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Biology subjects

Grah, R.

Publications and source records attributed to Grah, R..

3 recordsLinked to original sources

Linking Molecular Mechanisms to their Evolutionary Consequences: a primer

A major obstacle to predictive understanding of evolution stems from the complexity of biological systems, which prevents detailed characterization of key evolutionary properties. Here, we highlight some of the major sources of complexity that arise when relating molecular mechanisms to their evolutionary consequences and ask whether accounting for every mechanistic detail is important to accurately predict evolutionary outcomes. To do this, we developed a mechanistic model of a bacterial promoter regulated by two proteins, allowing us to connect any promoter genotype to six phenotypes that capture the dynamics of gene expression following an environmental switch. Accounting for the mechanisms that govern how this system works enabled us to provide an in-depth picture of how regulated bacterial promoters might evolve. More importantly, we used the model to explore which factors that contribute to the complexity of this system are essential for understanding its evolution, and which can be simplified without information loss. We found that several key evolutionary properties - the distribution of phenotypic and fitness effects of mutations, the evolutionary trajectories during selection for regulation - can be accurately captured without accounting for all, or even most, parameters of the system. Our findings point to the need for a mechanistic approach to studying evolution, as it enables tackling biological complexity and in doing so improves the ability to predict evolutionary outcomes.

evolutionary biology↗

Normative models of enhancer function

In prokaryotes, thermodynamic models of gene regulation provide a highly quantitative mapping from promoter sequences to gene expression levels that is compatible with in vivo and in vitro bio-physical measurements. Such concordance has not been achieved for models of enhancer function in eukaryotes. In equilibrium models, it is difficult to reconcile the reported short transcription factor (TF) residence times on the DNA with the high specificity of regulation. In non-equilibrium models, progress is difficult due to an explosion in the number of parameters. Here, we navigate this complexity by looking for minimal non-equilibrium enhancer models that yield desired regulatory phenotypes: low TF residence time, high specificity and tunable cooperativity. We find that a single extra parameter, interpretable as the "linking rate" by which bound TFs interact with Mediator components, enables our models to escape equilibrium bounds and access optimal regulatory phenotypes, while remaining consistent with the reported phenomenology and simple enough to be inferred from upcoming experiments. We further find that high specificity in non-equilibrium models is in a tradeoff with gene expression noise, predicting bursty dynamics -- an experimentally-observed hallmark of eukaryotic transcription. By drastically reducing the vast parameter space to a much smaller subspace that optimally realizes biological function prior to inference from data, our normative approach holds promise for mathematical models in systems biology.

biophysics↗

Transcriptional crosstalk varies between regulatory strategies

Genes differ in the frequency at which they are expressed and in the form of regulation used to control their activity. In particular, positive or negative regulation can lead to activation of a gene in response to an external signal. Previous works proposed that the form of regulation of a gene correlates with its frequency of usage: positive regulation when the gene is frequently expressed and negative regulation when infrequently expressed. Such network design means that, in the absence of their regulators, the genes are found in their least required activity state, hence regulatory intervention is often necessary. Due to the multitude of genes and regulators, spurious binding and unbinding events, called \"crosstalk\", could occur. To determine how the form of regulation affects the global crosstalk in the network, we used a mathematical model that includes multiple regulators and multiple target genes. We found that crosstalk depends non-monotonically on the availability of regulators. Our analysis showed that excess use of regulation entailed by the formerly suggested network design caused high crosstalk levels in a large part of the parameter space. We therefore considered the opposite idle design, where the default unregulated state of genes is their frequently required activity state. We found, that idle design minimized the use of regulation and thus minimized crosstalk. In addition, we estimated global crosstalk of S. cerevisiae using transcription factors binding data. We demonstrated that even partial network data could suffice to estimate its global crosstalk, suggesting its applicability to additional organisms. We found that S. cerevisiae estimated crosstalk is lower than that of a random network, suggesting that natural selection reduces crosstalk. In summary, our study highlights a new type of protein production cost which is typically overlooked: that of regulatory interference caused by the presence of excess regulators in the cell. It demonstrates the importance of whole-network descriptions, which could show effects missed by single-gene models.\n\nAuthor SummaryGenes differ in the frequency at which they are expressed and in the form of regulation used to control their activity. The basic level of regulation is mediated by different types of DNA-binding proteins, where each type regulates particular gene(s). We distinguish between two basic forms of regulation: positive - if a gene is activated by the binding of its regulatory protein, and negative - if it is active unless bound by its regulatory protein. Due to the multitude of genes and regulators, spurious binding and unbinding events, called \"crosstalk\", could occur. How does the form of regulation, positive or negative, affect the extent of regulatory crosstalk? To address this question, we used a mathematical model integrating many genes and many regulators. As intuition suggests, we found that in most of the parameter space, crosstalk increased with the availability of regulators. We propose, that crosstalk is usually reduced when networks are designed such that minimal regulation is needed, which we call the idle design. In other words: a frequently needed gene will use negative regulation and conversely, a scarcely needed gene will employ positive regulation. In both cases, the requirement for the regulators is minimized. In addition, we demonstrate how crosstalk can be calculated from available datasets and discuss the technical challenges in such calculation, specifically data incompleteness.

systems biology↗