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Fig. 6. Expression of constitutively active Cdk2 phenocopies the convergent
extension defects observed in Wee2-depleted embryos. (A) Both blastomeres of
two-cell embryos were microinjected with 230 pg of Cdk2WT or Cdk2AF mRNA as
indicated. These embryos were allowed to develop until stage 18 before being
processed for MyoD or XNot in situ analysis. Lateral limits of paraxial
mesoderm (MyoD expression) are noted by broken lines. Arrow indicates lack of
anterior neural fold. (B) The paraxial mesoderm of Cdk2 AF-treated embryos
fails to converge towards the midline. Representative Cdk2WT or Cdk2AF
treated, MyoD stained, stage 18 embryos from 6A were serially sectioned
transversely. The anteroposterior positions of the shown sections are
indicated by letters in right lower corner of panels as per
Fig. 4E. Dorsal towards the
top. Black arrow denotes the forming somitic ridge. (C) Expression of Cdk2AF
causes cell proliferation within the paraxial mesoderm but not the axial
mesoderm. The total number of nuclei within the paraxial and axial mesoderm of
representative embryos from 6A was determined as in
Fig. 2E. (D) Cdk2 AF treatment
compromises convergent extension driven elongation of dorsal explants. Embryos
were injected with Cdk2 WT or Cdk2 AF mRNA as in A and then processed for
dorsal explants. Explants were photographed when controls reached stage 24.
Scale bar: 1 mm. (E) Mesoderm specific gene expression is unchanged in Cdk2
AF-treated embryos. Quantitative RT-PCR for MyoD, XNot, Vent1, MA, MHC and ODC
from whole, stage 18 embryos injected as in A with Cdk2 AF mRNA, Cdk2 WT mRNA,
or nothing (Sibling).
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