Natalia L. Komarova

This study shows microbiomes alter host evolutionary dynamics by changing effective population size and selection coefficients, leading to different evolutionary outcomes than classical predictions.

The paper shows that hierarchical tissue structure creates history-dependent barriers to clonal invasion, with established clones affecting the invasion thresholds for subsequent mutants.

The paper shows that superspreaders in contact networks suppress selection, increase deleterious mutant persistence, and can accelerate or decelerate complex evolutionary processes.

The paper shows that in structured populations, variants with proportionally scaled birth and death rates can be advantageous or disadvantageous, altering their fixation probabilities compared to neutral mutants.

This paper shows spatial structure in cell populations can change how mutant burden depends on the death-to-birth ratio, explaining conflicting clinical observations about tumor turnover and patient outcomes.

The paper examines group averaging in rodent locomotion, finding that ensemble-averaged distributions differ from individual ones due to population heterogeneity and proposing a reference rodent model for personalized comparison.

This paper analyzes rodent movement patterns in open-field tests, finding two velocity modes and proposing a stochastic model to explain their behavior.

This study shows that Vibrio cholerae biofilms undergo surface remodeling and inversion of cell-matrix interactions, shifting from attractive to repulsive as biofilms age, which facilitates dispersal.

The paper derives scaling laws to predict mutant emergence in spatially expanding populations and shows gene amplifications promote mutant evolution in spatial settings but not in well-mixed populations.

The paper uses spatially explicit models to show that feedback regulation in cell lineages requires spatial feedforward loops to maintain tissue homeostasis.

The paper analyzes feedback regulation in bladder cancer to identify mechanisms causing cancer stem cell enrichment and chemoresistance.