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

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.

Pre-RC component Cdc6 is primed for origin licensing by phosphatases and Cdk1 inhibitor.

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.

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.

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.

Quantitative analysis of time-dependent transcription data elucidates the signal processing within the genetic network that regulates transcriptional cell cycle oscillations in yeast.

The S-phase checkpoint has roles in all phases of the cell cycle, which has implications for the majority of cancers that lack cell cycle controls.

The SCF-family of ubiquitin ligases regulates the key cancer proliferation node by controlling the degradation of RB-like tumor suppressor RBL2/p130.