Fitzpatrick V D, Percival-Smith A, Ingles C J, Krause H M
Banting and Best Department of Medical Research, Charles H. Best Institute, University of Toronto, Ontario, Canada.
Nature. 1992 Apr 16;356(6370):610-2. doi: 10.1038/356610a0.
The Drosophila segmentation gene fushi tarazu (ftz) encodes a homeodomain-containing protein, ftz, that can act as a DNA-binding activator of transcription. In the developing embryo, ftz is expressed in seven stripes which correspond to the even-numbered parasegments. These parasegments are missing in ftz- embryos. When ftz is expressed throughout blastoderm embryos under the control of a heat-shock promoter, the odd-numbered parasegments are lost. This 'anti-ftz' phenotype has been attributed to autoactivation of the endogenous ftz gene by the ectopically expressed protein. 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.
果蝇分节基因“成对规则基因”（ftz）编码一种含同源结构域的蛋白质ftz，它可作为转录的DNA结合激活因子。在发育中的胚胎里，ftz在七条条纹中表达，这些条纹对应偶数副节。在ftz基因缺失的胚胎中，这些副节缺失。当ftz在热休克启动子控制下在整个囊胚胚胎中表达时，奇数副节会缺失。这种“抗ftz”表型被认为是由异位表达的蛋白质对内源ftz基因的自激活作用导致的。在此我们表明，通过异位表达在同源结构域中有缺失的ftz多肽也能诱导相同的表型。因此，ftz可不直接结合DNA而改变基因表达。
