Kara Schmidlin

The paper shows that fitness variation across drug environments in yeast is organized by a low-dimensional phenotypic structure, revealing modular phenotypic modules that constrain adaptive mutations.

This study shows that evolving larger cell size reduces internal cellular density, as material accumulation does not keep pace with volume increase, both in experimental evolution and across species.

The paper investigates environment-by-environment interactions (ExE) across genetic backgrounds (ExExG) in yeast, showing that drug combinations vary in effectiveness among mutants and introducing a new predictive framework.

The paper uses single-cell RNA sequencing to analyze stress responses in yeast, finding that stressed cells show more variability than unstressed cells and that population-level analyses can obscure individual differences.

INgen enables DNA amplification within fixed cells, overcoming limitations in single-cell genomics by allowing sequencing without physical cell isolation.

The paper identifies distinct fitness tradeoff groups among fluconazole-resistant yeast mutants, suggesting different resistance mechanisms and implications for multidrug therapy design.

This paper introduces a high-throughput single-cell RNA-seq platform for yeasts that enables multiplexing of hundreds of strains and environments, revealing transcriptional heterogeneity within clonal populations.