arXiv subjects

Juan Manuel Pedraza

Publications and source records attributed to Juan Manuel Pedraza.

3 recordsLinked to original sources

arXiv2025

Intrinsic limits of timekeeping precision in gene regulatory cascades

Multiple cellular processes are triggered when the concentration of a regulatory protein reaches a critical threshold. Previous analyses have characterized timing statistics for single-gene systems. However, many biological timers are based on cascades of genes that activate each other sequentially. Here, we develop an analytical framework to describe the timing precision of such cascades using a burst-dilution hybrid stochastic model. We first revisit the single-gene case and recover the known result of an optimal activation threshold that minimizes first-passage-time (FPT) variability. Extending this concept to two-gene cascades, we identify three distinct optimization regimes determined by the ratio of intrinsic noise levels and the protein dilution rate, defining when coupling improves or worsens timing precision compared to a single-gene strategy. Generalizing to cascades of arbitrary gene length, we obtain a simple mathematical condition that determines when a new gene in the cascade can decrease the timing noise based on its intrinsic noise and protein dilution rate. In the specific case of a cascade of identical genes, our analytical results predict suppression of FPT noise with increasing cascade length and the existence of a mean time that decreases relative timing fluctuations. Together, these results define the intrinsic limits of timekeeping precision in gene regulatory cascades and provide a minimal analytical framework to explore timing control in biological systems.

q-bio.OT↗

arXiv2025

Information and fitness in two-state systems: self-replicating individuals in a fluctuating environment

A population of individuals with the same genes can present heterogeneous traits (phenotypes). The prevalence of this heterogeneity can be explained as a bet-hedging strategy that improves the population proliferation rate (fitness) in fluctuating environments. The phenotype distribution is influenced by factors such as competition between phenotypes, the duration of environmental states, and the rate of phenotype-switching. We illustrate these effects in a system where both the environment and the phenotype can adopt two states. This system includes scenarios such as symmetric bet-hedging and dormant-proliferating phenotypes. We examine how environmental and phenotypic states share mutual information, measured in bits, and explore the relationship between this information and population fitness. We propose that when fitness is measured relative to the case where phenotype and environment are independent, information and fitness can be treated as equivalent measures. We investigate strategies that individuals can use to improve this information, such as adjusting the rates of proliferation and phenotype-switching relative to the environmental fluctuation rate. Through these strategies, with fixed marginal distributions, an increase in information implies an increase in population fitness. We also identify limits to the maximum achievable fitness and information and discuss the value of the information in terms of this new normalized fitness. Our framework offers new insights into how organisms adapt to fluctuating environmental conditions.

q-bio.PE↗

arXiv2019

Characterization of cell division control strategies through continuous rate models

Recent experiments have supported the Adder model for E. coli division control. This model posits that bacteria grow, on average, a fixed size before division. It also predicts decorrelation between the noise in the added size and the size at birth. Here we use new experiments and a theoretical approach based on continuous rate models to explore deviations from the adder strategy, specifically, the division control of E. coli growing with glycerol as carbon source. In this medium, the division strategy is sizer-like, which means that the added size decreases with the size at birth. We found that in a sizer-like strategy the mean added size decreases with the size at birth while the noise in added size increases. We discuss possible molecular mechanisms underlying this strategy, and propose a general model that encompasses the different division strategies.

q-bio.CB↗