Anterior repression of a Drosophila stripe enhancer requires three position-specific mechanisms
Author:
Andrioli Luiz Paulo Moura1, Vasisht Vikram1, Theodosopoulou Ekaterina1, Oberstein Adam1, Small Stephen1
Affiliation:
1. Department of Biology, New York University, 1009 Main Building, 100 Washington Square East, New York, NY 10003-6688, USA
Abstract
The striped expression pattern of the pair-rule gene even skipped(eve) is established by five stripe-specific enhancers, each of which responds in a unique way to gradients of positional information in the earlyDrosophila embryo. The enhancer for eve stripe 2(eve 2) is directly activated by the morphogens Bicoid (Bcd) and Hunchback (Hb). As these proteins are distributed throughout the anterior half of the embryo, formation of a single stripe requires that enhancer activation is prevented in all nuclei anterior to the stripe 2 position. The gap genegiant (gt) is involved in a repression mechanism that sets the anterior stripe border, but genetic removal of gt (or deletion of Gt-binding sites) causes stripe expansion only in the anterior subregion that lies adjacent to the stripe border. We identify a well-conserved sequence repeat, (GTTT)4, which is required for repression in a more anterior subregion. This site is bound specifically by Sloppy-paired 1 (Slp1),which is expressed in a gap gene-like anterior domain. Ectopic Slp1 activity is sufficient for repression of stripe 2 of the endogenous eve gene,but is not required, suggesting that it is redundant with other anterior factors. Further genetic analysis suggests that the(GTTT)4-mediated mechanism is independent of the Gt-mediated mechanism that sets the anterior stripe border, and suggests that a third mechanism, downregulation of Bcd activity by Torso, prevents activation near the anterior tip. Thus, three distinct mechanisms are required for anterior repression of a single eve enhancer, each in a specific position. Ectopic Slp1 also represses eve stripes 1 and 3 to varying degrees,and the eve 1 and eve 3+7 enhancers each contain GTTT repeats similar to the site in the eve 2 enhancer. These results suggest a common mechanism for preventing anterior activation of three different eve enhancers.
Publisher
The Company of Biologists
Subject
Developmental Biology,Molecular Biology
Reference52 articles.
1. Adams, M. D. Celniker, S. E. Holt, R. A. Evans, C. A. Gocayne,J. D. Amanatides, P. G. Scherer, S. E. Li, P. W. Hoskins, R. A. Galle, R. F. et al. (2000). The genome sequence of Drosophila melanogaster. Science287,2185-2195. 2. Arnosti, D. N., Barolo, S., Levine, M. and Small, S.(1996). The eve stripe 2 enhancer employs multiple modes of transcriptional synergy. Development122,205-214. 3. Cadigan, K. M., Grossniklaus, U. and Gehring, W. J.(1994). Localized expression of sloppy paired protein maintains the polarity of Drosophila parasegments. Genes Dev.8, 899-913. 4. Capovilla, M., Eldon, E. D. and Pirrotta, V.(1992). The giant gene of Drosophila encodes a b-ZIP DNA-binding protein that regulates the expression of other segmentation gap genes.Development114,99-112. 5. Cirillo, L. A., Mcpherson, C. E., Bossard, P., Stevens, K.,Cherian, S., Shim, E.-Y., Clark, E. A., Burley, S. K. and Zaret, K. S.(1998). Binding of the winged-helix transcription factor HNF3 to a linker histone site on the nucleosome. EMBO J.17,244-254.
Cited by
39 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献
|
|