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Fig. 4. Loss of aPKC function expands basolateral membrane domain into the apical
side and disrupts the apical domain. (A) The aPKC NT construct has the
Par6-binding site but no kinase domain and so acts as a dominant-negative
fragment. (B) The effect of this construct can be rescued by overexpressing
full-length aPKC. Injections of 4.5 ng aPKC NT + 0.5 ng GFP, 4.5 ng aPKC NT +
0.5 ng aPKC, or 5 ng GFP were carried out. The average of four experiments
scored blind is shown. (C,D) aPKC NT dominant-negative fragment caused pigment
defects (D) compared with control (C) (5 ng of each). (E,H) aPKC NT
was co-injected with GFP showing that the pigment defects occurred in
the injected region. The arrows in C,E and D,H highlight the same cells. (F-J)
aPKC NT (I,J) caused ectopic localisation of the basolateral markers
ß1-integrin and occludin to the apical side (arrow) and tight junctions
were also lost (J, arrowhead) when compared with GFP control (F,G). (K)
Diagram of the observed phenotype. Colours are as above. Pigmented embryos
were injected as this allowed the affected area to be easily identified, they
were then fixed and stained for markers of cell polarity.
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