Bonus, a Drosophila homolog of TIF1 proteins, interacts with nuclear receptors and can inhibit beta FTZ-F1-dependent transcription

Citation
R. Beckstead et al., Bonus, a Drosophila homolog of TIF1 proteins, interacts with nuclear receptors and can inhibit beta FTZ-F1-dependent transcription, MOL CELL, 7(4), 2001, pp. 753-765
Citations number
61
Categorie Soggetti
Cell & Developmental Biology
Journal title
MOLECULAR CELL
ISSN journal
10972765 → ACNP
Volume
7
Issue
4
Year of publication
2001
Pages
753 - 765
Database
ISI
SICI code
1097-2765(200104)7:4<753:BADHOT>2.0.ZU;2-J
Abstract
The Drosophila bonus (bon) gene encodes a homolog of the vertebrate TIF1 tr anscriptional cofactors. bon is required for male viability, molting, and n umerous events in metamorphosis including leg elongation, bristle developme nt, and pigmentation. Most of these processes are associated with genes tha t have been implicated in the ecdysone pathway, a nuclear hormone receptor pathway required throughout Drosophila development. Bon is associated with sites on the polytene chromosomes and can interact with numerous Drosophila nuclear receptor proteins. Bon binds via an LxxLL motif to the AF-2 activa tion domain present in the ligand binding domain of beta FTZ-F1 and behaves as a transcriptional inhibitor in vivo.