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Reviews: (Lawrence and Struhl, 1996; Alcedo, 1997; Ingham, 1998; Aza-Blanc, 1999; Ingham and McMahon, 2001; Ingham, 2001; Stark, 2002)

Hh, a secreted signaling molecule, is made and released from the posterior compartment of the wing imaginal disc and crosses over into the anterior compartment. Hh binds to Patched (Ptc) releasing it’s repression on Smoothened (Smo). The signal then goes through the Ci signaling complex which is made up of Cos2, Fu, Su(fu), and Ci. The complex is released from microtubules and Ci goes into the nucleus and turns on Hh target genes.

Further anterior, where there is no Hh present, Ptc represses Smo since Hh can no longer repress Ptc. This leads to the retention of Ci in the cytoplasm. Ci also undergoes proteolysis by a mechanism including PKA, CK1, GSK3, Slimb, and the proteosome, changing the Ci-155kD form into a Ci-75kD form. The Ci-75 form can enter the nucleus and actively repress Hh target genes.

Additional info:

There is a region that is refractory to Hh signaling along the entire DV boundary of the wing imaginal disc. See (Glise, 2002)

The Glise, 2002 data indicate that, in the prospective wing margin, N, Wg, and Hh signalling exist in a delicate balance. In the wild type wing disc, N repression is dominant over Hh activation, leading to the differentiation of vein tissue at the margin, while Wg signalling counteracts Hh signalling to allow proper vein tissue and bristle formation (Glise, 2002)



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