Audrey Menegaz Proenca

This study shows that protein aggregation in E. coli drives aging by reducing intracellular space, leading to larger cell sizes and asymmetric divisions.

The paper investigates how single-cell damage dynamics under stress affect population fitness, finding that damage-dependent mortality is a key factor.

The paper shows that division asymmetry in E. coli has evolved to an optimum for population growth, with selective forces primarily acting on transcription signal asymmetry variance.

This paper shows that bacterial aging, through asymmetric damage inheritance, creates phenotypic heterogeneity that biases persistence rates during antibiotic treatment.