Gene regulatory architecture in antibiotic resistance is optimized for specific dynamic regimens
Listed in
This article is not in any list yet, why not save it to one of your lists.Abstract
Cellular responses to antibiotics face a fundamental trade-off: resistance must be deployed quickly enough to prevent the accumulation of drug inside the cell, but expression of resistance genes is costly in the absence of the drug. Therefore, antibiotic responses are typically regulated, controlling not only whether resistance is expressed, but also when, how strongly, and for how long. These regulatory strategies are implemented through the strength and arrangement of promoters and operators. However, it is still not clear how the dynamics of drug exposure select for specific regulatory strategies. Here, we develop a dynamical model of a typical antibiotic response, where a transcriptional repressor senses the drug and regulates expression of a resistance protein, coupled to the effects of the drug on cell growth and gene expression. We define a cost function that weighs the different burdens imposed on the cell over the course of the response, and perform in silico optimization of the regulatory parameters under different selective pressures for three architectures of increasing complexity: constitutive expression of resistance, repression by a constitutively expressed repressor, and repression by a self-regulated repressor. We find that strong drug exposures favor constitutive expression of resistance, high costs of basal expression favor repression by a constitutive repressor, and self-regulation of the repressor is favored only when the response must provide protection while also restraining overexpression of resistance. Stochastic simulations further show that self-regulation of the repressor protects cells against fluctuations in repressor levels, which cause unnecessary induction of resistance before exposure and failed induction after exposure. This framework links the dynamics of the environment to the evolution of gene regulation, providing a basis to predict which regulatory strategies are expected to arise under specific selective pressures.
Significance
Bacteria regulate the expression of antibiotic resistance genes to avoid the costs of producing resistance when it is not needed. However, regulated responses take time to activate, which can be fatal when cells are suddenly exposed to large drug doses. Here, we use a mathematical model of antibiotic responses to identify which regulatory strategies are optimal under different selective pressures. We show that the choice between constitutive and regulated expression of resistance, and the use of self-regulation by the repressor, depend on the dynamics of drug exposure and on which costs dominate the response. Noise in gene expression further favors self-regulation of the repressor near the limit of tolerable drug exposures. These results help explain the diversity of regulatory architectures found in natural resistance mechanisms, and the frequent loss of regulation in pathogens exposed to antibiotic treatments.
Article activity feed
-
Gene regulatory architecture in antibiotic resistance is optimized for specific dynamic regimens https://www.biorxiv.org/content/10.64898/2026.11.03.764017v1
-
Gene regulatory architecture in antibiotic resistance is optimized for specific dynamic regimens https://www.biorxiv.org/content/10.64898/2026.11.03.764017v1
-