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Fig. 5. nlk MO enhances the mesoderm defect of wnt8 MOs. (A,B,C)
Wild type, (D,E,F) wnt8 MOs, (G,H,I) nlk MO and (J,K,L)
nlk MO/wnt8 MOs. A,D,G,J were stained for tbx6 at
90% epiboly (vegetal view; dorsal to the top). B,E,H,K were stained with a mix
of opl, pax2, krox20 and myod at 6 to 7 somites (dorsal
view; bars indicate the extent of opl expression). C,F,I,L were left
to develop to 24 hpf (lateral view). tbx6 expression is reduced in
wnt8 (D) and nlk (G) compared with wild type (A), whereas
nlk/wnt8 morphants have a dramatic reduction in tbx6 (J;
double-headed arrows indicate dorsal region of margin where tbx6 is
excluded). wnt8 MO embryos have a greatly expanded opl
domain, and a slightly wider notochord (E; notochord domain delineated by
longitudinal stripes of adaxial myod expression), reflecting the
defects in AP patenting of the neuroectoderm and in DV patterning in the
mesoderm, characteristic of wnt8 morphants. nlk morphants
(H) are slightly shorter than wild type, but have no significant defects in
neuroectoderm or mesoderm patterning. nlk/wnt8 morphants (K) are
dramatically shortened, with significantly broadened expression of neural
markers, reflecting increased dorsalization of the embryos. Only a few trunk
somites are formed, and tail formation does not occur. nlk/wnt8
morphants at 24 hpf (L) are significantly shorter than wild type (C),
wnt8 MO (F) or nlk MO (I), and show a dorsal curvature of
the tail characteristic of severely dorsalized embryos.
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