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Register a new userMean-field methods in evolutionary duplication-innovation-loss models for the genome-level repertoire of protein domains
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We present a combined mean-field and simulation approach to different models describing the dynamics of classes formed by elements that can appear, disappear or copy themselves. These models, related to a paradigm duplication-innovation model known as Chinese Restaurant Process, are devised to reproduce the scaling behavior observed in the genome-wide repertoire of protein domains of all known species. In view of these data, we discuss the qualitative and quantitative differences of the alternative model formulations, focusing in particular on the roles of element loss and of the specificity of empirical domain classes.
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Much evolutionary information is stored in the fluctuations of protein length distributions. The genome size and non-coding DNA content can be calculated based only on the protein length distributions. So there is intrinsic relationship between the coding DNA size and non-coding DNA size. According to the correlations and quasi-periodicity of protein length distributions, we can classify life into three domains. Strong evidences are found to support the order in the structures of protein length distributions.
With the development of high throughput sequencing technology, it becomes possible to directly analyze mutation distribution in a genome-wide fashion, dissociating mutation rate measurements from the traditional underlying assumptions. Here, we sequenced several genomes of Escherichia coli from colonies obtained after chemical mutagenesis and observed a strikingly nonrandom distribution of the induced mutations. These include long stretches of exclusively G to A or C to T transitions along the genome and orders of magnitude intra- and inter-genomic differences in mutation density. Whereas most of these observations can be explained by the known features of enzymatic processes, the others could reflect stochasticity in the molecular processes at the single-cell level. Our results demonstrate how analysis of the molecular records left in the genomes of the descendants of an individual mutagenized cell allows for genome-scale observations of fixation and segregation of mutations, as well as recombination events, in the single genome of their progenitor.
As the infection of 2019-nCoV coronavirus is quickly developing into a global pneumonia epidemic, careful analysis of its transmission and cellular mechanisms is sorely needed. In this report, we re-analyzed the computational approaches and findings presented in two recent manuscripts by Ji et al. (https://doi.org/10.1002/jmv.25682) and by Pradhan et al. (https://doi.org/10.1101/2020.01.30.927871), which concluded that snakes are the intermediate hosts of 2019-nCoV and that the 2019-nCoV spike protein insertions shared a unique similarity to HIV-1. Results from our re-implementation of the analyses, built on larger-scale datasets using state-of-the-art bioinformatics methods and databases, do not support the conclusions proposed by these manuscripts. Based on our analyses and existing data of coronaviruses, we concluded that the intermediate hosts of 2019-nCoV are more likely to be mammals and birds than snakes, and that the novel insertions observed in the spike protein are naturally evolved from bat coronaviruses.
The ongoing global pandemic of infection disease COVID-19 caused by the 2019 novel coronavirus (SARS-COV-2, formerly 2019-nCoV) presents critical threats to public health and the economy since it was identified in China, December 2019. The genome of SARS-CoV-2 had been sequenced and structurally annotated, yet little is known of the intrinsic organization and evolution of the genome. To this end, we present a mathematical method for the genomic spectrum, a kind of barcode, of SARS-CoV-2 and common human coronaviruses. The genomic spectrum is constructed according to the periodic distributions of nucleotides, and therefore reflects the unique characteristics of the genome. The results demonstrate that coronavirus SARS-CoV-2 exhibits dinucleotide TT islands in the non-structural proteins 3, 4, 5, and 6. Further analysis of the dinucleotide regions suggests that the dinucleotide repeats are increased during evolution and may confer the evolutionary fitness of the virus. The special dinucleotide regions in the SARS-CoV-2 genome identified in this study may become diagnostic and pharmaceutical targets in monitoring and curing the COVID-19 disease.
The problem of the directionality of genome evolution is studied from the information-theoretic view. We propose that the function-coding information quantity of a genome always grows in the course of evolution through sequence duplication, expansion of code, and gene transfer between genomes. The function-coding information quantity of a genome consists of two parts, p-coding information quantity which encodes functional protein and n-coding information quantity which encodes other functional elements except amino acid sequence. The relation of the proposed law to the thermodynamic laws is indicated. The evolutionary trends of DNA sequences revealed by bioinformatics are investigated which afford further evidences on the evolutionary law. It is argued that the directionality of genome evolution comes from species competition adaptive to environment. An expression on the evolutionary rate of genome is proposed that the rate is a function of Darwin temperature (describing species competition) and fitness slope (describing adaptive landscape). Finally, the problem of directly experimental test on the evolutionary directionality is discussed briefly.
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