Additional Supporting Information may be found in the online version of this article.

hep26554-sup-0001-suppinfo.tif237KSupporting Figure 1. Cell motility in Pkhd1del4/del4 cholangiocytes is Cdc42- and RhoA-independent. Cell motility was examined by the Boyden chamber assay. Cells that had migrated to the underside of the porous polycarbonate membrane were quantified under a phase-contrast microscope. Treatment with the Cdc42 inhibitor, casin, or with the RhoA inhibitor, Y-27632, did not inhibit cell motility in Pkhd1del4/del4 cholangiocytes neither at baseline nor after treatment with forskolin (F). (*p<0.05 vs unstimulated cells (C)).
hep26554-sup-0002-suppinfo.tif114KSupporting Figure 2. β-catenin silencing in Pkhd1del4/del4 cholangiocytes. Representative Western blot and quantitative analysis showing a significant reduction in β-catenin expression in cells treated with siRNA but not with scramble negative control. (*p<0.01 vs controls (C) or scramble (Scr).
hep26554-sup-0003-suppinfo.tif6104KSupporting Figure 3. Liver cyst show different morphology between PC-KO and Pkhd1del4/del4mice. Hematoxylin-eosin stained micrographs of liver samples from PC-KO and Pkhd1del4/del4mice showing the different morphology between liver cysts in polycystin defects (PC-KO) and in fibropolycystic diseases (Pkhd1del4/del4). (Magnification 100x A,C; 400x B,D. Scale bar is 100 μm in panels A, C and 20 μm in panels B, D).

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