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Gene Review

ftz  -  fushi tarazu

Drosophila melanogaster

Synonyms: BG:DS07876.1, CG2047, Dm-Ftz, Dm-ftz, DmFtz, ...
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Disease relevance of ftz

  • The embryonic ftz protein migrates more slowly on SDS-polyacrylamide gels than protein made either in E. coli or in a reticulocyte lysate system in vitro, indicating that it is modified in the embryo [1].
  • To demonstrate this, we targeted the promoter of the well-characterized fushi tarazu (ftz) gene with a ZFP TF activator using the VP16 activation domain from Herpes simplex virus, and ZFP TF repressors using the Drosophila methyl-CpG binding domain (MBD)-like Delta protein [2].
  • If the ftz gene is prevented from functioning, alternating portions of the body normally derived from the active stripes fail to develop, resulting in larvae which lack the denticle bands normally formed by the mesothorax and odd-numbered abdominal segments (that is, thoracic segment T2 and abdominal segments A1, A3, A5 and A7) [3].

High impact information on ftz

  • Naked, microinjected fushi tarazu (ftz) transcripts do not localize in blastoderm embryos, indicating that cytoplasmic mechanisms alone are insufficient for apical targeting [4].
  • Certain genes, such as ftz, are largely negatively regulated in the interstripes through proximal upstream elements by the striped expression of other pair-rule genes, while others, such as hairy and eve, are largely regulated through distal upstream elements by the aperiodic gap genes (Figure 7) [5].
  • Fushi tarazu and engrailed are two of the genes required for proper segmentation of the Drosophila embryo [6].
  • Using a cotransfection assay, we have shown that homeodomain proteins encoded by the homeotic gene Antennapedia (Antp) and the segmentation gene fushi tarazu, as well as a hybrid homeodomain protein, are activators of transcription from specific promoters in cultured Drosophila cells [7].
  • The altered specificity Bicoid mutants recognized DNA sites bound by Ultrabithorax, fushi tarazu, and other related homeo-domain proteins [8].

Chemical compound and disease context of ftz


Biological context of ftz

  • We report a systematic mutational analysis of the helix-turn-helix motif (HTH) of the fushi tarazu (ftz) homeo domain (HD) of Drosophila [11].
  • Direct activation of homeotic gene control regions by ftz (or eve) protein may be a regulatory step which is generally used to align expression of homeotic genes with parasegmental boundaries [12].
  • Using a heat-shock-inducible run transgene, we found that ectopic run expression leads to rapid repression of eve stripes and a somewhat delayed expansion of ftz stripes [13].
  • We show that fusion gene expression is transcriptionally regulated, such that ectopic expression is suppressed when pattern is established, and present evidence indicating that interstripe hb-ftz expression is repressed by eve [14].
  • Examination of the phenotype of ftz Rg-pbx- double-mutant embryos did not reveal a clear pattern of epistasis between the genes nor was absolute additivity of phenotype seen [15].

Anatomical context of ftz

  • Regulation of segment polarity genes in the Drosophila blastoderm by fushi tarazu and even skipped [16].
  • In addition, en and twi products activate the enhancer, probably directly. en broadens the parasegmental stripe while twi cooperates with ftz to enhance expression in the mesoderm [17].
  • In contrast, the Fushi Tarazu homeodomain protein is an activator, both in cultured cells and in Drosophila embryos, where it activates several known target genes, including its own gene [18].
  • The Fushi tarazu homeodomain also causes neurite outgrowth in UR61 cells and the neurotrophic activities of Engrailed and Fushi tarazu homeodomains correlate with their DNA binding specificities [19].
  • In the absence of ftz CNS expression, some neurons appear normal (for example, the aCC, pCC, and RP1), whereas the RP2 neuron extends its growth cone along an abnormal pathway, mimicking its sibling (RP1), suggesting a transformation in neuronal identity [20].

Associations of ftz with chemical compounds

  • These effects appear to result from stabilization of the ftz protein, since ftz stripes decay much more slowly in mutant embryos than in wild type after injection of the protein synthesis inhibitor cycloheximide [21].
  • The mobility shift assay was used to study the competition of the minor groove binder distamycin A with either an Antennapedia homeodomain (Antp HD) peptide or derivatives of a fushi tarazu homeodomain (ftz HD) peptide for their AT-rich DNA binding site [22].
  • FTZ-F1, a steroid hormone receptor-like protein implicated in the activation of fushi tarazu [23].
  • This interaction required the AF-2 core and putative ligand-binding domain of FTZ-F1 and the LXXLL motif of FTZ [24].
  • Here we show that the activity of the glutamine-rich fushi tarazu activation domain is indeed blocked by truncated TFIIB derivatives in Drosophila Schneider L2 cells, suggesting that it is mediated by interactions with TFIIB [25].

Physical interactions of ftz


Regulatory relationships of ftz


Other interactions of ftz

  • We propose that the anterior margin of each ftz stripe is normally defined by the posterior even-skipped (eve) boundary [36].
  • We have observed that the transcription of several genes, including ftz, is triggered in embryos at a critical nuclear density; therefore, we suggest that titration of transcription factors like ttk by the nucleocytoplasmic ratio triggers zygotic transcription in Drosophila [37].
  • Footprint analysis and tests in transformed embryos of constructs bearing mutated footprint regions suggest that ftz protein acts directly as a transcriptional activator of Ubx [12].
  • DNA from each of these 3' exons also hybridized weakly to DNA from the fushi tarazu locus of the ANT-C [38].
  • By contrast, the specific combination of Runt + Ftz is sufficient for slp1 repression in all blastoderm nuclei [39].

Analytical, diagnostic and therapeutic context of ftz


  1. Expression, modification, and localization of the fushi tarazu protein in Drosophila embryos. Krause, H.M., Klemenz, R., Gehring, W.J. Genes Dev. (1988) [Pubmed]
  2. Controlling gene expression in Drosophila using engineered zinc finger protein transcription factors. Jamieson, A.C., Guan, B., Cradick, T.J., Xiao, H., Holmes, M.C., Gregory, P.D., Carroll, P.M. Biochem. Biophys. Res. Commun. (2006) [Pubmed]
  3. Near-reciprocal phenotypes caused by inactivation or indiscriminate expression of the Drosophila segmentation gene ftz. Struhl, G. Nature (1985) [Pubmed]
  4. Squid hnRNP protein promotes apical cytoplasmic transport and localization of Drosophila pair-rule transcripts. Lall, S., Francis-Lang, H., Flament, A., Norvell, A., Schüpbach, T., Ish-Horowicz, D. Cell (1999) [Pubmed]
  5. Zebra patterns in fly embryos: activation of stripes or repression of interstripes? Carroll, S.B. Cell (1990) [Pubmed]
  6. Binding site-dependent direct activation and repression of in vitro transcription by Drosophila homeodomain proteins. Ohkuma, Y., Horikoshi, M., Roeder, R.G., Desplan, C. Cell (1990) [Pubmed]
  7. Transcriptional activation by the Antennapedia and fushi tarazu proteins in cultured Drosophila cells. Winslow, G.M., Hayashi, S., Krasnow, M., Hogness, D.S., Scott, M.P. Cell (1989) [Pubmed]
  8. DNA specificity of the bicoid activator protein is determined by homeodomain recognition helix residue 9. Hanes, S.D., Brent, R. Cell (1989) [Pubmed]
  9. The location, modification, and function of the fushi tarazu protein during Drosophila embryogenesis. Krause, H.M., Gehring, W.J. Prog. Clin. Biol. Res. (1988) [Pubmed]
  10. Role of the TATA binding protein-transcription factor IIB interaction in supporting basal and activated transcription in plant cells. Pan, S., Czarnecka-Verner, E., Gurley, W.B. Plant Cell (2000) [Pubmed]
  11. In vivo analysis of the helix-turn-helix motif of the fushi tarazu homeo domain of Drosophila melanogaster. Furukubo-Tokunaga, K., Müller, M., Affolter, M., Pick, L., Kloter, U., Gehring, W.J. Genes Dev. (1992) [Pubmed]
  12. Sharp anterior boundary of homeotic gene expression conferred by the fushi tarazu protein. Müller, J., Bienz, M. EMBO J. (1992) [Pubmed]
  13. Control of segmental asymmetry in Drosophila embryos. Manoukian, A.S., Krause, H.M. Development (1993) [Pubmed]
  14. Mis-regulating segmentation gene expression in Drosophila. Parkhurst, S.M., Ish-Horowicz, D. Development (1991) [Pubmed]
  15. A development genetic analysis of the gene regulator of postbithorax in Drosophila melanogaster. Bender, M., Turner, F.R., Kaufman, T.C. Dev. Biol. (1987) [Pubmed]
  16. Regulation of segment polarity genes in the Drosophila blastoderm by fushi tarazu and even skipped. Ingham, P.W., Baker, N.E., Martinez-Arias, A. Nature (1988) [Pubmed]
  17. Molecular mechanisms of pattern formation by the BRE enhancer of the Ubx gene. Qian, S., Capovilla, M., Pirrotta, V. EMBO J. (1993) [Pubmed]
  18. Inserting the Ftz homeodomain into engrailed creates a dominant transcriptional repressor that specifically turns off Ftz target genes in vivo. John, A., Smith, S.T., Jaynes, J.B. Development (1995) [Pubmed]
  19. Neuronal differentiation of PC12 cells induced by engrailed homeodomain is DNA-binding specific and independent of MAP kinases. Cosgaya, J.M., Aranda, A., Cruces, J., Martín-Blanco, E. J. Cell. Sci. (1998) [Pubmed]
  20. Expression and function of the segmentation gene fushi tarazu during Drosophila neurogenesis. Doe, C.Q., Hiromi, Y., Gehring, W.J., Goodman, C.S. Science (1988) [Pubmed]
  21. Mutations affecting the stability of the fushi tarazu protein of Drosophila. Kellerman, K.A., Mattson, D.M., Duncan, I. Genes Dev. (1990) [Pubmed]
  22. Distamycin-induced inhibition of homeodomain-DNA complexes. Dorn, A., Affolter, M., Müller, M., Gehring, W.J., Leupin, W. EMBO J. (1992) [Pubmed]
  23. FTZ-F1, a steroid hormone receptor-like protein implicated in the activation of fushi tarazu. Lavorgna, G., Ueda, H., Clos, J., Wu, C. Science (1991) [Pubmed]
  24. Segmentation gene product Fushi tarazu is an LXXLL motif-dependent coactivator for orphan receptor FTZ-F1. Suzuki, T., Kawasaki, H., Yu, R.T., Ueda, H., Umesono, K. Proc. Natl. Acad. Sci. U.S.A. (2001) [Pubmed]
  25. Interaction between a transcriptional activator and transcription factor IIB in vivo. Colgan, J., Wampler, S., Manley, J.L. Nature (1993) [Pubmed]
  26. The interaction of proteins encoded by Drosophila homeotic and segmentation genes with specific DNA sequences. Laughon, A., Howell, W., Scott, M.P. Development (1988) [Pubmed]
  27. The tramtrack gene encodes a Drosophila finger protein that interacts with the ftz transcriptional regulatory region and shows a novel embryonic expression pattern. Harrison, S.D., Travers, A.A. EMBO J. (1990) [Pubmed]
  28. The Drosophila nuclear receptors FTZ-F1 alpha and FTZ-F1 beta compete as monomers for binding to a site in the fushi tarazu gene. Ohno, C.K., Ueda, H., Petkovich, M. Mol. Cell. Biol. (1994) [Pubmed]
  29. The correct activation of Antennapedia and bithorax complex genes requires the fushi tarazu gene. Ingham, P.W., Martinez-Arias, A. Nature (1986) [Pubmed]
  30. In vivo interactions of the Drosophila Hairy and Runt transcriptional repressors with target promoters. Jiménez, G., Pinchin, S.M., Ish-Horowicz, D. EMBO J. (1996) [Pubmed]
  31. Ectopic expression of the Drosophila tramtrack gene results in multiple embryonic defects, including repression of even-skipped and fushi tarazu. Read, D., Levine, M., Manley, J.L. Mech. Dev. (1992) [Pubmed]
  32. Computational Identification of Ftz/Ftz-F1 downstream target genes. Bowler, T., Kosman, D., Licht, J.D., Pick, L. Dev. Biol. (2006) [Pubmed]
  33. Low-level ectopic expression of Fushi tarazu in Drosophila melanogaster results in ftz(Ual/Rpl)-like phenotypes and rescues ftz phenotypes. Argiropoulos, B., Ho, J., Blachuta, B.J., Tayyab, I., Percival-Smith, A. Mech. Dev. (2003) [Pubmed]
  34. How does the fushi tarazu gene activate engrailed in the Drosophila embryo? Lawrence, P.A., Pick, L. Dev. Genet. (1998) [Pubmed]
  35. Chromatin remodeling mediated by Drosophila GAGA factor and ISWI activates fushi tarazu gene transcription in vitro. Okada, M., Hirose, S. Mol. Cell. Biol. (1998) [Pubmed]
  36. Autocatalytic ftz activation and metameric instability induced by ectopic ftz expression. Ish-Horowicz, D., Pinchin, S.M., Ingham, P.W., Gyurkovics, H.G. Cell (1989) [Pubmed]
  37. Activation of transcription in Drosophila embryos is a gradual process mediated by the nucleocytoplasmic ratio. Pritchard, D.K., Schubiger, G. Genes Dev. (1996) [Pubmed]
  38. Structural relationships among genes that control development: sequence homology between the Antennapedia, Ultrabithorax, and fushi tarazu loci of Drosophila. Scott, M.P., Weiner, A.J. Proc. Natl. Acad. Sci. U.S.A. (1984) [Pubmed]
  39. Ftz modulates Runt-dependent activation and repression of segment-polarity gene transcription. Swantek, D., Gergen, J.P. Development (2004) [Pubmed]
  40. Cloning and transcriptional analysis of the segmentation gene fushi tarazu of Drosophila. Kuroiwa, A., Hafen, E., Gehring, W.J. Cell (1984) [Pubmed]
  41. Non-periodic cues generate seven ftz stripes in the Drosophila embryo. Yu, Y., Pick, L. Mech. Dev. (1995) [Pubmed]
  42. Human DNA sequences homologous to a protein coding region conserved between homeotic genes of Drosophila. Levine, M., Rubin, G.M., Tjian, R. Cell (1984) [Pubmed]
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