA-injected
cdx1a/cdx4-deficient, isl1:GFP transgenic embryos show
GFP-positive branchiomotor neurons throughout the posterior CNS. (D-I) At the
20-somite stage (19 hpf), hoxc6a and hoxa9a overexpression
in cdx1a/cdx4-deficient embryos results in reduced krx20
expression in r3 and r5 and its loss in the posterior CNS (E,F,H,I, red;
caudal expression indicated with an arrowhead), as compared with uninjected
controls (D,G and Fig. 2).
(D-F) val expression is maintained in r5/6 and posterior CNS of
cdx1a/cdx4-deficient embryos overexpressing posterior Hox genes (see
Fig. 2 for wild-type control).
(G,I) Posterior Hox gene overexpression does not rescue spinal cord
olig2 expression in cdx1a/cdx4-deficient embryos (see
Fig. 1 for wild-type control).
Embryos shown in lateral (A-C) or dorsal (D-I) views, anterior to the left.
Asterisk indicates val expression in hindbrain and posterior CNS.
Arrowhead indicates ectopic krx20 expression in the posterior CNS. A
minimum of 15 embryos in three independent experiments were analyzed, with
more than 90% of embryos displaying the phenotypes shown. Scale bars: 100
µm.
|
