Ebi alleviates excessive growth signaling through multiple epigenetic functions in D rosophila

As multicellular organisms develop, many cells permanently stop dividing and undergo terminal differentiation. The G 1 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 G 1 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 D rosophila 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 D rosophila homologue of retinoblastoma, and regulating the expression of specific target genes of the R bf/ E 2 F pathway. Furthermore, ebi also sustained expression of certain genes, including R bf , encoding factors that inhibit progression out of G 1. Our genetic studies suggest that the antagonistic function of ebi against the P olycomb group silencing complex plays a role in the G 1/ S phase transition.