Post-transcriptional control by YTHDC2 is required to turn off the mitotic proliferation program and facilitate proper expression of the meiotic program to allow a clean cell fate transition in the germline stem cell lineage.

The kinase that controls maternal mRNA translation is regulated by phosphorylation of its activating subunit to restrict kinase activity to the developmental window between meiosis completion and early embryogenesis.

Ribosomal profiling reveals that translational repression is an important mechanism for cell cycle control and can complement protein degradation.

The mouse gene Ythdc2 exemplifies an evolutionarily ancient family of crucial regulators of the transition from germline stem cell divisions to meiosis.

During centrosome maturation, pericentrin is delivered to the centrosome co-translationally by a microtubule- and dynein-dependent process, as pericentrin mRNA is undergoing active translation near the centrosome.

The switch from mitotic cell cycles to the one meiotic cell cycle in each generation is triggered through dramatic upregulation of a broad gene expression program by transcriptional regulator STRA8.

Quantitative live-cell microscopy and molecular perturbations in Drosophila and human cells reveal a crosstalk between molecular 'rulers' (Aurora B) and 'clocks' (Cdk1) that coordinates mitotic exit in space and time.

High-resolution single-cell mass accumulation and protein synthesis rate measurements are used to quantify the extent, dynamics and consequences of animal cell growth in mitosis and cytokinesis.

Multiple steps of the atypical cell cycles underlying Plasmodium gametogony are controlled by a divergent cyclin/cyclin-dependent complex.

Experiments with mammalian cells and Xenopus egg extracts elucidate how three proteins cooperate to shape the reticular endoplasmic reticulum network.