STRUCTURE AND REGULATION OF THE FUSHI-TARAZU GENE FROM DROSOPHILA-HYDEI

The Drosophila melanogaster segmentation gene fushi tarazu (ftz) encod es a homeodomain-type transcription factor involved in the control of larval pattern formation. Loss of function mutations cause an embryoni c lethal, pair-rule phenotype. The segmentation defects, but not the l ethality, can be partially rescued by the ftz orthologue from Drosophi la hydei. In this work, the primary structure, expression and regulati on of the D. hydei ftz gene was characterized. Sequence comparisons cl assify ftz as a rather fast evolving gene. However, since the homeodom ain of the D. hydei FTZ protein is highly similar to that of D. melano gaster, proper regulation of D. melanogaster frz downstream genes woul d be expected. In D. melanogaster embryos, a D. hydei ftz transgene is expressed normally, independent of endogenous ftz gene activity, sugg esting that D. hydei ftz regulatory sequences are correctly recognized by D. melanogaster transcription factors. Accordingly, lacZ fusion co nstructs driven by the D, hydei ftz upstream element are expressed nor mally in D, melanogaster embryos. Altogether, the similarities between the two ftz orthologues by far outweigh the differences. The limited success of the trans-species rescue might be, therefore, a consequence of the accumulation of too many subtle changes in gene function, exce eding the limits of developmental plasticity during fly embryogenesis.