dc.contributor.author | Harms, Klaus | |
dc.contributor.author | Lunnan, Asbjørn | |
dc.contributor.author | Hulter, Nils | |
dc.contributor.author | Mourier, Tobias | |
dc.contributor.author | Vinner, Lasse | |
dc.contributor.author | Andam, Cheryl P | |
dc.contributor.author | Marttinen, Pekka | |
dc.contributor.author | Fridholm, Helena | |
dc.contributor.author | Hansen, Anders Johannes | |
dc.contributor.author | Hanage, William P | |
dc.contributor.author | Nielsen, Kaare Magne | |
dc.contributor.author | Willerslev, Eske | |
dc.contributor.author | Johnsen, Pål Jarle | |
dc.date.accessioned | 2017-02-27T12:07:51Z | |
dc.date.available | 2017-02-27T12:07:51Z | |
dc.date.issued | 2016-12-27 | |
dc.description.abstract | In a screen for unexplained mutation events we identified a previously unrecognized mechanism generating clustered DNA polymorphisms such as microindels and cumulative SNPs. The mechanism, short-patch double illegitimate recombination (SPDIR), facilitates short single-stranded DNA molecules to invade and replace genomic DNA through two joint illegitimate recombination events. SPDIR is controlled by key components of the cellular genome maintenance machinery in the gram-negative bacterium Acinetobacter baylyi. The source DNA is primarily intragenomic but can also be acquired through horizontal gene transfer. The DNA replacements are nonreciprocal and locus independent. Bioinformatic approaches reveal occurrence of SPDIR events in the gram-positive human pathogen Streptococcus pneumoniae and in the human genome. | en_US |
dc.description.sponsorship | The cancer work was supported by The Danish National Advanced Technology foundation (The GenomeDenmark platform, Grant 019-2011-2). This work was supported by The Arctic University of Norway and the Danish National Research Foundation (K.H.), the Academy of Finland Grant 251170 (to P.M.), the Finnish Centre of Excellence in Computational Inference Research Grant 259272 (to P.M.), and also by Norwegian Research Council Grant 204263/F20 (to P.J.J.). | en_US |
dc.description | Source: <a href=http://dx.doi.org/10.1073/pnas.1615819114>doi: 10.1073/pnas.1615819114</a> | en_US |
dc.identifier.citation | Harms K, Lunnan, Hulter, Mourier, Vinner, Andam, Marttinen P, Fridholm, Hansen, Hanage, Nielsen KM, Willerslev E, Johnsen Pj. Substitutions of short heterologous DNA segments of intragenomic or extragenomic origins produce clustered genomic polymorphisms. Proceedings of the National Academy of Sciences of the United States of America. 2016;113(52):15066-15071 | en_US |
dc.identifier.cristinID | FRIDAID 1439775 | |
dc.identifier.doi | 10.1073/pnas.1615819114 | |
dc.identifier.issn | 0027-8424 | |
dc.identifier.issn | 1091-6490 | |
dc.identifier.uri | https://hdl.handle.net/10037/10367 | |
dc.language.iso | eng | en_US |
dc.publisher | National Academy of Sciences | en_US |
dc.relation.journal | Proceedings of the National Academy of Sciences of the United States of America | |
dc.rights.accessRights | openAccess | en_US |
dc.subject | VDP::Medisinske Fag: 700::Basale medisinske, odontologiske og veterinærmedisinske fag: 710::Farmakologi: 728 | en_US |
dc.subject | VDP::Medical disciplines: 700::Basic medical, dental and veterinary science disciplines: 710::Pharmacology: 728 | en_US |
dc.title | Substitutions of short heterologous DNA segments of intragenomic or extragenomic origins produce clustered genomic polymorphisms | en_US |
dc.type | Journal article | en_US |
dc.type | Tidsskriftartikkel | en_US |
dc.type | Peer reviewed | en_US |