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dc.contributor.authorCastañeda-García, Alfredoes_ES
dc.contributor.authorPrieto Márquez, Ana Isabeles_ES
dc.contributor.authorRodríguez Beltrán, Jerónimoes_ES
dc.contributor.authorAlonso, N.es_ES
dc.contributor.authorCostas, Colomaes_ES
dc.contributor.authorRojas, A. M.es_ES
dc.contributor.authorBlázquez Gómez, Jesúses_ES
dc.identifier.citationNature Communications 8: 14246 (2017)es_ES
dc.descriptionCastañeda-García, Alfredo et al.es_ES
dc.description.abstractMismatch repair (MMR) is a near ubiquitous pathway, essential for the maintenance of genome stability. Members of the MutS and MutL protein families perform key steps in mismatch correction. Despite the major importance of this repair pathway, MutS–MutL are absent in almost all Actinobacteria and many Archaea. However, these organisms exhibit rates and spectra of spontaneous mutations similar to MMR-bearing species, suggesting the existence of an alternative to the canonical MutS–MutL-based MMR. Here we report that Mycobacterium smegmatis NucS/EndoMS, a putative endonuclease with no structural homology to known MMR factors, is required for mutation avoidance and anti-recombination, hallmarks of the canonical MMR. Furthermore, phenotypic analysis of naturally occurring polymorphic NucS in a M. smegmatis surrogate model, suggests the existence of M. tuberculosis mutator strains. The phylogenetic analysis of NucS indicates a complex evolutionary process leading to a disperse distribution pattern in prokaryotes. Together, these findings indicate that distinct pathways for MMR have evolved at least twice in nature.es_ES
dc.description.sponsorshipJ.B. was supported by Plan Nacional de I+D+i and Instituto de Salud Carlos III, Subdirección General de Redes y Centros de Investigación Cooperativa, Ministerio de Economía y Competitividad, Spanish Network for Research in Infectious Diseases (REIPI RD12/0015) – co-financed by European Development Regional Fund ‘A way to achieve Europe’ ERDF and SAF2015-72793-EXP and BFU2016-78250-P from Spanish Ministry of Science and Competitiveness (MINECO)-FEDER). A.J.D. was supported by a grant from the Biotechnology and Biological Sciences Research Council (BB/J018643/1). A.C.-G. and J.R.-B. were supported by contracts from REIPI RD15/0012 and A.C.-G. also by a Ramon Areces fellowship for Life Sciences. A.I.P. was supported by a ‘Sara Borrell’ contract, Instituto de Salud Carlos III. T.T. was supported by the Research Council of Norway, GLOBVAC project 234506.es_ES
dc.publisherNature Publishing Groupes_ES
dc.relation.isversionofPublisher's versiones_ES
dc.titleA non-canonical mismatch repair pathway in prokaryoteses_ES
dc.description.peerreviewedPeer reviewedes_ES
dc.contributor.funderInstituto de Salud Carlos IIIes_ES
dc.contributor.funderMinisterio de Economía y Competitividad (España)es_ES
dc.contributor.funderEuropean Commissiones_ES
dc.contributor.funderBiotechnology and Biological Sciences Research Council (UK)es_ES
dc.contributor.funderFundación Ramón Areceses_ES
dc.contributor.funderResearch Council of Norwayes_ES
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