Fig. 6

Fig. 6 The role of different tissues in posterior body axis elongation.

Diagrams of posterior elongating tissues in wild-type, tbx16^−/−, noto^−/−, and vangl2^−/− mutants, illustrating the high-level tissue flows caused by cell movements. The near-complete failure to differentiate PSM in tbx16^−/− does not disrupt posterior body axis elongation, as the enlarged MPZ continues to move posteriorly. The loss of the notochord in noto^−/− reduces fluidity in the MPZ and vortices are lost from the MPZ/PSM boundary, but posterior body axis elongation is not disrupted. Disrupted planar polarity movements and dorsal cell movements in vangl2^−/− leads to greatly slowed posterior body axis elongation, with ventral tissue movements scaled to the altered proportions of the posterior tissues.