Abstract
THE Drosophila segmentation gene fushi tarazu (ftz) encodes a homeodomain-containing protein, ftz, that can act as a DNA-binding activator of transcription1–5. In the developing embryo, ftz is expressed in seven stripes6 which correspond to the even-numbered parasegments7. These parasegments are missing in ftz' embryos8. When ftz is expressed throughout blastoderm embryos under the control of a heat-shock promoter, the odd-numbered parasegments are lost9. This 'anti-ftz' phenotype has been attributed to autoactivation of the endogenous ftz gene by the ectopically expressed protein10. Here we show that the same phenotype is induced by ectopic expression of a ftz polypeptide containing a deletion in the homeodomain. Thus, ftz can alter gene expression without binding directly to DNA.
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Fitzpatrick, V., Percival-Smith, A., Ingles, C. et al. Homeodomain-independent activity of the fushi tarazu polypeptide in Drosophila embryos. Nature 356, 610–612 (1992). https://doi.org/10.1038/356610a0
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DOI: https://doi.org/10.1038/356610a0
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