The decision to commit to cell division-the Start transition-in budding yeast is governed by time integration of G1 cyclin-CDK activity by the transcription factor Whi5.

Cells accumulate damaged proteins during aging and, by compromising the function of chaperones in folding newly synthesized G1 cyclins, proteostasis breakdown inhibits cell-cycle entry and drives yeast cells into senescence.

A G1 cyclin shows key properties expected of a protein that could link cell cycle progression to cell growth.

Investigation of how cells rewire their transcriptional programs during transition from mitotic to meiotic cell fate reveals a two-pronged mechanism for inactivating a key mitotic transcription factor.

Impaired GABAergic and glutamatergic synaptic function and loss of interneurons in the amygdala, hippocampus, and cerebellum cause characteristic disease symptoms in a mouse model juvenile neuronal ceroid lipofuscinosis.

Inhibition of phosphatases by kinases develops Whi5 phosphorylation and cell cycle function in low cyclin-dependent kinase activity.

Yeast cell size homeostasis is not controlled by a G1-specific mechanism alone but is likely to be an emergent property resulting from the integration of several mechanisms that coordinate cell and bud growth with division.

Two novel subsets of microglia identified by their unique autofluorescence profiles differ in their subcellular organization, proteomic signatures and in their response to aging and lysosomal dysfunction.

Cell cycle network evolution in a fungal ancestor was punctuated by the arrival of a viral DNA-binding protein that was permanently incorporated into the regulatory network controlling cell cycle entry.

The endo-lysosomal system plays a positive essential role in the initiation of the cell cycle in yeast.