John J. Tyson

This study identifies a novel feedback system regulating Cdk function through Spo12, a small disordered protein that inhibits PP2A, and shows its role in enhancing cell proliferation in fission yeast.

The paper develops a dynamical model of the cell cycle as two mutually inhibitory oscillators, showing how this framework can explain various cell cycle behaviors.

FindingNemo improves ultra-long nanopore sequencing by optimizing DNA extraction and library preparation for higher yields and scalability.

The paper analyzes experimental data on fission yeast cell cycle transitions and proposes a stochastic model to assess bistability of the G2/M checkpoint.

This paper shows that dysregulation of CycB:CDK disrupts cell cycle switches, leading to genome doubling, a common event in tumorigenesis.

The paper develops a stochastic Boolean model of the budding yeast cell cycle that accurately replicates wild-type and mutant phenotypes, providing a validated framework for studying cell cycle regulation.

The paper shows that mitotic kinase oscillations control cell cycle latches, and disrupting these leads to endocycles in yeast.

The paper builds a computational model of the nutrient signaling network in budding yeast to reconcile experimental data with a proposed molecular mechanism and test predictions in mutant strains.

The paper develops a computational model to explain DNA re-replication in fission yeast mutants, showing how protein overproduction leads to transitions between endoreplication and over-replication.

The paper identifies a generic network motif of coupled positive and negative feedback loops governing bistable transitions in the eukaryotic cell cycle.

The paper analyzes the robustness of oscillations in a circadian clock model by modifying parameter constraints and feedback loops to achieve realistic biological parameters.

This study experimentally shows that Per2AS regulates circadian clock amplitude through a negative feedback loop with Per2, without producing a protein.

The paper quantitatively estimates genetic interactions between 36 yeast cell-cycle genes using high-throughput phenotyping of 7,350 mutants and refines a mathematical cell cycle model.

This paper develops a hybrid stochastic model to study noise effects on budding yeast cell cycle control, achieving efficient simulations matching experimental data.

The paper presents a stochastic model to study how kinase and phosphatase activities affect error correction and spindle assembly checkpoint signaling in budding yeast.

This study uses mathematical models to investigate size control mechanisms in budding yeast, finding that titration of Cln3 against genomic binding sites provides a more accurate explanation than inhibitor dilution.

The paper performs a bifurcation analysis of a mammalian circadian clock model to understand how gene expression and protein activity influence oscillatory dynamics and feedback loops.

The paper uses an engineered SAC activator to study the biochemical and physiological mechanisms of the Spindle Assembly Checkpoint.