Abstract
The protein encoded by the Drosophila pair-rule gene fushi tarazu (ftz) is required for the formation of the even-numbered parasegments. Here we analyze the phenotypes of ectopic expression of FTZ and FTZ protein deletions from the Tubulin alpha1 (Tubalpha1) promoter. Fusion of ftz to the Tubalpha1 promoter resulted in low-level ectopic expression of FTZ relative to FTZ expressed from the endogenous ftz gene. The effects of ectopic expression of four FTZ proteins, FTZ(1-413) (full length wild-type FTZ), FTZ(delta257-316) (a complete deletion of the HD), FTZ(delta101-150) (a deletion that includes the major FTZ-F1 binding site) and FTZ(delta151-209) were determined. Ectopic expression of FTZ(1-413), FTZ(delta257-316) and FTZ(delta101-151) did not result in an anti-ftz phenotype; however, ectopic expression of FTZ(1-413), and FTZ(delta257-316) did result in a ftz(Ual/Rpl)-like phenotype. In addition, low-level ectopic expression of FTZ(1-413) and FTZ(delta257-316) rescued ftz phenotypes. This was an important observation because the even-numbered parasegment pattern of FTZ expression is considered important for normal segmentation. Therefore, the rescue of ftz phenotypes by low-level FTZ expression in all cells of the embryo suggests that the even-numbered parasegment expression pattern of FTZ is not the sole factor restricting FTZ action. Low-level ectopic expression of FTZ(delta151-209) resulted in the anti-ftz phenotype and rescued hypomorphic ftz-f1 phenotypes indicating that FTZ(delta151-209) is a hyperactive FTZ molecule. Therefore, the region encompassing amino acids 151-209 of FTZ is required in some manner for repression of FTZ activity. These results are discussed in relation to the current understanding of the mechanism of FTZ action.
