Budding yeast relies on G cyclin specificity to couple cell cycle progression with morphogenetic development.

Two models have been put forward for cyclin-dependent kinase (Cdk) control of the cell cycle. In the qualitative model, cell cycle events are ordered by distinct substrate specificities of successive cyclin waves. Alternatively, in the quantitative model, the gradual rise of Cdk activity from G phase to mitosis leads to ordered substrate phosphorylation at sequential thresholds.

Analysis of Cell Cycle Progression in the Budding Yeast S. cerevisiae.

The cell cycle is an ordered series of events by which cells grow and divide to give rise to two daughter cells. In eukaryotes, cyclin-cyclin-dependent kinase (cyclin-Cdk) complexes act as master regulators of the cell division cycle by phosphorylating numerous substrates. Their activity and expression profiles are regulated in time.

MST2 kinase suppresses rDNA transcription in response to DNA damage by phosphorylating nucleolar histone H2B.

The heavily transcribed rDNA repeats that give rise to the ribosomal RNA are clustered in a unique chromatin structure, the nucleolus. Due to its highly repetitive nature and transcriptional activity, the nucleolus is considered a hotspot of genomic instability. Breaks in rDNA induce a transient transcriptional shut down to conserve energy and promote rDNA repair; however, how nucleolar chromatin is modified and impacts on rDNA repair is unknown.