- THIS ARTICLE
- Full Text (PDF)
- Alert me when this article is cited
- Alert me if a correction is posted
- SERVICES
- Similar articles in this journal
- Similar articles in PubMed
- Alert me to new issues of the journal
- Download to citation manager
- Reprints & Permissions
- CITING ARTICLES
- Citing Articles via HighWire
- Citing Articles via Google Scholar
- GOOGLE SCHOLAR
- Articles by Hyduk, D.
- Articles by Percival-Smith, A.
- Search for Related Content
- PUBMED
- PubMed Citation
- Articles by Hyduk, D.
- Articles by Percival-Smith, A.
Genetics, Vol 142, 481-492, Copyright © 1996
INVESTIGATIONS |
Genetic Characterization of the Homeodomain-Independent Activity of the Drosophila fushi tarazu Gene Product
D. Hyduk and A. Percival-Smith
Department of Zoology, University of Western Ontario, London, Ontario, Canada N6A 5B7
The gene product of fushi tarazu (FTZ) has a homeodomain (HD)-independent activity. Ectopic expression of a FTZ protein that lacks half the HD in embryos results in the anti-ftz phenotype. We have characterized this FTZ HD-independent activity further. Ectopic expression of the HD-independent FTZ activity, in the absence of FTZ activity expressed from the endogenous ftz gene, was sufficient to result in the anti-ftz phenotype. Since the anti-ftz phenotype is a first instar larvae composed nearly entirely of FTZ-dependent cuticular structures derived from the even-numbered parasegments, this result suggests that expression of the HD-independent FTZ activity is sufficient to establish FTZ-dependent cuticle. Activation of FTZ-dependent Engrailed (EN) expression and activation of the ftz enhancer were HD-independent. The ftz enhancer element, AE-1, was activated by the HD-independent FTZ activity; however, the ftz enhancer element, AE-BS2CCC, which is the same as AE-1 except for the inactivation of two FTZ HD DNA-binding sites, was not. Activation of the ftz enhancer by ectopic expression of FTZ activity was effective only during gastrulation and germ band extension. In the discussion, we propose an explanation for these results.
This article has been cited by other articles:
 |
|
 |
|
  E. Rubin, X. Wu, T. Zhu, J. C.Y. Cheung, H. Chen, A. Lorincz, R. K. Pandita, G. G. Sharma, H. C. Ha, J. Gasson, et al. A Role for the HOXB7 Homeodomain Protein in DNA Repair Cancer Res., February 15, 2007; 67(4): 1527 - 1535. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Suzuki, H. Kawasaki, R. T. Yu, H. Ueda, and K. Umesono Segmentation gene product Fushi tarazu is an LXXLL motif-dependent coactivator for orphan receptor FTZ-F1 PNAS, October 5, 2001; (2001) 221552998. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A Nasiadka, A Grill, and H. Krause Mechanisms regulating target gene selection by the homeodomain-containing protein Fushi tarazu Development, January 7, 2000; 127(13): 2965 - 2976. [Abstract] [PDF]
|
|
|
|
 |
|
 A. Percival-Smith and D. J. Hayden Analysis in Drosophila melanogaster of the Interaction Between Sex Combs Reduced and Extradenticle Activity in the Determination of Tarsus and Arista Identity Genetics, September 1, 1998; 150(1): 189 - 198. [Abstract] [Full Text]
|
|
|
|
|
|
B Florence, A Guichet, A Ephrussi, and A Laughon Ftz-F1 is a cofactor in Ftz activation of the Drosophila engrailed gene Development, January 2, 1997; 124(4): 839 - 847. [Abstract] [PDF]
|
|
|
|
|
|
T. Suzuki, H. Kawasaki, R. T. Yu, H. Ueda, and K. Umesono Segmentation gene product Fushi tarazu is an LXXLL motif-dependent coactivator for orphan receptor FTZ-F1 PNAS, October 23, 2001; 98(22): 12403 - 12408. [Abstract] [Full Text] [PDF]
|
|