Fig. 7. SmoC activates low signaling and interferes with high signaling. All tissue is from MS1096 hemizygotes grown at 25°C, except for F and G which were grown at 18°C. (A-E,P,Q) Homozygous UasSmoC. (F) UasSmoC/+; UasSmoC/+ and (G) UasSmoC/+; UasSmoC/Pcos⁺ siblings. (H-J) Doubly heterozygous smo³ SmoC2, SmoC3 with Pcos⁺ (I) or UasFu (J). (K,L) homozygous UasSmoC with heterozygous UasSmo (K) or EP941 (K). SmoC 4x expanded L3 anteriorly to fill the L2/3 intervein (square brackets), reduced the L3/4 intervein, and expanded the costa or reduced the size of the anterior compartment (A,F,H), though the extent was sensitive to genetic background and growth conditions. SmoC expanded expression of Iro (bracket in B) and dpp(C), as well as the reduced expression of ptc (D) and col (E). At 18°C SmoC consistently produced costal overgrowth (F) that was eliminated in siblings carrying a third copy of wild-type cos (G). Pcos⁺ reduced the L3/4 narrowing and ectopic venation caused by SmoC, relative to siblings (compare H with I). Pcos⁺ failed to suppress the L3/4 narrowing of high SSF (O). Pcos⁺ also suppressed the costal overgrowth of 4x FFS (M) and the ectopic venation of 4x Smo (N). Fu enhanced the ectopic venation and costal overgrowth of SmoC, as well as suppressing the L3/4 narrowing (J). The L3/4 narrowing and ectopic venation of 4x Sm°C was suppressed in siblings carrying 2x Smo (compare K with A). SmoC enhanced the growth reduction caused by Ptc, so that the wing is virtually eliminated (compare L with Fig. 4F). SmoC reduced accumulation of Ci155 near the compartment border (P) in the wing pouch where MS1096 is expressed relative to the notum where MS1096 is not expressed (bracket). It also caused abnormal accumulation of Ci155 in the costal primordium (arrowhead). SmoC promoted nuclear access of Ci155 far from compartment border (arrow) in LMB-treated imaginal discs (Q).

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