XB-IMG-83165
Xenbase Image ID: 83165
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Figure 8. Regulation of Gli21-799, an analogue Gli2 mutant of zebrafish Yot, by Dzip1 and Spop. (A) Western blot results showing that knockdown of Dzip1 stabilized Gli21-799 in Xenopus embryos. RNAs encoding Gli21-799 and MT-GFP were injected into controls and embryos that had received a prior injection of DMO. Embryos were harvested at the neurula stage and subjected to Western blotting. MT-GFP served as an injection and loading control. (B) Forced Spop expression decreased the protein stability of Gli21-799. MT- Gli21-799 and MT-GFP were transfected alone, or in combination with MT-Spop into NIH3T3 cells. Cell lysates were subjected to Western blot with the anti-myc antibody to detect the levels of Spop. (C) Model of Dzip1 functions during Hh signaling. Dzip1 supports ciliogenesis and maintains the proper expression level of Gli proteins through controlling the stability of Spop (left panel). Partial knockdown of Dzip1 has no effect on the formation of cilia, but induces degradation of Spop, leading to increased levels of Gli proteins. When exposed to Shh, these cells produce more Gli activators, resulting in a more robust Hh target gene expression (middle panel). When Dzip1 is depleted more completely, ciliogenesis is disrupted. Although these cells have increased levels of Gli, they cannot receive Shh. This prevents the formation of Gli activators. Consequently, gene expression induced by Shh is inhibited (right panel). Under normal conditions, cells located at a distance from the source of Shh are not exposed to Shh. Whether these cells form cilia or not are not important. However, when Dizp1 is depleted, destabilization of Spop will induce accumulation of full-length Gli proteins (not Gli activators). This will lead to weak ectopic Hh target gene expression in embryos. Image published in: Schwend T et al. (2013) Copyright © 2013. Image reproduced with permission of the publisher and the copyright holder. This is an Open Access article distributed under the terms of the Creative Commons Attribution License. Larger Image Printer Friendly View |