Mobile genetic elements最新文献

{"title":"Uncovering novel mobile genetic elements and their dynamics through an extra-chromosomal sequencing approach.","authors":"Douglas R Deutsch,&nbsp;Bryan Utter,&nbsp;Vincent A Fischetti","doi":"10.1080/2159256X.2016.1189987","DOIUrl":"https://doi.org/10.1080/2159256X.2016.1189987","url":null,"abstract":"<p><p>Staphylococcus aureus is a major clinically important pathogen with well-studied phage contributions to its virulence potential. In this commentary, we describe our method to enrich and sequence stealth extra-chromosomal DNA elements in the bacterial cell, allowing the identification of novel extra-chromosomal prophages in S. aureus clinical strains. Extra-chromosomal sequencing is a useful and broadly applicable tool to study bacterial genomics, giving a temporal glance at the extra-chromosomal compartment of the cell and allowing researchers to uncover lower-copy plasmidial elements (e.g., prophages) as well as gain a greater understanding of mobile genetic elements that shuffle on and off the chromosome. Here, we describe how episomal and plasmidial DNA elements can have profound downstream effects on the host cell and surrounding bacterial population, and discuss specific examples of their importance in Gram-positive bacteria. We also offer potential avenues of future research where extra-chromosomal sequencing may play a key role in our understanding of the complete virulence potential of infectious bacteria. </p>","PeriodicalId":89441,"journal":{"name":"Mobile genetic elements","volume":"6 4","pages":"e1189987"},"PeriodicalIF":0.0,"publicationDate":"2016-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/2159256X.2016.1189987","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34407306","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":"Ordered orthology as a tool in prokaryotic evolutionary inference","authors":"S. Snir","doi":"10.1080/2159256X.2015.1120576","DOIUrl":"https://doi.org/10.1080/2159256X.2015.1120576","url":null,"abstract":"ABSTRACT Molecular data is accumulated at exponentially increasing pace. This deluge of information should have brought us closer to resolving one of the most fundamental issues in biology - deciphering the history of life on Earth. So far, however, this abundance of data only seems to blur our understanding of the problem. This is largely due to horizontal gene transfer (HGT), the transfer of genetic material between evolutionarily unrelated organisms that transforms the prokaryotic tree into a network of relationships. Recently, we developed a method to infer evolutionary relationships among closely related species where the conventional evolutionary markers do not provide a strong enough signal. The method relies on the loss of synteny, gene order conservation among species that provides a stronger signal, sufficient to classify even strains of a given species. Here we elaborate on this method and suggest further uses of it in the context of detecting HGT events and genome architecture.","PeriodicalId":89441,"journal":{"name":"Mobile genetic elements","volume":"6 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/2159256X.2015.1120576","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"60153796","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":"Rapid compensatory evolution promotes the survival of conjugative plasmids.","authors":"Ellie Harrison,&nbsp;Calvin Dytham,&nbsp;James P J Hall,&nbsp;David Guymer,&nbsp;Andrew J Spiers,&nbsp;Steve Paterson,&nbsp;Michael A Brockhurst","doi":"10.1080/2159256X.2016.1179074","DOIUrl":"https://doi.org/10.1080/2159256X.2016.1179074","url":null,"abstract":"<p><p>Conjugative plasmids play a vital role in bacterial adaptation through horizontal gene transfer. Explaining how plasmids persist in host populations however is difficult, given the high costs often associated with plasmid carriage. Compensatory evolution to ameliorate this cost can rescue plasmids from extinction. In a recently published study we showed that compensatory evolution repeatedly targeted the same bacterial regulatory system, GacA/GacS, in populations of plasmid-carrying bacteria evolving across a range of selective environments. Mutations in these genes arose rapidly and completely eliminated the cost of plasmid carriage. Here we extend our analysis using an individual based model to explore the dynamics of compensatory evolution in this system. We show that mutations which ameliorate the cost of plasmid carriage can prevent both the loss of plasmids from the population and the fixation of accessory traits on the bacterial chromosome. We discuss how dependent the outcome of compensatory evolution is on the strength and availability of such mutations and the rate at which beneficial accessory traits integrate on the host chromosome. </p>","PeriodicalId":89441,"journal":{"name":"Mobile genetic elements","volume":"6 3","pages":"e1179074"},"PeriodicalIF":0.0,"publicationDate":"2016-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/2159256X.2016.1179074","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34747048","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":"TE-domestication and horizontal transfer in a putative Nef-AP1mu mimic of HLA-A cytoplasmic domain re-trafficking.","authors":"Joseph S Murray,&nbsp;Elaina H Murray","doi":"10.1080/2159256X.2016.1176634","DOIUrl":"https://doi.org/10.1080/2159256X.2016.1176634","url":null,"abstract":"<p><p>Genes of the major histocompatibility complex (MHC; also called HLA in human) are polymorphic elements in the genomes of sharks to humans. Class-I and class-II MHC loci appear responsible for much of the genetic linkage to myriad disease states via the capacity to bind short (~8-15 a.a.) peptides of a given pathogen's proteome, or in some cases, the altered proteomes of cancerous cells, and even (in autoimmunity) certain nominal 'self' peptides (Janeway, 2004).(1) Unfortunately, little is known about how the canonical structure of the MHC-I/-II peptide-presenting gene evolved, particularly since beyond ~500 Mya (sharks) no paralogs exist.(2,3) We previously reported that HLA-A isotype alleles with the α1-helix, R65 motif, are wide-spread in phylogeny, but that the α 2-helix, H151R motif, has apparently segregated out of most species. Surprisingly, an uncharacterized orf in T. syrichta (Loc-103275158) encoded R151, but within a truncated A-23 like gene containing 5'- and 3'- footprints of the transposon (TE), tigger-1; the extant tarsier A-23 allele is totally missing exon-3 and part-of exon-4; together, suggesting TE-mediated inactivation of an intact/ancestral A-23 allele (Murray, 2015a).(4) The unique Loc-103275158 orf encodes a putative 15-exon transcript with no apparent paralogs throughout phylogeny. However, an HLA-A11 like gene in M. leucophaeus with a shortened C-terminal domain, and an HLA-A like orf in C. atys with two linked α1/α2/α3 domains, both contain a second transmembrane segment, which is conserved in Loc-103275158. Thus, we could model the putative protein with its Nef-like tail domain docked to its MHC-I like α3 domain (i.e., on the same side of a membrane). This modeled tertiary structure is strikingly similar to the solved structure of the Nef:MHC-I CD:AP1mu transporter (Jia, 2012).(5) Nef:AP1mu binds the CD of MHC-I in trafficking MHC-I away from the trans-golgi and into the endocytic pathway in HIV-1 infected cells. The CD loop of the Loc-103275158 provisional protein conserved the nominal MHC-I CD tyrosine phosphorylation site, and it has an N-terminal SH3 domain that we docked in one conformation to its internal Nef-like domain. Here, we suggest that phosphorylation of the protein's CD-loop signals an exchange between the internal Nef-like domain and a lentiviral-Nef for binding the N-terminal SH3 domain - freeing the Nef-like domain to bind MHC-I CD. Since the 5'-tigger sequence encodes part of the pseudo α1/α2 MHC-I domain, and the 3'-tigger part of the Nef-like domain, we speculate that transposition proceeded phylogenetically disparate horizontal transfers, involving adjacent 5'- and 3'- parasitic footprints, which we also found in the Loc-103275158 orf. </p>","PeriodicalId":89441,"journal":{"name":"Mobile genetic elements","volume":"6 3","pages":"e1176634"},"PeriodicalIF":0.0,"publicationDate":"2016-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/2159256X.2016.1176634","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34652700","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":"Transposable elements and miRNA: Regulation of genomic stability and plasticity.","authors":"Irene Munk Pedersen,&nbsp;Dimitrios G Zisoulis","doi":"10.1080/2159256X.2016.1175537","DOIUrl":"https://doi.org/10.1080/2159256X.2016.1175537","url":null,"abstract":"<p><p>Transposable elements, the class of mobile DNA sequences that change their copies or positions within the genome have an ever increasing role in shaping the genetic and evolutionary landscape. Approximately half of the mammalian genome is composed of repetitive elements, including LINE-1 (L1) elements. Because of their ability to \"copy and paste\" into other regions of the genome, their activation represent an opportunity as well as a threat, as L1-induced mutations results in genomic instability and plasticity. On one hand L1 retrotransposition and integration fosters genomic diversity and on the other, de-repressed L1 functions as a driver of diseases such as cancer. The regulation of L1 is an area of intense research and novel epigenetic mechanisms have recently been discovered to now include DNA methylation, histone modifications, and miR-induced L1 silencing. During development, reprogramming and in transformed cells, specific classes of repetitive elements are upregulated, presumably due to the loss of epigenetic regulation in this process, increasing the risk of L1-induced mutations. Here we discuss how miR regulation of L1 activation fits into the complex picture of L1 repression in somatic cells and touch on some of the possible implications. </p>","PeriodicalId":89441,"journal":{"name":"Mobile genetic elements","volume":"6 3","pages":"e1175537"},"PeriodicalIF":0.0,"publicationDate":"2016-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/2159256X.2016.1175537","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34747080","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":"Endogenous non-retroviral RNA virus elements evidence a novel type of antiviral immunity.","authors":"Tomoyuki Honda,&nbsp;Keizo Tomonaga","doi":"10.1080/2159256X.2016.1165785","DOIUrl":"https://doi.org/10.1080/2159256X.2016.1165785","url":null,"abstract":"<p><p>Vertebrate genomes contain many virus-related sequences derived from both retroviruses and non-retroviral RNA and DNA viruses. Such non-retroviral RNA sequences are possibly produced by reverse-transcription and integration of viral mRNAs of ancient RNA viruses using retrotransposon machineries. We refer to this process as transcript reversion. During an ancient bornavirus infection, transcript reversion may have left bornavirus-related sequences, known as endogenous bornavirus-like nucleoproteins (EBLNs), in the genome. We have recently demonstrated that all Homo sapiens EBLNs are expressed in at least one tissue. Because species with EBLNs appear relatively protected against infection by a current bornavirus, Borna disease virus, it is speculated that EBLNs play some roles in antiviral immunity, as seen with some endogenous retroviruses. EBLNs can function as dominant negative forms of viral proteins, small RNAs targeting viral sequences, or DNA or RNA elements modulating the gene expression. Growing evidence reveals that various RNA viruses are reverse-transcribed and integrated into the genome of infected cells, suggesting transcript reversion generally occurs during ongoing infection. Considering this, transcript reversion-mediated interference with related viruses may be a novel type of antiviral immunity in vertebrates. Understanding the biological significance of transcript reversion will provide novel insights into host defenses against viral infections. </p>","PeriodicalId":89441,"journal":{"name":"Mobile genetic elements","volume":"6 3","pages":"e1165785"},"PeriodicalIF":0.0,"publicationDate":"2016-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/2159256X.2016.1165785","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34745257","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":"<i>Helitrons</i> in <i>Drosophila</i>: Chromatin modulation and tandem insertions.","authors":"Guilherme B Dias,&nbsp;Pedro Heringer,&nbsp;Gustavo C S Kuhn","doi":"10.1080/2159256X.2016.1154638","DOIUrl":"https://doi.org/10.1080/2159256X.2016.1154638","url":null,"abstract":"<p><p>Although <i>Helitrons</i> were discovered 15 y ago, they still represent an elusive group of transposable elements (TEs). They are thought to transpose via a rolling-circle mechanism, but no transposition assay has yet been conducted. We have recently characterized a group of <i>Helitrons</i> in <i>Drosophila</i>, named <i>DINE-TR1</i>, that display interesting features, including pronounced enrichment at β-heterochromatin, multiple tandem insertions (TIs) of the entire TE, and that experienced at least 2 independent expansion events of its internal tandem repeats (TRs) in distant <i>Drosophila</i> lineages. Here we discuss 2 aspects of TE dynamics displayed by the <i>DINE-TR1 Helitrons</i>: (i) the general evolutionary impact of piRNA-guided heterochromatin formation via TE-derived TR expansion and (ii) the possible mechanisms that could account for the recurrent TIs of <i>Helitrons</i>.</p>","PeriodicalId":89441,"journal":{"name":"Mobile genetic elements","volume":"6 2","pages":"e1154638"},"PeriodicalIF":0.0,"publicationDate":"2016-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/2159256X.2016.1154638","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34450123","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":"Ty1 escapes restriction by the self-encoded factor p22 through mutations in capsid.","authors":"Jessica M Tucker,&nbsp;David J Garfinkel","doi":"10.1080/2159256X.2016.1154639","DOIUrl":"https://doi.org/10.1080/2159256X.2016.1154639","url":null,"abstract":"<p><p>Ty1 is a long terminal repeat (LTR) retrotransposon belonging to the Ty1/<i>copia</i> family and is present in up to 32 full-length copies in <i>Saccharomyces</i>. Like retroviruses, Ty1 contains <i>GAG</i> and <i>POL</i> genes, LTRs, and replicates via an RNA intermediate within a virus-like particle (VLP). Although Ty1 retrotransposition is not infectious, uncontrolled replication can lead to detrimental effects on the host genome, including insertional mutagenesis and chromosomal rearrangements. Ty1 copy number control (CNC) limits replication and is mediated through a self-encoded protein called p22. p22 is translated from a subgenomic Ty1 RNA and encodes an amino-truncated version of the Gag protein. We highlight a recent study identifying Ty1 Gag, which comprises the VLP capsid and provides nucleic acid chaperone functions, as a direct target of p22-mediated inhibition. CNC-resistant (CNC^R) mutations map within predicted helical domains of Gag, including those in the Ty1/<i>copia</i> pfam domain Retrotran_gag_2 (formerly UBN2) and a central region we refer to as the CNC^R domain. CNC^R Gag forms VLPs that exclude p22, thus restoring Ty1 replication. We discuss possible mechanisms for p22 inclusion in Ty1 VLPs and compare Ty1 CNC with retroviral restriction factors targeting capsid (CA).</p>","PeriodicalId":89441,"journal":{"name":"Mobile genetic elements","volume":"6 2","pages":"e1154639"},"PeriodicalIF":0.0,"publicationDate":"2016-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/2159256X.2016.1154639","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34450124","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":"Characterizing the functions of Ty1 Gag and the Gag-derived restriction factor p22/p18.","authors":"Katarzyna Pachulska-Wieczorek,&nbsp;Leszek Błaszczyk,&nbsp;Julita Gumna,&nbsp;Yuri Nishida,&nbsp;Agniva Saha,&nbsp;Marcin Biesiada,&nbsp;David J Garfinkel,&nbsp;Katarzyna J Purzycka","doi":"10.1080/2159256X.2016.1154637","DOIUrl":"https://doi.org/10.1080/2159256X.2016.1154637","url":null,"abstract":"<p><p>The long terminal repeat (LTR) and non-LTR retrotransposons comprise approximately half of the human genome, and we are only beginning to understand their influence on genome function and evolution. The LTR retrotransposon Ty1 is the most abundant mobile genetic element in the <i>S. cerevisiae</i> reference genome. Ty1 replicates via an RNA intermediate and shares several important structural and functional characteristics with retroviruses. However, unlike retroviruses Ty1 retrotransposition is not infectious. Retrotransposons integrations can cause mutations and genome instability. Despite the fact that <i>S. cerevisiae</i> lacks eukaryotic defense mechanisms such as RNAi, they maintain a relatively low copy number of the Ty1 retrotransposon in their genomes. A novel restriction factor derived from the C-terminal half of Gag (p22/p18) and encoded by internally initiated transcript inhibits retrotransposition in a dose-dependent manner. Therefore, Ty1 evolved a specific <i>GAG</i> organization and expression strategy to produce products both essential and antagonistic for retrotransposon movement. In this commentary we discuss our recent research aimed at defining steps of Ty1 replication influenced by p22/p18 with particular emphasis on the nucleic acid chaperone functions carried out by Gag and the restriction factor.</p>","PeriodicalId":89441,"journal":{"name":"Mobile genetic elements","volume":"6 2","pages":"e1154637"},"PeriodicalIF":0.0,"publicationDate":"2016-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/2159256X.2016.1154637","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34514620","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":"Horizontal transfer - imperative mission of acellular life forms, <i>Acytota</i>.","authors":"Eduard Kejnovsky,&nbsp;Edward N Trifonov","doi":"10.1080/2159256X.2016.1154636","DOIUrl":"https://doi.org/10.1080/2159256X.2016.1154636","url":null,"abstract":"<p><p><i>Acytota</i> is a kingdom of life covering satellites, plasmids, transposable elements, viroids and viruses, all outside the conventional tree of life but satisfying most life definitions. This review focuses on some aspects of <i>Acytota</i>, their \"genomes\" and life styles, the dominance of transposable elements and their evolutionary influence on other life forms in order to vindicate the <i>Acytota</i> as a life kingdom no more polyphyletic than other kingdoms and its members no more parasitic than other life forms.</p>","PeriodicalId":89441,"journal":{"name":"Mobile genetic elements","volume":"6 2","pages":"e1154636"},"PeriodicalIF":0.0,"publicationDate":"2016-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/2159256X.2016.1154636","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34514619","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}