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- W2092620011 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." @default.
- W2092620011 created "2016-06-24" @default.
- W2092620011 creator A5020363278 @default.
- W2092620011 creator A5023779268 @default.
- W2092620011 creator A5065151779 @default.
- W2092620011 date "2013-08-06" @default.
- W2092620011 modified "2023-10-04" @default.
- W2092620011 title "Ebi alleviates excessive growth signaling through multiple epigenetic functions in<i>Drosophila</i>" @default.
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- W2092620011 doi "https://doi.org/10.1111/gtc.12088" @default.
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