Table 1

The various Ptc constructs used to evaluate Ptc regulation. Differences between constructs come from the amount of protein expressed, which was low (L), high (H), or very high (UAS). None of these transgenes were expressed from promoters that are responsive to Hh signaling, and therefore, the abundance of the produced proteins is controlled through posttranscriptional mechanisms. Transgenic proteins differ in their activity toward Smo. Normal activity means that binding of Hh alleviates Smo repression by Ptc and, in the absence of Hh, Ptc inhibits Smo.

Transgene	Relative abundance of the encoded protein	Activity toward Smo	Hh binding	Internalization- competent	NPXY motif present
L>Ptc-GFP	Low	Normal	Yes	Yes	Yes
L>Ptc^Δ2-GFP	Low	Constitutively active (Smo inhibited)^*	No	Yes	Yes
H>Ptc^Δ2-GFP	High	Constitutively active (Smo inhibited)^†	No	Yes	Yes
L>Ptc^AAAA-GFP	Low	Normal	Yes	No	No
H>Ptc¹⁴-GFP	High	Normal	Yes	No	Yes
UAS-Ptc	Very high	Normal	Yes	Yes	Yes
UAS-Ptc^Δ2	Very high	Constitutively active (Smo inhibited)^†	No	Yes	Yes
UAS-Ptc^S2	Very high	Dominant negative (Smo active)	Yes	Yes	Yes
UAS Ptc^ΔCTD	Very high	No activity	Yes	No	No
UAS Ptc^LDL	Very high	No activity	Yes	Yes	No
UAS Ptc^AAAA	Very high	Normal	Yes	No	No

*This transgene expresses a low amount of Ptc^Δ2, which inhibits Smo constitutively only in a ptc⁻ mutant background; in a wild-type background, endogenous Ptc bound to Hh is enough to shift the ratio of unbound to bound Ptc and activate the pathway.

†These transgenes express high amounts of Ptc^Δ2, which are enough to inhibit Smo constitutively even in the presence of endogenous Ptc bound to Hh.