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. Author manuscript; available in PMC: 2013 Oct 1.
Published in final edited form as: Birth Defects Res A Clin Mol Teratol. 2012 Aug 3;94(10):804–816. doi: 10.1002/bdra.23052

Figure 7. Perturbations of the apicobasal polarity pathway are sufficient to induce HP formation.

Figure 7

(A–B) Unlike controls (A), high (5μg/μl) LGL-GFP misexpression is sufficient to induce ectopic HPs (arrowhead, B). (C–D) Control (C) and high LGL-GFP misexpression (D) demonstrating apical LGL, loss of apical PAR3 and apical constriction (arrowhead, D). (E) Compared to controls (A), nuclei are basally migrated at ectopic HPs induced by high LGL-GFP (E). (F, G) Aberrant, basal mitosis (arrowheads in G) following high LGL-GFP electroporations. (H–I′) Biochemical interactions between pSMAD 1,5,8 and PAR3 in EGFP-electroporated whole cell lysates immunoprecipitated with PAR3 and immunoblotted with pSMAD 1,5,8 antibody (H). pSMAD 1,5,8 and PAR3 interactions demonstrated by reversing pSMAD 1,5,8 and PAR3 antibodies (H′). Compared to controls (H, H′), biochemical interactions between pSMAD 1,5,8 and PAR3 are reduced in noggin-electroporated lysates (I, I′).