FB2025_01 , released February 20, 2025
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Citation
Beckstead, R., Ortiz, J.A., Sanchez, C., Prokopenko, S.N., Chambon, P., Losson, R., Bellen, H.J. (2001). Bonus, a Drosophila homolog of TIF1 proteins, interacts with nuclear receptors and can inhibit FTZ-F1-dependent transcription.  Mol. Cell 7(4): 753--765.
FlyBase ID
FBrf0135890
Publication Type
Research paper
Abstract
The Drosophila bonus (bon) gene encodes a homolog of the vertebrate TIF1 transcriptional cofactors. bon is required for male viability, molting, and numerous events in metamorphosis including leg elongation, bristle development, and pigmentation. Most of these processes are associated with genes that 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 activation domain present in the ligand binding domain of betaFTZ-F1 and behaves as a transcriptional inhibitor in vivo.
PubMed ID
PubMed Central ID
PMC3800173 (PMC) (EuropePMC)
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Secondary IDs
    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Mol. Cell
    Title
    Molecular Cell
    Publication Year
    1997-
    ISBN/ISSN
    1097-2765 1097-4164
    Data From Reference
    Aberrations (2)
    Alleles (6)
    Genes (9)
    Physical Interactions (7)
    Insertions (3)
    Transgenic Constructs (1)