Mobile genetic elementsPub Date : 2016-01-25eCollection Date: 2016-01-01DOI: 10.1080/2159256X.2015.1137380
Rohan Maddamsetti
{"title":"Gene flow in microbial communities could explain unexpected patterns of synonymous variation in the <i>Escherichia coli</i> core genome.","authors":"Rohan Maddamsetti","doi":"10.1080/2159256X.2015.1137380","DOIUrl":"https://doi.org/10.1080/2159256X.2015.1137380","url":null,"abstract":"<p><p>Researchers contest the importance of gene flow in bacterial core genomes, as traditionalists view microbes as predominantly clonal, asexually reproducing organisms. Contrary to the traditional perspective, <i>Escherichia coli</i> core genes vary greatly in their levels of synonymous genetic diversity. This observation indicates that the relative importance of evolutionary forces such as mutation, selection, and recombination varies from gene to gene. In this paper, I highlight why the synonymous diversity observation is broadly relevant to researchers interested in the evolutionary dynamics of microbial populations and communities. I explain how a model of evolution called the coalescent relates neutral diversity (i.e. mutations with negligible fitness effects) to mutation rates, evolutionary time, and a parameter called effective population size. I then describe the possible ways in which mutation, selection, and recombination can explain observed patterns of synonymous diversity in <i>E. coli.</i> Finally, I describe a model for <i>E. coli</i> genome evolution in which different loci are subject to varying levels of gene flow among co-occurring microbes and viruses in the environment. Researchers can falsify the gene flow hypothesis by sequencing genes and strains isolated from stable microbiomes or by carrying out evolution experiments that trace gene genealogies in real-time.</p>","PeriodicalId":89441,"journal":{"name":"Mobile genetic elements","volume":"6 1","pages":"e1137380"},"PeriodicalIF":0.0,"publicationDate":"2016-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/2159256X.2015.1137380","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34755233","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mobile genetic elementsPub Date : 2016-01-13eCollection Date: 2016-01-01DOI: 10.1080/2159256X.2015.1123796
Dor Salomon
{"title":"MIX and match: mobile T6SS MIX-effectors enhance bacterial fitness.","authors":"Dor Salomon","doi":"10.1080/2159256X.2015.1123796","DOIUrl":"https://doi.org/10.1080/2159256X.2015.1123796","url":null,"abstract":"<p><p>Protein secretion systems that mediate interbacterial competition secret a wide repertoire of antibacterial toxins. A major player in these competitions is the newly discovered bacterial type VI secretion system (T6SS). We recently found that a subset of polymorphic MIX-effectors, which are a widespread class of effectors secreted by T6SSs, are horizontally shared between marine bacteria and are used to diversify their T6SS effector repertoires, thus enhancing their environmental fitness. In this commentary, I expand on the ideas that were introduced in the previous report, and further speculate on the possible mobility of other MIX-effectors. In addition, I discuss the possible role of horizontal gene transfer in the dissemination of MIX-effectors through bacterial genomes, as well as its possible role in diversifying the T6SS effector repertoire.</p>","PeriodicalId":89441,"journal":{"name":"Mobile genetic elements","volume":"6 1","pages":"e1123796"},"PeriodicalIF":0.0,"publicationDate":"2016-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/2159256X.2015.1123796","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34741724","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mobile genetic elementsPub Date : 2015-12-30eCollection Date: 2016-01-01DOI: 10.1080/2159256X.2015.1136375
Mizue Naito, Teresa E Pawlowska
{"title":"The role of mobile genetic elements in evolutionary longevity of heritable endobacteria.","authors":"Mizue Naito, Teresa E Pawlowska","doi":"10.1080/2159256X.2015.1136375","DOIUrl":"https://doi.org/10.1080/2159256X.2015.1136375","url":null,"abstract":"<p><p>The movement of mobile genetic elements (MGEs), including bacteriophages, insertion sequence (IS) elements, and integrative and conjugative elements (ICEs) can have profound effects on bacterial evolution by introducing novel genes, or disrupting the existing ones. Obligate endobacteria are a distinctive group of bacteria that reside within the intracellular compartments of their eukaryotic hosts. Many obligate endobacteria are reproductively dependent on their hosts. Vertical transmission, in addition to degenerative genome contraction and loss of MGEs, makes heritable endobacteria vulnerable to Muller's ratchet, a process that jeopardizes evolutionary longevity of small populations. Mycoplasma-related endobacteria (MRE) are ancient heritable endosymbionts of arbuscular mycorrhizal fungi. Their genomes harbour numerous MGEs. To explore the significance of MGEs in the evolution of MRE and other obligate endobacteria, we analyze the impact of transmission mode, recombination, and evolutionary age on the maintenance of MGEs. Furthermore, we discuss the ability of MGEs to act as sites of gene conversion and recombination in endobacterial genomes. We propose that MGEs are important instruments of genome shuffling, contributing to population heterogeneity and evolutionary longevity in heritable obligate endobacteria.</p>","PeriodicalId":89441,"journal":{"name":"Mobile genetic elements","volume":"6 1","pages":"e1136375"},"PeriodicalIF":0.0,"publicationDate":"2015-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/2159256X.2015.1136375","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34741722","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mobile genetic elementsPub Date : 2015-12-29eCollection Date: 2016-01-01DOI: 10.1080/2159256X.2015.1133267
Siqi Hu, Chen Liang, Fei Guo
{"title":"Stress out the LINEs.","authors":"Siqi Hu, Chen Liang, Fei Guo","doi":"10.1080/2159256X.2015.1133267","DOIUrl":"https://doi.org/10.1080/2159256X.2015.1133267","url":null,"abstract":"<p><p>Occupying 17% of human genome, the mobile long interspersed element 1 (LINE-1 or L1) continues to modulate the landscape of our genome by inserting into new loci and, as a result, causing sporadic diseases. It is not surprising that human cells have evolved a battery of mechanisms to control and limit the activity of LINE-1. Our recent study unravels such a mechanism that is imposed by the stress granule pathway. This mechanism functions by sequestering the LINE-1 RNA-protein complex within the cytoplasmic stress granules and thus inhibiting the nuclear import of LINE-1 RNA and its subsequent reverse transcription and integration into cellular DNA. Conditions that promote stress granule formation, such as expression of the SAMHD1 protein, further reduce LINE-1 retrotransposition.</p>","PeriodicalId":89441,"journal":{"name":"Mobile genetic elements","volume":"6 1","pages":"e1133267"},"PeriodicalIF":0.0,"publicationDate":"2015-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/2159256X.2015.1133267","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34741723","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mobile genetic elementsPub Date : 2015-12-04eCollection Date: 2016-01-01DOI: 10.1080/2159256X.2015.1119927
Anthony V Furano, Pamela R Cook
{"title":"The challenge of ORF1p phosphorylation: Effects on L1 activity and its host.","authors":"Anthony V Furano, Pamela R Cook","doi":"10.1080/2159256X.2015.1119927","DOIUrl":"https://doi.org/10.1080/2159256X.2015.1119927","url":null,"abstract":"<p><p>L1 non-LTR retrotransposons are autonomously replicating genetic elements that profoundly affected their mammalian hosts having generated upwards of 40% or more of their genomes. Although deleterious, they remain active in most mammalian species, and thus the nature and consequences of the interaction between L1 and its host remain major issues for mammalian biology. We recently showed that L1 activity requires phosphorylation of one of its 2 encoded proteins, ORF1p, a nucleic acid chaperone and the major component of the L1RNP retrotransposition intermediate. Reversible protein phosphorylation, which is effected by interacting cascades of protein kinases, phosphatases, and ancillary proteins, is a mainstay in the regulation and coordination of many basic biological processes. Therefore, demonstrating phosphorylation-dependence of L1 activity substantially enlarged our knowledge of the scope of L1 / host interaction. However, developing a mechanistic understanding of what this means for L1 or its host is a formidable challenge, which we discuss here.</p>","PeriodicalId":89441,"journal":{"name":"Mobile genetic elements","volume":"6 1","pages":"e1119927"},"PeriodicalIF":0.0,"publicationDate":"2015-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/2159256X.2015.1119927","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34391726","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mobile genetic elementsPub Date : 2015-12-04eCollection Date: 2016-01-01DOI: 10.1080/2159256X.2015.1119926
Maria A Nilsson
{"title":"The devil is in the details: Transposable element analysis of the Tasmanian devil genome.","authors":"Maria A Nilsson","doi":"10.1080/2159256X.2015.1119926","DOIUrl":"https://doi.org/10.1080/2159256X.2015.1119926","url":null,"abstract":"<p><p>The third marsupial genome was sequenced from the Tasmanian devil (<i>Sarcophilus harrisii</i>), a species that currently is driven to extinction by a rare transmissible cancer. The transposable element (TE) landscape of the Tasmanian devil genome revealed that the main driver of retrotransposition the <b>L</b>ong <b>IN</b>terspersed <b>E</b>lement 1 (LINE1) seem to have become inactivated during the past 12 million years. Strangely, the <b>S</b>hort <b>IN</b>terspersed <b>E</b>lements (SINE), that normally hijacks the LINE1 retrotransposition system, became inactive prior to LINE1 at around 30 million years ago. The SINE inactivation was in vitro verified in several species. Here I discuss that the apparent LINE1 inactivation might be caused by a genome assembly artifact. The repetitive fraction of any genome is highly complex to assemble and the observed problems are not unique to the Tasmanian devil genome.</p>","PeriodicalId":89441,"journal":{"name":"Mobile genetic elements","volume":"6 1","pages":"e1119926"},"PeriodicalIF":0.0,"publicationDate":"2015-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/2159256X.2015.1119926","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34391725","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"New clues on the regulation of the CRISPR-Cas immune system","authors":"Magnus Lundgren","doi":"10.1080/2159256X.2015.1117169","DOIUrl":"https://doi.org/10.1080/2159256X.2015.1117169","url":null,"abstract":"Research into the CRISPR-Cas immune system of prokaryotes is progressing at a tremendous pace given both its important biological function and its role as a source of new genetic tools. However, a few areas of the field have remained largely unaddressed. A recent report provides information on one such overlooked area: how the cell regulates the CRISPR-Cas immune system. The processes, despite their importance, have remained illusive. In Pectobacterium atrosepticum regulation is, perhaps surprisingly, based on metabolic factors responding to glucose levels in the cell. Regulators include both activators and repressors of cas gene expression. It remains an open question why and how this regulatory system have evolved, and if it is a typical example of how CRISPR-as systems are regulated or not.","PeriodicalId":89441,"journal":{"name":"Mobile genetic elements","volume":"5 1","pages":"109 - 111"},"PeriodicalIF":0.0,"publicationDate":"2015-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/2159256X.2015.1117169","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"60153725","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Alu elements and DNA double-strand break repair","authors":"T. White, M. E. Morales, P. Deininger","doi":"10.1080/2159256X.2015.1093067","DOIUrl":"https://doi.org/10.1080/2159256X.2015.1093067","url":null,"abstract":"Alu elements represent one of the most common sources of homology and homeology in the human genome. Homeologous recombination between Alu elements represents a major form of genetic instability leading to deletions and duplications. Although these types of events have been studied extensively through genomic sequencing to assess the impact of Alu elements on disease mutations and genome evolution, the overall abundance of Alu elements in the genome often makes it difficult to assess the relevance of the Alu elements to specific recombination events. We recently reported a powerful new reporter gene system that allows the assessment of various cis and trans factors on the contribution of Alu elements to various forms of genetic instability. This allowed a quantitative measurement of the influence of mismatches on Alu elements and instability. It also confirmed that homeologous Alu elements are able to stimulate non-homologous end joining events in their vicinity. This appears to be dependent on portions of the mismatch repair pathway. We are now in a position to begin to unravel the complex influences of Alu density, mismatch and location with alterations of DNA repair processes in various tissues and tumors.","PeriodicalId":89441,"journal":{"name":"Mobile genetic elements","volume":"5 1","pages":"81 - 85"},"PeriodicalIF":0.0,"publicationDate":"2015-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/2159256X.2015.1093067","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"60153259","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The dualistic nature of integrative and conjugative elements","authors":"Nicolas Carraro, Vincent Burrus","doi":"10.1080/2159256X.2015.1102796","DOIUrl":"https://doi.org/10.1080/2159256X.2015.1102796","url":null,"abstract":"Integrative and conjugative elements (ICEs) are mobile genetic elements that play a key role in bacterial adaptation. Such elements are found in almost every bacterial genera and species, and often code for adaptive traits conferring selective advantages to their host. ICEs maintain by integrating into and replicating along with a replicon of the host genome. ICEs can propagate by conjugative transfer toward a recipient cell following excision from the replicon as a circular covalently-closed molecule. For a long time, the excised form of ICEs was assumed to be non-replicative. This assumption predicts that excised ICEs are sensitive to loss during cell division, unless they carry stabilization systems such as addiction modules or antibiotic resistance genes. Over the past few years, growing evidence have been presented that support conditional replication of the circular intermediate as an intrinsic feature of ICEs. We recently confirmed this feature in the large family of SXT/R391 ICEs, which thrive in several species of Enterobacteriaceae and Vibrionaceae. Furthermore, we demonstrated that SXT/R391 ICEs encode a functional plasmid-like type II partition system that enhances their stability, such systems being probably encoded by other ICEs. The lifecycle of ICEs is therefore much more complex than initially thought as many ICEs may use plasmid-like features to improve their stability and dissemination.","PeriodicalId":89441,"journal":{"name":"Mobile genetic elements","volume":"5 1","pages":"98 - 102"},"PeriodicalIF":0.0,"publicationDate":"2015-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/2159256X.2015.1102796","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"60153650","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"LINE retrotransposition and host DNA repair machinery.","authors":"Katsumi Yamaguchi, Masaki Kajikawa, Norihiro Okada","doi":"10.1080/2159256X.2015.1096998","DOIUrl":"10.1080/2159256X.2015.1096998","url":null,"abstract":"<p><p>Long interspersed elements (LINEs), or non-long-terminal repeat (LTR) retrotransposons, are mobile genetic elements that exist in the genomic DNA of most eukaryotes, comprising a considerable portion of the host chromosomes. LINEs constitute endogenous mutagens that cause insertional mutations in host chromosomes and have a large impact on host genome evolution. Despite their importance, however, the molecular mechanism of LINE retrotransposition is not fully understood. Several studies suggest that host proteins that participate in the repair of DNA breaks modulate LINE retrotransposition. Recently, we provided evidence that there are 2 distinct pathways-annealing and direct-that join the 5'-end of LINEs to host chromosomal DNA. These pathways appear to be used distinctively by zebrafish LINEs and the human L1 in DT40 cells. In HeLa cells, only the annealing pathway appears to be used. This implies that different characteristics of the 2 LINEs and also host factors dictate which pathway is selected. Here, we discuss the 5'-end-joining pathways of LINE retrotransposition and propose that the pathways of LINE integration adopt certain host repair factors.</p>","PeriodicalId":89441,"journal":{"name":"Mobile genetic elements","volume":"5 1","pages":"92-97"},"PeriodicalIF":0.0,"publicationDate":"2015-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4760211/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"60153625","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}