scholarly journals Symmetry and simplicity spontaneously emerge from the algorithmic nature of evolution

2021 ◽  
Author(s):  
Iain Johnston ◽  
Kamaludin Dingle ◽  
Sam F Greenbury ◽  
Chico Q. Camargo ◽  
Jonathan P K Doye ◽  
...  

Engineers routinely design systems to be modular and symmetric in order to increase robustness to perturbations and to facilitate alterations at a later date. Biological structures also frequently exhibit modularity and symmetry, but the origin of such trends is much less well understood. It can be tempting to assume -- by analogy to engineering design -- that symmetry and modularity arise from natural selection. But evolution, unlike engineers, cannot plan ahead, and so these traits must also afford some immediate selective advantage which is hard to reconcile with the breadth of systems where symmetry is observed. Here we introduce an alternative non-adaptive hypothesis based on an algorithmic picture of evolution. It suggests that symmetric structures preferentially arise not just due to natural selection, but also because they require less specific information to encode, and are therefore much more likely to appear as phenotypic variation through random mutations. Arguments from algorithmic information theory can formalise this intuition, leading to the prediction that many genotype-phenotype maps are exponentially biased towards phenotypes with low descriptional complexity. A preference for symmetry is a special case of this bias towards compressible descriptions. We test these predictions with extensive biological data, showing that that protein complexes, RNA secondary structures, and a model gene-regulatory network all exhibit the expected exponential bias towards simpler (and more symmetric) phenotypes. Lower descriptional complexity also correlates with higher mutational robustness, which may aid the evolution of complex modular assemblies of multiple components.

Parasitology ◽  
1983 ◽  
Vol 86 (2) ◽  
pp. 335-344 ◽  
Author(s):  
D. J. Minchella ◽  
P. T. Loverde

SUMMARYA method of interrupting the life-cycle of the human blood fluke Schistosoma by increasing the proportion of genetically insusceptible intermediate host snails in natural populations was first proposed nearly 25 years ago. The method assumes that insusceptible snails will be at a selective advantage over susceptible snails when the schistosome parasite is present, and therefore natural selection will act to increase the proportion of alleles for insusceptibility. A major objection to the proposed technique is ‘If insusceptible snails are at a selective advantage, then why are they not predominant in natural populations that transmit disease?’ One explanation of this paradox is that insusceptibility may be associated with a disadvantageous character or a physiological defect. This study tests this hypothesis by measuring the relative reproductive success of susceptible and insusceptible snails under controlled conditions. Results indicate that insusceptible (unsuitable) snails are negatively affected in the presence of either susceptible snails or schistosome parasites. Furthermore, in the presence of both susceptible snails and schistosome parasites, insusceptible snails are selectively disadvantaged compared to susceptible snails. These results obtained under laboratory-controlled conditions suggest a plausible answer as to why insusceptible snails are not predominant in natural populations that transmit disease.


Parasitology ◽  
2014 ◽  
Vol 142 (S1) ◽  
pp. S108-S119 ◽  
Author(s):  
PAUL CAPEWELL ◽  
ANNELI COOPER ◽  
CAROLINE CLUCAS ◽  
WILLIAM WEIR ◽  
ANNETTE MACLEOD

SUMMARYTrypanosoma brucei is the causative agent of African sleeping sickness in humans and one of several pathogens that cause the related veterinary disease Nagana. A complex co-evolution has occurred between these parasites and primates that led to the emergence of trypanosome-specific defences and counter-measures. The first line of defence in humans and several other catarrhine primates is the trypanolytic protein apolipoprotein-L1 (APOL1) found within two serum protein complexes, trypanosome lytic factor 1 and 2 (TLF-1 and TLF-2). Two sub-species of T. brucei have evolved specific mechanisms to overcome this innate resistance, Trypanosoma brucei gambiense and Trypanosoma brucei rhodesiense. In T. b. rhodesiense, the presence of the serum resistance associated (SRA) gene, a truncated variable surface glycoprotein (VSG), is sufficient to confer resistance to lysis. The resistance mechanism of T. b. gambiense is more complex, involving multiple components: reduction in binding affinity of a receptor for TLF, increased cysteine protease activity and the presence of the truncated VSG, T. b. gambiense-specific glycoprotein (TgsGP). In a striking example of co-evolution, evidence is emerging that primates are responding to challenge by T. b. gambiense and T. b. rhodesiense, with several populations of humans and primates displaying resistance to infection by these two sub-species.


2019 ◽  
Vol 20 (S18) ◽  
Author(s):  
Wenxiang Zhang ◽  
Xiujuan Lei (IEEE member) ◽  
Chen Bian

Abstract Background It’s a very urgent task to identify cancer genes that enables us to understand the mechanisms of biochemical processes at a biomolecular level and facilitates the development of bioinformatics. Although a large number of methods have been proposed to identify cancer genes at recent times, the biological data utilized by most of these methods is still quite less, which reflects an insufficient consideration of the relationship between genes and diseases from a variety of factors. Results In this paper, we propose a two-rounds random walk algorithm to identify cancer genes based on multiple biological data (TRWR-MB), including protein-protein interaction (PPI) network, pathway network, microRNA similarity network, lncRNA similarity network, cancer similarity network and protein complexes. In the first-round random walk, all cancer nodes, cancer-related genes, cancer-related microRNAs and cancer-related lncRNAs, being associated with all the cancer, are used as seed nodes, and then a random walker walks on a quadruple layer heterogeneous network constructed by multiple biological data. The first-round random walk aims to select the top score k of potential cancer genes. Then in the second-round random walk, genes, microRNAs and lncRNAs, being associated with a certain special cancer in corresponding cancer class, are regarded as seed nodes, and then the walker walks on a new quadruple layer heterogeneous network constructed by lncRNAs, microRNAs, cancer and selected potential cancer genes. After the above walks finish, we combine the results of two-rounds RWR as ranking score for experimental analysis. As a result, a higher value of area under the receiver operating characteristic curve (AUC) is obtained. Besides, cases studies for identifying new cancer genes are performed in corresponding section. Conclusion In summary, TRWR-MB integrates multiple biological data to identify cancer genes by analyzing the relationship between genes and cancer from a variety of biological molecular perspective.


2011 ◽  
Vol 135-136 ◽  
pp. 602-608
Author(s):  
Ya Meng ◽  
Xue Qun Shang ◽  
Miao Miao ◽  
Miao Wang

Mining functional modules with biological significance has attracted lots of attention recently. However, protein-protein interaction (PPI) network and other biological data generally bear uncertainties attributed to noise, incompleteness and inaccuracy in practice. In this paper, we focus on received PPI data with uncertainties to explore interesting protein complexes. Moreover, some novel conceptions extended from known graph conceptions are used to develop a depth-first algorithm to mine protein complexes in a simple uncertain graph. Our experiments take protein complexes from MIPS database as standard of accessing experimental results. Experiment results indicate that our algorithm has good performance in terms of coverage and precision. Experimental results are also assessed on Gene Ontology (GO) annotation, and the evaluation demonstrates proteins of our most acquired protein complexes show a high similarity. Finally, several experiments are taken to test the scalability of our algorithm. The result is also observed.


2019 ◽  
Vol 20 (9) ◽  
pp. 2129 ◽  
Author(s):  
Daniel Hatlem ◽  
Thomas Trunk ◽  
Dirk Linke ◽  
Jack C. Leo

The SpyCatcher-SpyTag system was developed seven years ago as a method for protein ligation. It is based on a modified domain from a Streptococcus pyogenes surface protein (SpyCatcher), which recognizes a cognate 13-amino-acid peptide (SpyTag). Upon recognition, the two form a covalent isopeptide bond between the side chains of a lysine in SpyCatcher and an aspartate in SpyTag. This technology has been used, among other applications, to create covalently stabilized multi-protein complexes, for modular vaccine production, and to label proteins (e.g., for microscopy). The SpyTag system is versatile as the tag is a short, unfolded peptide that can be genetically fused to exposed positions in target proteins; similarly, SpyCatcher can be fused to reporter proteins such as GFP, and to epitope or purification tags. Additionally, an orthogonal system called SnoopTag-SnoopCatcher has been developed from an S. pneumoniae pilin that can be combined with SpyCatcher-SpyTag to produce protein fusions with multiple components. Furthermore, tripartite applications have been produced from both systems allowing the fusion of two peptides by a separate, catalytically active protein unit, SpyLigase or SnoopLigase. Here, we review the current state of the SpyCatcher-SpyTag and related technologies, with a particular emphasis on their use in vaccine development and in determining outer membrane protein localization and topology of surface proteins in bacteria.


Science ◽  
2020 ◽  
Vol 370 (6521) ◽  
pp. eabb5962
Author(s):  
Jia Zheng ◽  
Ning Guo ◽  
Andreas Wagner

Natural selection can promote or hinder a population’s evolvability—the ability to evolve new and adaptive phenotypes—but the underlying mechanisms are poorly understood. To examine how the strength of selection affects evolvability, we subjected populations of yellow fluorescent protein to directed evolution under different selection regimes and then evolved them toward the new phenotype of green fluorescence. Populations under strong selection for the yellow phenotype evolved the green phenotype most rapidly. They did so by accumulating mutations that increase both robustness to mutations and foldability. Under weak selection, neofunctionalizing mutations rose to higher frequency at first, but more frequent deleterious mutations undermined their eventual success. Our experiments show how selection can enhance evolvability by enhancing robustness and create the conditions necessary for evolutionary success.


1981 ◽  
Vol 13 (3) ◽  
pp. 337-343 ◽  
Author(s):  
Gérard Métral

SummaryReproductive performance of the human female is simulated by Monte Carlo methods. The results clearly suggest the operation of natural selection on the length of the female menstrual cycle, brought about by differential fertility. It is argued that the selection pressure towards a shorter cycle, with a selective advantage of approximately 1% per day of shortening, is balanced by internal physiological determinants preventing excessive shortening, so the result is a situation of stabilizing natural selection.


2015 ◽  
Vol 2015 ◽  
pp. 1-9
Author(s):  
Peng Liu ◽  
Lei Yang ◽  
Daming Shi ◽  
Xianglong Tang

A method for predicting protein-protein interactions based on detected protein complexes is proposed to repair deficient interactions derived from high-throughput biological experiments. Protein complexes are pruned and decomposed into small parts based on the adaptivek-cores method to predict protein-protein interactions associated with the complexes. The proposed method is adaptive to protein complexes with different structure, number, and size of nodes in a protein-protein interaction network. Based on different complex sets detected by various algorithms, we can obtain different prediction sets of protein-protein interactions. The reliability of the predicted interaction sets is proved by using estimations with statistical tests and direct confirmation of the biological data. In comparison with the approaches which predict the interactions based on the cliques, the overlap of the predictions is small. Similarly, the overlaps among the predicted sets of interactions derived from various complex sets are also small. Thus, every predicted set of interactions may complement and improve the quality of the original network data. Meanwhile, the predictions from the proposed method replenish protein-protein interactions associated with protein complexes using only the network topology.


2013 ◽  
Vol 81 (11) ◽  
pp. 2023-2033 ◽  
Author(s):  
Min Wu ◽  
Zhipeng Xie ◽  
Xiaoli Li ◽  
Chee‐Keong Kwoh ◽  
Jie Zheng

Sign in / Sign up

Export Citation Format

Share Document