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.

TransgeneRelative
abundance of the
encoded protein
Activity toward
Smo
Hh
binding
Internalization-
competent
NPXY motif
present
L>Ptc-GFPLowNormalYesYesYes
L>PtcΔ2-GFPLowConstitutively active (Smo inhibited)*NoYesYes
H>PtcΔ2-GFPHighConstitutively active (Smo inhibited)NoYesYes
L>PtcAAAA-GFPLowNormalYesNoNo
H>Ptc14-GFPHighNormalYesNoYes
UAS-PtcVery highNormalYesYesYes
UAS-PtcΔ2Very highConstitutively active (Smo inhibited)NoYesYes
UAS-PtcS2Very highDominant negative (Smo active)YesYesYes
UAS PtcΔCTDVery highNo activityYesNoNo
UAS PtcLDLVery highNo activityYesYesNo
UAS PtcAAAAVery highNormalYesNoNo

*This transgene expresses a low amount of PtcΔ2, 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 PtcΔ2, which are enough to inhibit Smo constitutively even in the presence of endogenous Ptc bound to Hh.