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Carballo-Pacheco, M.

Publications and source records attributed to Carballo-Pacheco, M..

4 recordsLinked to original sources

Macroecological Laws Can Naturally Arise from Chaotic Internal Species Dynamics

Macroecological relationships that connect various statistical descriptors of long-term and short-term species dynamics represent some of the most general laws in ecology and biology. These macroecological laws have been observed across diverse ecologies of plants and animals, and more recently, also in microbiota. Yet it remains unclear why strikingly similar macroecological relationships often arise in very different biological communities and various environmental contexts. Here, we investigated whether chaotic internal dynamics in spatially heterogeneous communities could underlie multiple macroecological relationships. Our analyses reveal that very general constraints on species interactions and spatial migration parameters can simultaneously lead to multiple macroecological laws found in microbial ecosystems without requiring external sources of noise. Our study also identifies the mechanistic origins of many empirically observed macroecological relationships, such as Taylors law, anomalous abundance diffusion, the Laplace distribution of short-term abundance changes, and the distribution of species residence times. Overall, we demonstrate how macroecological laws can arise from interaction-driven chaotic dynamics and common ecological constraints, thereby providing a unifying explanation for their widespread prevalence in nature.

ecology↗

Multiple macroecological laws do characterize various aspects of microbiota dynamics

In this letter we address the potential confusion related to our recent demonstration that multiple macroecological laws describe short- and long-term dynamics of microbial communities. Specifically, we clarify that these laws, similarly to many other relationships observed in nature, are characterized not just by the existence of scaling, but also by certain characteristic values of the scaling exponents. By performing proper statistical analysis, we demonstrate that the relationships sensitive to temporal bacterial dynamics are not reproduced in the shuffled data. We also discuss that there is no clear evidence in the data that macroecological relationships in microbiota are primarily driven by external or environmental factors. Proper statistical analyses of the data suggest that the dynamics of gut microbiota, even on a constant diet, contains rich temporal structure. Therefore, it is likely that complex and non-linear internal dynamics may be primarily responsible for the observed macroecological laws in microbiota and other ecological communities.

microbiology↗

Phenotypic delay: mechanistic models and their implications for the evolution of resistance to antibiotics

Phenotypic delay - the time delay between genetic mutation and expression of the corresponding phenotype - is generally neglected in evolutionary models, yet recent work suggests that it may be more common than previously assumed. Here, we use computer simulations and theory to investigate the significance of phenotypic delay for the evolution of bacterial resistance to antibiotics. We consider three mechanisms which could potentially cause phenotypic delay: effective polyploidy, dilution of antibiotic-sensitive molecules and accumulation of resistance-enhancing molecules. We find that the accumulation of resistant molecules is relevant only within a narrow parameter range, but both the dilution of sensitive molecules and effective polyploidy can cause phenotypic delay over a wide range of parameters. We further investigate whether these mechanisms could affect population survival under drug treatment and thereby explain observed discrepancies in mutation rates estimated by Luria-Delbruck fluctuation tests. While the effective polyploidy mechanism does not affect population survival, the dilution of sensitive molecules leads both to decreased probability of survival under drug treatment and underestimation of mutation rates in fluctuation tests. The dilution mechanism also changes the shape of the Luria-Delbruck distribution of mutant numbers, and we show that this modified distribution provides an improved fit to previously published experimental data. Author SummaryUnderstanding precisely how some bacteria survive exposure to antibiotics is a major research focus. Specific mutations in the bacterial genome are known to provide protection. However, it remains unclear how much time passes between a bacterium acquiring the genetic change and being able to tolerate antibiotics - termed the phenotypic delay - and what controls this delay. Here, using computer simulations and mathematical arguments we discuss three biologically plausible mechanisms of phenotypic delay. We investigate how each mechanism would affect the outcome of laboratory experiments often used to study the evolution of antibiotic resistance, and we highlight how the delay might be detected in such experiments. We also show that the existence of the delay could explain an observed discrepancy in the measurement of mutation rates, and demonstrate that one of our models provides a superior fit to experimental data. Our work exposes how molecular details at the intracellular level can have a direct effect on evolution at the population level.

evolutionary biology↗

Receptor crosstalk improves concentration sensing of multiple ligands

Cells need to reliably sense external ligand concentrations to achieve various biological functions such as chemotaxis or signaling. The molecular recognition of ligands by surface receptors is degenerate in many systems leading to crosstalk between different receptors. Crosstalk is often thought of as a deviation from optimal specific recognition, as the binding of non-cognate ligands can interfere with the detection of the receptors cognate ligand, possibly leading to a false triggering of a downstream signaling pathway. Here we quantify the optimal precision of sensing the concentrations of multiple ligands by a collection of promiscuous receptors. We demonstrate that crosstalk can improve precision in concentration sensing and discrimination tasks. To achieve superior precision, the additional information about ligand concentrations contained in short binding events of the noncognate ligand should be exploited. We present a proofreading scheme to realize an approximate estimation of multiple ligand concentrations that reaches a precision close to the derived optimal bounds. Our results help rationalize the observed ubiquity of receptor crosstalk in molecular sensing.

cell biology↗