Michael Hinczewski

The paper models myosin-V-like motor proteins to show how they can achieve both high velocity and long run distances, identifying a trade-off and theoretical limits.

This study investigates gap formation between interacting bacterial colonies using experiments and modeling, finding that nutrient competition and direct growth inhibition drive this phenomenon.

The paper shows that public good-producing subclones can invade non-producer populations in structured environments due to spatial effects, challenging classical evolutionary game theory predictions.

This paper introduces SHEPHERD, a method combining population genetics and MDPs to design adaptive drug policies that reduce disease fitness in heterogeneous populations, showing effectiveness in synthetic multi-drug landscapes.

The paper quantifies de novo mutations from maize Mutator transposons across tissues, revealing tissue-specific patterns and reinterpreting genetic experiments.

This paper introduces a new metric, edge flip fraction, to compare fitness landscapes and shows it predicts evolutionary trajectories and drug sequence optimality.

The paper studies how asymmetric interactions affect mutant survival during population range expansions using simulations and a mathematical model.

This study investigates how phosphomimetic substitutions at C-terminal sites of TDP-43's low complexity domain alter liquid-liquid phase separation, revealing a biphasic salt dependence and changes in phase separation mechanisms.

The paper demonstrates that Wiener-Kolmogorov bounds can be violated in nonlinear signaling systems, though the violations are biologically negligible.

The paper analyzes the energetic costs of cellular signaling, showing that ATP consumption and chemical potential determine the information capacity of kinase-phosphatase loops, with yeast signaling pathways approaching optimality.