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Alvaro Sanchez

Publications and source records attributed to Alvaro Sanchez.

2 recordsLinked to original sources

A tradeoff between the ecological and evolutionary stabilities of public goods genes in microbial populations

Microbial populations often rely on the cooperative production of extracellular \"public goods\" molecules. The cooperative nature of public good production may lead to minimum viable population sizes, below which populations collapse. In addition, \"cooperator\" public goods producing cells face evolutionary competition from non-producing mutants, or \"freeloaders\". Thus, public goods cooperators have to be stable not only to the invasion of freeloaders, but also to ecological perturbations that may push their numbers too small to be sustainable. Through a combination of experiments with microbial populations and mathematical analysis of the Ecological Public Goods Game, we show that game parameters and experimental conditions that improve the evolutionary stability of cooperators also lead to a low ecological stability of the cooperator population. Complex regulatory strategies mimicking those used by microbes in nature may allow cooperators to beat this eco-evolutionary stability tradeoff and become resistant to freeloaders while at the same time maximizing their ecological stability. Our results thus identify the coupled eco-evolutionary stability as being key for the long-term viability of microbial public goods cooperators.

Evolutionary Biology

Integrating regulatory information via combinatorial control of the transcription cycle

Combinatorial regulation of gene expression by multiple transcription factors (TFs) enables cells to carry out sophisticated computations that are key to cellular decision-making. How is the information contained in multiple TF binding sites integrated to dictate the rate of transcription? The dominant model is that direct or indirect physical interactions between TFs enable them to combinatorially recruit each other and RNA polymerase to the promoter. Here we develop a quantitative framework to explore an alternative model, where combinatorial gene regulation can result from TFs working on different kinetic steps of the transcription cycle. Our results clarify the null hypotheses for independent action of TFs and show that combinatorial control of the transcription cycle can generate a wide range of analog and Boolean computations without requiring the input regulators to be simultaneously co-localized in the nucleus. This work emphasizes the importance of deciphering TF function beyond activation and repression, highlights the role of the basal promoter in processing regulatory information and suggests qualitative explanations for the flexibility of regulatory evolution.

Systems Biology