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Citation
Lim, Y.M., Yamasaki, Y., Tsuda, L. (2013). Ebi alleviates excessive growth signaling through multiple epigenetic functions in Drosophila.  Genes Cells 18(11): 909--920.
FlyBase ID
FBrf0223067
Publication Type
Research paper
Abstract

As multicellular organisms develop, many cells permanently stop dividing and undergo terminal differentiation. The G1 phase of the cell cycle is thought to be the critical decision point for differentiation. Many growth factors, such as epidermal growth factor, are involved in regulating the G1 to S phase transition, and aberrant activation of growth factor signaling is one of the critical causes of tumor formation. Therefore, each cell must have proper mechanisms to suppress inappropriate/excessive activation of growth factor signaling, but the underlying molecular mechanisms remain undefined. Here, we found that ebi, a Drosophila homologue of genes encoding transducin-β-like 1 and transducin-β-like 1-related protein, mitigated excess growth stimulation by taking advantage of its distinct epigenetic functions. Ebi acted as a corepressor of transcription by forming a complex with retinoblastoma family protein (RBF), a Drosophila homologue of retinoblastoma, and regulating the expression of specific target genes of the Rbf/E2F pathway. Furthermore, ebi also sustained expression of certain genes, including Rbf, encoding factors that inhibit progression out of G1. Our genetic studies suggest that the antagonistic function of ebi against the Polycomb group silencing complex plays a role in the G1/S phase transition.

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    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Genes Cells
    Title
    Genes to cells : devoted to molecular & cellular mechanisms
    Publication Year
    1996-
    ISBN/ISSN
    1356-9597
    Data From Reference
    Genes (15)
    Physical Interactions (1)
    Cell Lines (1)