# Publications

*E. coli*to be non-exponential. Our analysis shows that in the later stages of the cell cycle the growth rate is faster than exponential.

*Escherichia coli*is growth-rate dependent. 2021. bioRxivAbstract

*Escherichia coli*different data sets and models have supported a range of conclusions from one extreme where these two processes are tightly linked to another extreme where these processes are completely independent of each other. Using high throughput optical microscopy and cell cycle modeling, we show that in slow growth conditions replication and division processes are strongly correlated, indicating a significant coupling between replication and division. This coupling weakens as the growth rate of cells increases. Our data suggest that the underlying control mechanism in slow growth conditions is related to unreplicated chromosome blocking the onset of constriction at the midcell. We show that the nucleoid occlusion protein SlmA does not play a role in this process and neither do other known factors involved in positioning bacterial Z-ring relative to the chromosome. Altogether this work reconciles different ideas from the past and brings out a more nuanced role of replication in controlling the division process in a growth-rate dependent manner.

*a priori*knowledge of the underlying gene expression dynamics. We apply this method to experimental data of single-cell bacterial gene expression. The results allow us to estimate the average copy numbers and the translation burst parameters of the studied proteins.

*E. coli*transcription network, we find that the biological network is significantly more stable than its randomized counterpart, suggesting that stability constraints may have shaped network structure during the course of evolution.

In biological contexts as diverse as development, apoptosis, and synthetic microbial consortia, collections of cells or sub-cellular components have been shown to overcome the slow signaling speed of simple diffusion by utilizing diffusive relays, in which the presence of one type of diffusible signaling molecule triggers participation in the emission of the same type of molecule. This collective effect gives rise to fast-traveling diffusive waves. Here, in the context of cell signaling, we show that system dimensionality – the shape of the extracellular medium and the distribution of cells within it – can dramatically affect the wave dynamics, but that these dynamics are insensitive to details of cellular activation. As an example, we show that neutrophil swarming experiments exhibit dynamical signatures consistent with the proposed signaling motif. We further show that cell signaling relays generate much steeper concentration profiles than does simple diffusion, which may facilitate neutrophil chemotaxis.

*explicit*relationship between observables obtained from a single lineage and the population growth rate? We show that a population’s growth rate can be represented in terms of averages over isolated lineages. This lineage representation is related to a large deviation principle that is a generic feature of exponentially proliferating populations. Due to the large deviation structure of growing populations, the number of lineages needed to obtain an accurate estimate of the growth rate depends exponentially on the duration of the lineages, leading to a nonmonotonic convergence of the estimate, which we verify in both synthetic and experimental data sets.

*maximum*of i.i.d. variables may converge to a distribution belonging to one of three universality classes (Gumbel, Weibull and Fréchet). Here, we rederive these known results following a mathematically non-rigorous yet highly transparent renormalization-group-inspired approach that captures both of these universal results following a nearly identical procedure.

*GAL1*promoter to make the Whi5 concentration independent of cell size. At an expression level that equalizes the mean cell size with that of wild-type cells, the size distributions of cells with galactose-induced Whi5 expression and wild-type cells are indistinguishable. Fluorescence microscopy confirms that the endogenous and

*GAL1*promoters produce different relationships between Whi5 concentration and cell volume without diminishing size control in the G1 phase. We also expressed Cln3 from the GAL1 promoter, finding that the spread in cell sizes for an asynchronous population is unaffected by this perturbation. Our findings indicate that size control in budding yeast does not fundamentally originate from the linear accumulation of Whi5, contradicting a previous claim and demonstrating the need for further models of cell-cycle regulation to explain how cell size controls passage through Start.