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Fig. 1. A highly simplified schematic illustrating the central components and the
general mechanism of HH signal transduction. In cells not responding to HH
(the "OFF" state), PTC — a
twelve-transmembrane-domain-containing protein and the receptor for HH ligands
— represses the activity of SMO, a G-protein-coupled receptor-like
seven-transmembrane-domain-containing protein. The intracellular consequence
of this repression is the PKA-mediated inactivation or conversion of the GLI
family of transcription factors (CI in Drosophila) into repressors
(GLIRep) and constitutive repression of HH target genes. On
reception of HH through its binding with PTC (the "ON" state), SMO
inhibition is somehow relieved and this results in the nuclear accumulation of
activated forms of GLIs (GLIAct) that induce HH target gene
transcription. A conserved target is ptc itself, as upregulation of
PTC by HH serves to restrict its signalling range. In vertebrates,
Gli1, like ptc, also appears to be transcriptionally
regulated by HH through the activities of other GLI proteins. For further
details and modulations of the pathway see Ingham and McMahon
(Ingham and McMahon,
2001 ).
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