Biology subjects

Juan F Poyatos

Publications and source records attributed to Juan F Poyatos.

4 recordsLinked to original sources

bioRxiv2016

Genetic redundancies enhance information transfer in noisy regulatory circuits

Cellular decision making is based on regulatory circuits that associate signal thresholds to specific physiological actions. This transmission of information is subjected to molecular noise what can decrease its fidelity. Here, we show instead how such intrinsic noise enhances information transfer in the presence of multiple circuit copies. The result is due to the contribution of noise to the generation of autonomous responses by each copy, which are altogether associated with a common decision. Moreover, factors that correlate the responses of the redundant units (extrinsic noise or regulatory cross-talk) contribute to reduce fidelity, while those that further uncouple them (heterogeneity within the copies) can lead to stronger information gain. Overall, our study emphasizes how the interplay of signal thresholding, redundancy, and noise influences the accuracy of cellular decision making. Understanding this interplay provides a basis to explain collective cell signaling mechanisms, and to engineer robust decisions with noisy genetic circuits.

Systems Biology↗

bioRxiv2016

Exploitation by cheaters facilitates the preservation of essential public goods in microbial communities

How are public goods1-4 maintained in bacterial cooperative populations? The presence of these compounds is usually threatened by the rise of cheaters that do not contribute but just exploit the common resource5,6. Minimizing cheater invasions appears then as a necessary maintenance mechanism7,8. However, that invasions can instead add to the persistence of cooperation is a prospect that has yet remained largely unexplored6. Here, we show that the detrimental consequences of cheaters can actually preserve public goods, at the cost of recurrent collapses and revivals of the population. The result is made possible by the interplay between spatial constraints and the essentiality of the shared resource. We validate this counter-intuitive effect by carefully combining theory and experiment, with the engineering of an explicit synthetic community in which the public compound allows survival to a bactericidal stress. Notably, the characterization of the experimental system identifies additional factors that can matter, like the impact of the lag phase on the tolerance to stress, or the appearance of spontaneous mutants. Our work emphasizes the unanticipated consequences of the eco-evolutionary feedbacks that emerge in microbial communities relying on essential public goods to function, feedbacks that reveal fundamental for the adaptive change of ecosystems at all scales.

Systems Biology↗

bioRxiv2014

Dual autogenous control of the multiple antibiotic resistance phenotype in Escherichia coli

Bacteria can defend against diverse antibiotics by mounting a multiple antibiotic resistance (mar) phenotype. The resistance is linked to a chromosomal locus that encodes an activator and a repressor regulating their own expression. Here, we investigated how this dual autogenous control determines the dynamics of the response. We found that the regulatory architecture provides a mechanism to enable rapid induction, generate pulses of activation, and increase the range of sensing. The response is also graded and homogeneous across the population. Moreover, the interaction of a third regulator with the core module fine tunes the previous features, while limiting the cross-talk with metabolic signals. A minimal model accurately anticipates these properties, and emphasizes how specific attributes of the circuit components constrain the appearance of other potential behaviors associated to the regulatory design. Our results integrate both molecular and circuit-level characteristics to fully elucidate the dynamic emergence of the mar phenotype.

Systems Biology↗

bioRxiv2014

Rewiring of genetic networks in response to modification of genetic background

Genome-scale genetic interaction networks are progressively contributing to map the molecular circuitry that determines cellular behaviour. To what extent this mapping changes in response to different environmental or genetic conditions is however largely unknown. Here we assembled a genetic network using an in silico model of metabolism in yeast to explicitly ask how separate genetic backgrounds alter network structure. Backgrounds defined by single deletions of metabolically active enzymes induce strong rewiring when the deletion corresponds to a catabolic gene, evidencing a broad redistribution of fluxes to alternative pathways. We also show how change is more pronounced in interactions linking genes in distinct functional modules, and in those connections that present weak epistasis. These patterns reflect overall the distributed robustness of catabolism. In a second class of genetic backgrounds, in which a number of neutral mutations accumulate, we dominantly observe modifications in the negative interactions that together with an increase in the number of essential genes indicate a global reduction in buffering. Notably, neutral trajectories that originate considerable changes in the wild-type network comprise mutations that diminished the environmental plasticity of the corresponding metabolism, what emphasizes a mechanistic integration of genetic and environmental buffering. More generally, our work demonstrates how the specific mechanistic causes of robustness influence the architecture of multiconditional genetic interaction maps.

Systems Biology↗