466 research outputs found
Hierarchy and Feedback in the Evolution of the E. coli Transcription Network
The E.coli transcription network has an essentially feedforward structure,
with, however, abundant feedback at the level of self-regulations. Here, we
investigate how these properties emerged during evolution. An assessment of the
role of gene duplication based on protein domain architecture shows that (i)
transcriptional autoregulators have mostly arisen through duplication, while
(ii) the expected feedback loops stemming from their initial cross-regulation
are strongly selected against. This requires a divergent coevolution of the
transcription factor DNA-binding sites and their respective DNA cis-regulatory
regions. Moreover, we find that the network tends to grow by expansion of the
existing hierarchical layers of computation, rather than by addition of new
layers. We also argue that rewiring of regulatory links due to
mutation/selection of novel transcription factor/DNA binding interactions
appears not to significantly affect the network global hierarchy, and that
horizontally transferred genes are mainly added at the bottom, as new target
nodes. These findings highlight the important evolutionary roles of both
duplication and selective deletion of crosstalks between autoregulators in the
emergence of the hierarchical transcription network of E.coli.Comment: to appear in PNA
Neutral forces acting on intragenomic variability shape the Escherichia coli regulatory network topology
Cis-regulatory networks (CRNs) play a central role in cellular decision
making. Like every other biological system, CRNs undergo evolution,
which shapes their properties by a combination of adaptive
and nonadaptive evolutionary forces. Teasing apart these forces is
an important step toward functional analyses of the different components
of CRNs, designing regulatory perturbation experiments,
and constructing synthetic networks. Although tests of neutrality
and selection based on molecular sequence data exist, no such tests
are currently available based on CRNs. In this work, we present
a unique genotype model of CRNs that is grounded in a genomic
context and demonstrate its use in identifying portions of the
CRN with properties explainable by neutral evolutionary forces
at the system, subsystem, and operon levels.We leverage our model
against experimentally derived data from Escherichia coli. The
results of this analysis show statistically significant and substantial
neutral trends in properties previously identified as adaptive
in originラdegree distribution, clustering coefficient, and motifsラ
within the E. coli CRN. Our model captures the tightly coupled genomeヨ
interactome of an organism and enables analyses of how
evolutionary events acting at the genome level, such as mutation,
and at the population level, such as genetic drift, give rise to neutral
patterns that we can quantify in CRNs
Selective Constraints on Amino Acids Estimated by a Mechanistic Codon Substitution Model with Multiple Nucleotide Changes
Empirical substitution matrices represent the average tendencies of
substitutions over various protein families by sacrificing gene-level
resolution. We develop a codon-based model, in which mutational tendencies of
codon, a genetic code, and the strength of selective constraints against amino
acid replacements can be tailored to a given gene. First, selective constraints
averaged over proteins are estimated by maximizing the likelihood of each 1-PAM
matrix of empirical amino acid (JTT, WAG, and LG) and codon (KHG) substitution
matrices. Then, selective constraints specific to given proteins are
approximated as a linear function of those estimated from the empirical
substitution matrices.
Akaike information criterion (AIC) values indicate that a model allowing
multiple nucleotide changes fits the empirical substitution matrices
significantly better. Also, the ML estimates of transition-transversion bias
obtained from these empirical matrices are not so large as previously
estimated. The selective constraints are characteristic of proteins rather than
species. However, their relative strengths among amino acid pairs can be
approximated not to depend very much on protein families but amino acid pairs,
because the present model, in which selective constraints are approximated to
be a linear function of those estimated from the JTT/WAG/LG/KHG matrices, can
provide a good fit to other empirical substitution matrices including cpREV for
chloroplast proteins and mtREV for vertebrate mitochondrial proteins.
The present codon-based model with the ML estimates of selective constraints
and with adjustable mutation rates of nucleotide would be useful as a simple
substitution model in ML and Bayesian inferences of molecular phylogenetic
trees, and enables us to obtain biologically meaningful information at both
nucleotide and amino acid levels from codon and protein sequences.Comment: Table 9 in this article includes corrections for errata in the Table
9 published in 10.1371/journal.pone.0017244. Supporting information is
attached at the end of the article, and a computer-readable dataset of the ML
estimates of selective constraints is available from
10.1371/journal.pone.001724
Degeneracy: a link between evolvability, robustness and complexity in biological systems
A full accounting of biological robustness remains elusive; both in terms of the mechanisms by which robustness is achieved and the forces that have caused robustness to grow over evolutionary time. Although its importance to topics such as ecosystem services and resilience is well recognized, the broader relationship between robustness and evolution is only starting to be fully appreciated. A renewed interest in this relationship has been prompted by evidence that mutational robustness can play a positive role in the discovery of adaptive innovations (evolvability) and evidence of an intimate relationship between robustness and complexity in biology.
This paper offers a new perspective on the mechanics of evolution and the origins of complexity, robustness, and evolvability. Here we explore the hypothesis that degeneracy, a partial overlap in the functioning of multi-functional components, plays a central role in the evolution and robustness of complex forms. In support of this hypothesis, we present evidence that degeneracy is a fundamental source of robustness, it is intimately tied to multi-scaled complexity, and it establishes conditions that are necessary for system evolvability
Three-dimensional simulations of inorganic aerosol distributions in east Asia during spring 2001
In this paper, aerosol composition and size distributions in east Asia are simulated using a comprehensive chemical transport model. Three-dimensional aerosol simulations for the TRACE-P and ACE-Asia periods are performed and used to help interpret actual observations. The regional chemical transport model, STEM-2K3, which includes the on-line gas-aerosol thermodynamic module SCAPE II, and explicitly considers chemical aging of dust, is used in the analysis. The model is found to represent many of the important observed features. The Asian outflow during March and April of 2001 is heavily polluted with high aerosol loadings. Under conditions of low dust loading, SO_2 condensation and gas phase ammonia distribution determine the nitrate size and gas-aerosol distributions along air mass trajectories, a situation that is analyzed in detail for two TRACE-P flights. Dust is predicted to alter the partitioning of the semivolatile components between the gas and aerosol phases as well as the size distributions of the secondary aerosol constituents. Calcium in the dust affects the gas-aerosol equilibrium by shifting the equilibrium balance to an anion-limited status, which benefits the uptake of sulfate and nitrate, but reduces the amount of aerosol ammonium. Surface reactions on dust provide an additional mechanism to produce aerosol nitrate and sulfate. The size distribution of dust is shown to be a critical factor in determining the size distribution of secondary aerosols. As much of the dust mass is found in the supermicron mode (70–90%), appreciable amounts of sulfate and nitrate are found in the supermicron particles. For sulfate the observations and the analysis indicate that 10–30% of sulfate is in the supermicron fraction during dust events; in the case of nitrate, more than 80% is found in the supermicron fraction
Networked buffering: a basic mechanism for distributed robustness in complex adaptive systems
A generic mechanism - networked buffering - is proposed for the generation of robust traits in complex systems. It requires two basic conditions to be satisfied: 1) agents are versatile enough to perform more than one single functional role within a system and 2) agents are degenerate, i.e. there exists partial overlap in the functional capabilities of agents. Given these prerequisites, degenerate systems can readily produce a distributed systemic response to local perturbations. Reciprocally, excess resources related to a single function can indirectly support multiple unrelated functions within a degenerate system. In models of genome:proteome mappings for which localized decision-making and modularity of genetic functions are assumed, we verify that such distributed compensatory effects cause enhanced robustness of system traits. The conditions needed for networked buffering to occur are neither demanding nor rare, supporting the conjecture that degeneracy may fundamentally underpin distributed robustness within several biotic and abiotic systems. For instance, networked buffering offers new insights into systems engineering and planning activities that occur under high uncertainty. It may also help explain recent developments in understanding the origins of resilience within complex ecosystems. \ud
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Functional Compensation of Primary and Secondary Metabolites by Duplicate Genes in Arabidopsis thaliana
It is well known that knocking out a gene in an organism often causes no phenotypic effect. One possible explanation is the existence of duplicate genes; that is, the effect of knocking out a gene is compensated by a duplicate copy. Another explanation is the existence of alternative pathways. In terms of metabolic products, the relative roles of the two mechanisms have been extensively studied in yeast but not in any multi-cellular organisms. Here, to address the functional compensation of metabolic products by duplicate genes, we quantified 35 metabolic products from 1,976 genes in knockout mutants of Arabidopsis thaliana by a high-throughput Liquid chromatography-Mass spectrometer (LC-MS) analysis. We found that knocking out either a singleton gene or a duplicate gene with distant paralogs in the genome tends to induce stronger metabolic effects than knocking out a duplicate gene with a close paralog in the genome, indicating that only duplicate genes with close paralogs play a significant role in functional compensation for metabolic products in A. thaliana. To extend the analysis, we examined metabolic products with either high or low connectivity in a metabolic network. We found that the compensatory role of duplicate genes is less important when the metabolite has a high connectivity, indicating that functional compensation by alternative pathways is common in the case of high connectivity. In conclusion, recently duplicated genes play an important role in the compensation of metabolic products only when the number of alternative pathways is small
Extensive Copy-Number Variation of Young Genes across Stickleback Populations
MM received funding from the Max Planck innovation funds for this project. PGDF was supported by a Marie Curie European Reintegration Grant (proposal nr 270891). CE was supported by German Science Foundation grants (DFG, EI 841/4-1 and EI 841/6-1). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript
Gene duplication and phenotypic changes in the evolution of Mammalian metabolic networks
Metabolic networks attempt to describe the complete suite of biochemical reactions available to an organism. One notable feature of these networks in mammals is the large number of distinct proteins that catalyze the same reaction. While the existence of these isoenzymes has long been known, their evolutionary significance is still unclear. Using a phylogenetically-aware comparative genomics approach, we infer enzyme orthology networks for sixteen mammals as well as for their common ancestors. We find that the pattern of isoenzymes copy-number alterations (CNAs) in these networks is suggestive of natural selection acting on the retention of certain gene duplications. When further analyzing these data with a machine-learning approach, we found that that the pattern of CNAs is also predictive of several important phenotypic traits, including milk composition and geographic range. Integrating tools from network analyses, phylogenetics and comparative genomics both allows the prediction of phenotypes from genetic data and represents a means of unifying distinct biological disciplines
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