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Fig. 3. Ci-FGF3 is required for notochord CE. (A-C')
Phenotypic series of embryos co-injected with Ci-FGF3 splice
morpholinos (MOs) and Bra::GFP (green) and counterstained with phalloidin
(red). The notochord displays progressively stronger intercalation defects
ranging from an occasional two cells per row (A,A', category II),
two-cell row (B,B', category III) and more than two cells per row
(C,C', category IV). (D) Summary of MO phenotypes. n,
number of embryos examined. (E) Distribution of actin protrusion
abundance and ML/AP ratio in wild-type and MO embryos. The MO embryos display
a more severe reduction in protrusions and loss of ML polarity than
dnFGFR notochord (see Fig.
1J). (F-I') Misexpression of Ci-FGF3
disrupts notochord intercalation non-cell-autonomously. Notochord
(F,F'), ventral and dorsal nerve cord (G,G'), muscle (H,H')
and endodermal strand (I,I') enhancer-driven Ci-FGF3 causes
varying degrees of intercalation defects (number of defective embryos/total
embryos) in the notochord. All embryos are co-electroporated with Bra::GFP
(green) and counterstained with phalloidin (red). Images in A'-I'
are magnifications from A-I, respectively.
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