Xenbase Image ID: 129061

Figure 6. Conserved and divergent aspects of Smo signaling(a) Smo−/− MEFs, stably expressing mSmo or the cilia-localized chimera mFz7mSmoICD were incubated with control media, 20-OHC (10 μM), Shh, or wnt3a. The cells were processed for Q-PCR, to measure Gli1 transcription. Error bars show standard deviation (n=3 independent experiments). MFz7mSmoICD did not rescue Hh signaling in Smo−/− cells, irrespective of the presence of Wnt3a.(b) As in (a), but with stable expression of the chimera rMAcChRmSmoICD, which is recruited to cilia by treatment with acetylcholine (AcCh, 100 μM). RMAcChRmSmoICDdoes not rescue Hh signaling, in the presence or absence of AcCh.(c) As in (a) but with stable expression of low levels of DrSmomSmoICD. DrSmomSmoICD is constitutively active, and is not further activated by 20-OHC (10 μM), Shh, or SAG (400 nM). In contrast, DrSmo is inactive in Smo−/− MEFs.(d) As in (c), but with addition of 20 μM forskolin (FSK), to block Hh signaling downstream of Smo. Signaling by both mSmo and DrSmomSmoICD is blocked by FSK.(e) Schematic of the mSmo protein and of the location of Sites A and B. For each site, activators are in blue, while inhibitors are in red.(f) Regulation of vertebrate Smo. Inhibition of Ptch by Shh results in Smo Site A activation; it is unclear if Site B is also activated by Shh. The oxysterol 20-OHC, which binds to Site B in the extracellular domain of Smo, potentiates Site A activation. Active Smo then signals to the cytoplasm. Image published in: Nedelcu D et al. (2013) Image downloaded from an Open Access article in PubMed Central. Image reproduced on Xenbase with permission of the publisher and the copyright holder. Larger Image Printer Friendly View

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