Frederick R. Cross

TL;DR: The present method is general and affords a quantitative description of cellular differences at the level of protein expression and modification, thus providing information that is critical to the understanding of complex biological phenomena.

TL;DR: A new human cyclin, named cyclin E, was isolated by complementation of a triple cln deletion in S. cerevisiae, suggesting that it functioned at START by interacting with the CDC28 protein.

TL;DR: It is shown that a mathematical model built on a consensus picture of this control system is largely successful in explaining the phenotypes of mutants described so far and allows one to frame and critique hypotheses about how the division cycle is regulated in wild-type and mutant cells, to predict the phenotypic properties of new mutant combinations, and to estimate the effective values of biochemical rate constants that are difficult to measure directly in vivo.

TL;DR: Using strains where CLN1 was expressed conditionally, the essential function of ClN proteins was found to be limited to the G1 phase, consistent with the hypothesis that Cln proteins activate the Cdc28 protein kinase, shown to be essential for the G 1 to S phase transition in S. cerevisiae.

TL;DR: In budding yeast, a single Cdk is activated by multiple cyclins, and the ability of these cyclins to target specific proteins and to initiate different cell-cycle events might reflect the timing of the expression of the cyclins.