Figure 5.—

sax⁵ produces more severe phenotypes than sax⁴. (A) Dark field image of a wild-type wing. Longitudinal veins 2 (L2), 4 (L4), and 5(L5) are indicated. (B and C) Wings resulting from sax mutant clones as described in Bangi and Wharton (2006b). Clones marked with shv appear dark in images. (B) A sax⁴ clone encompassing the entire posterior compartment shows no patterning defects. Consistent with previous studies (Singer et al. 1997; Bangi and Wharton 2006b), a small sax⁴ clone in the anterior compartment leads to an ectopic L2 (eL2) vein. (C) A sax⁵ clone in the posterior compartment results in the loss of L4 (arrow) and a narrowing of the L4/L5 intervein, a phenotype never seen in an equivalent sax⁴ clone. The more severe phenotype of sax⁵ suggests that the presence of a defective Sax receptor is more detrimental to BMP signaling during wing patterning than the complete loss of the Sax receptor. (D) A cell-based BMP signaling assay indicates that the sax⁵ mutation is able to negatively affect BMP signaling mediated by Tkv. S2 cells were cotransfected with the Su(H)/brk-lacZ reporter construct, Su(H), and N* constructs to stimulate transcription (sample 1), and tkv, and/or sax and sax⁵ constructs under the control of the actin 5C promoter (samples 2–9). Values depicted are the fold activation of β-galactosidase over the basal activity of the reporter construct alone. All values represent the average of samples measured in triplicate and normalized for transfection efficiency.