RESUMO
Jak/STAT is an important signaling pathway mediating multiple events in development. We describe participation of metazoan co-activator SAYP/PHF10 in this pathway downstream of STAT. The latter, via its activation domain, interacts with the conserved core of SAYP. STAT is associated with the SAYP-containing co-activator complex BTFly and recruits BTFly onto genes. SAYP is necessary for stimulating STAT-driven transcription of numerous genes. Mutation of SAYP leads to maldevelopments similar to those observed in STAT mutants. Thus, SAYP is a novel co-activator mediating the action of STAT.
Assuntos
Proteínas de Drosophila/metabolismo , Fatores de Transcrição STAT/metabolismo , Fatores de Transcrição/metabolismo , Ativação Transcricional , Animais , Linhagem Celular , Drosophila/genética , Proteínas de Drosophila/química , Proteínas de Drosophila/genética , Mutação , Fenótipo , Domínios e Motivos de Interação entre Proteínas , Fatores de Transcrição STAT/química , Fatores de Transcrição/química , Fatores de Transcrição/genéticaRESUMO
The role of metazoan coactivator SAYP in nuclear receptor-driven gene activation in the ecdysone cascade of Drosophila is considered. SAYP interacts with DHR3 nuclear receptor and activates the corresponding genes by recruiting the BTFly (Brahma and TFIID) coactivator supercomplex. The knockdown of SAYP leads to a decrease in the level of DHR3-activated transcription. DHR3 and SAYP interact during development and have multiple common targets across the genome.