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. Author manuscript; available in PMC: 2013 Jan 16.
Published in final edited form as: Angiogenesis. 2008 Sep 17;11(4):347–360. doi: 10.1007/s10456-008-9116-2

Fig. 2.

Fig. 2

Dvl2 mutants disrupt endothelial cell polarity. a Diagram of HA-Dvl2 constructs in pCMV5 (HA-tags on the N-terminal of each construct are not depicted). Each of the functional domains have been individually deleted. In addition, one construct was generated through the introduction of a point mutation to yield the PCP-inhibitory K446M-Dvl2 construct. Caveolin-1 localization (b–f, green) in MPE cells expressing various HA-Dvl2 (red) constructs: b Dvl2, c ΔDIX-Dvl2, d ΔPDZ-Dvl2, e ΔDEP-Dvl2 and f K446M-Dvl2. Normal asymmetrical caveolin-1 localization was observed in Dvl2 and ΔDIX-Dvl2-expressing cells but was either diminished or mis-localized in cells expressing the others constructs. The minimal K446M point-mutation in Dvl2 was sufficient to bring about this phenotype. Dashed lines encircle cells to facilitate their visualization