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Epigenomic Landscape of Lyme Disease Spirochetes Reveals Novel Motifs

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F60076658%3A12310%2F21%3A43903629" target="_blank" >RIV/60076658:12310/21:43903629 - isvavai.cz</a>

  • Result on the web

    <a href="https://journals.asm.org/doi/10.1128/mBio.01288-21" target="_blank" >https://journals.asm.org/doi/10.1128/mBio.01288-21</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1128/mBio.01288-21" target="_blank" >10.1128/mBio.01288-21</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Epigenomic Landscape of Lyme Disease Spirochetes Reveals Novel Motifs

  • Original language description

    Borrelia burgdorferi, the etiological agent of Lyme disease, persists in nature through an enzootic cycle consisting of a vertebrate host and an Ixodes tick vector. The sequence motifs modified by two well-characterized restriction/modification (R/M) loci of B. burgdorferi type strain B31 were recently described, but the methylation profiles of other Lyme disease Borrelia bacteria have not been characterized. Here, the methylomes of B. burgdorferi type strain B31 and 7 clonal derivatives, along with B. burgdorferi N40, B. burgdorferi 297, B. burgdorferi CA-11, B. afzelii PKo, B. afzelii BO23, and B. garinii PBr, were defined through PacBio single-molecule realtime (SMRT) sequencing. This analysis revealed 9 novel sequence motifs methylated by the plasmid-encoded restriction/modification enzymes of these Borrelia strains. Furthermore, while a previous analysis of B. burgdorferi B31 revealed an epigenetic impact of methylation on the global transcriptome, the current data contradict those findings; our analyses of wild-type B. burgdorferi B31 revealed no consistent differences in gene expression among isogenic derivatives lacking one or more restriction/ modification enzymes. IMPORTANCE The principal causative agent of Lyme disease in humans in the United States is Borrelia burgdorferi, while B. burgdorferi, B. afzelii, and B. garinii, collectively members of the Borrelia burgdorferi sensu lato species complex, cause Lyme disease in Europe and Asia. Two plasmid-encoded restriction/modification systems have been shown to limit the genetic transformation of B. burgdorferi type strain B31 with foreign DNA, but little is known about the restriction/modification systems of other Lyme disease Borrelia bacteria. This paper describes the methylation motifs present on genomic DNAs of multiple B. burgdorferi, B. afzelii, and B. garinii strains. Contrary to a previous report, we did not find evidence for an epigenetic impact on gene expression by methylation. Knowledge of the motifs recognized and methylated by the restriction/modification enzymes of Lyme disease Borrelia will facilitate molecular genetic investigations of these important human pathogens. Additionally, the similar motifs methylated by orthologous restriction/modification systems of Lyme disease Borrelia bacteria and the presence of these motifs within recombinogenic loci suggest a biological role for these ubiquitous restriction/modification systems in horizontal gene transfer.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    10606 - Microbiology

Result continuities

  • Project

  • Continuities

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2021

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    mBio

  • ISSN

    2150-7511

  • e-ISSN

  • Volume of the periodical

    12

  • Issue of the periodical within the volume

    3

  • Country of publishing house

    US - UNITED STATES

  • Number of pages

    20

  • Pages from-to

  • UT code for WoS article

    000693451600003

  • EID of the result in the Scopus database

    2-s2.0-85112119847