Michael Manhart

This study examines how different fitness statistics in high-throughput microbial experiments affect interpretations of mutant fitness and evolutionary dynamics.

This study shows milk urea increases during lactation, is conserved across mammals, and supports infant gut microbiome establishment through urea-metabolizing bacteria.

The paper shows that sublinear density dependence can arise from sequential shifts in resource limitation, without needing other factors like predation, and predicts superlinear dependence at high and low densities.

This study shows that cross-feeding between E. coli auxotrophs globally and idiosyncratically changes mutant fitness by altering selection pressures on specific genetic variants.

This paper develops a theoretical framework to explain how ecological interactions between microbes influence the distribution of fitness effects of mutations.

A gut consumer-resource model with explicit metabolic pathways yields competition-dominated healthy and cooperation-dominated dysbiotic states; an interaction-balance index (ENBI) detects this shift in human disease cohorts.

The paper models and experimentally tests how plasmid transfer and loss probabilities influence antibiotic resistance spread between colliding bacterial colonies.

The paper tests if yeast populations can regain lost function in a synthetic gene circuit by exposing mutants to drug and inducer, revealing adaptation scenarios with or without restoring the circuit's function.

The paper proposes a method to distinguish between direct and indirect targets of selection by analyzing mutational accessibility of phenotypic changes.