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. Author manuscript; available in PMC: 2017 Jan 28.
Published in final edited form as: Genesis. 2015 Aug 10;53(9):612–626. doi: 10.1002/dvg.22879

Figure 4. Evc2 mutations result in abrogated ciliary localization and compromised Hedgehog signaling.

Figure 4

(a–h) Immunoflorescence visualized localizations of EVC2 (a, c, e, g) and EVC (b, d, f, h) (green) within primary cilium (acetylated tubulin, Ac Tu; a, b e, f, red) or next to the centrosome (gamma tubulin, Ga Tu; c, d, g, h, red) of primary chondrocytes from Evc2ex12/ex12 (a–d), Evc2dE/dE (e–h) or their littermate controls. (i–n) MEF cells from Evc2ex12/ex12 (i, j), Evc2dE/dE (k, l) or Evc2ex12/dE (m, n) and their littermate controls were treated by Hedgehog conditioned medium (CM) or smoothen agonist (SAG). After 24 hours, expression levels of Ptch1 (i, k, m) or Gli1 (j, l, n) were quantified. Folds of induction were calculated using amount of RNA after treatment divided by amount of RNA with no treatment (n=3, *, p<0.01). (o–p) Changes in Hedgehog signaling levels in growth plates of Evc2dE/dE and its litter mate mice were visualized by lacZ staining after introduction of Ptch1-lacZ (o) and Gli1-lacZ (p) into the Evc2dE/dE background. Bar: 10 um for a–h, 200 um for o–p.