dFMRP and Caprin, translational regulators of synaptic plasticity, control the cell cycle at the Drosophila mid-blastula transition

摘要: The molecular mechanisms driving the conserved metazoan developmental shift referred to as mid-blastula transition (MBT) remain mysterious. Typically, cleavage divisions give way longer asynchronous cell cycles with acquisition of a gap phase. In Drosophila, rapid synchronous nuclear must pause at MBT allow formation cellular blastoderm through special form cytokinesis termed cellularization. Drosophila Fragile X mental retardation protein (dFMRP; FMR1), transcript-specific translational regulator, is required for role FMRP has been most extensively studied in nervous system because loss activity neurons causes misexpression specific mRNAs synaptic plasticity, resulting and autism humans. Here, we show that early embryo dFMRP associates specifically Caprin, another regulator implicated eIF4G, key initiation. Caprin collaborate control cycle by directly mediating normal repression maternal Cyclin B mRNA activation zygotic fruhstart mRNA. These findings identify two new targets regulation implicate regulatory processes diverse learning, memory embryonic development.