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).