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Campo DC | Valor | Lengua/Idioma |
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dc.contributor.author | Fornelos, Nadine | - |
dc.contributor.author | Butala, Matej | - |
dc.contributor.author | Hodnik, Vesna | - |
dc.contributor.author | Anderluh, Gregor | - |
dc.contributor.author | Bamford, Jaana K. | - |
dc.contributor.author | Salas, Margarita | - |
dc.date.issued | 2015-06-05 | - |
dc.identifier | doi: 10.1093/nar/gkv634 | - |
dc.identifier | issn: 1362-4962 | - |
dc.identifier.citation | Nucleic Acids Research 43(15): 7315-7329 (2015) | - |
dc.identifier.uri | http://hdl.handle.net/10261/124131 | - |
dc.description.abstract | The SOS response in Eubacteria is a global response to DNA damage and its activation is increasingly associated with the movement of mobile genetic elements. The temperate phage GIL01 is induced into lytic growth using the host's SOS response to genomic stress. LexA, the SOS transcription factor, represses bacteriophage transcription by binding to a set of SOS boxes in the lysogenic promoter P1. However, LexA is unable to efficiently repress GIL01 transcription unless the small phage-encoded protein gp7 is also present. We found that gp7 forms a stable complex with LexA that enhances LexA binding to phage and cellular SOS sites and interferes with RecA-mediated auto-cleavage of LexA, the key step in the initiation of the SOS response. Gp7 did not bind DNA, alone or when complexed with LexA. Our findings suggest that gp7 induces a LexA conformation that favors DNA binding but disfavors LexA auto-cleavage, thereby altering the dynamics of the cellular SOS response. This is the first account of an accessory factor interacting with LexA to regulate transcription. | - |
dc.description.sponsorship | Finnish Centre of Excellence in Biological Interactions [252411]; (cofunded under the Marie Curie Actions of the European Commission) [FP7-COFUND];EMBO[ASTF 286-2013 to N.F.]; Academy of Finland [251106 to J.K.B.]; Slovenian Research Agency [P1-0207 to M.B. and I0-0021 to V.H. and G.A.]; Spanish Ministry of Economy and Competitiveness [BFU2011-23645 to M.S.]. Funding for open access charge: Academy of Finland. | - |
dc.publisher | Oxford University Press | - |
dc.relation.isversionof | Publisher's version | - |
dc.rights | openAccess | - |
dc.title | Bacteriophage GIL01 gp7 interacts with host LexA repressor to enhance DNA binding and inhibit RecA-mediated auto-cleavage | - |
dc.type | artículo | - |
dc.identifier.doi | 10.1093/nar/gkv634 | - |
dc.date.updated | 2015-10-29T12:44:08Z | - |
dc.description.version | Peer Reviewed | - |
dc.language.rfc3066 | eng | - |
dc.contributor.funder | Fonds National de la Recherche Luxembourg | - |
dc.contributor.funder | Slovenian Research Agency | - |
dc.contributor.funder | Ministerio de Economía y Competitividad (España) | - |
dc.contributor.funder | European Commission | - |
dc.contributor.funder | Centre of Excellence in Biological Interactions (Finland) | - |
dc.contributor.funder | Academy of Finland | - |
dc.relation.csic | Sí | - |
dc.identifier.funder | http://dx.doi.org/10.13039/501100001866 | es_ES |
dc.identifier.funder | http://dx.doi.org/10.13039/501100003329 | es_ES |
dc.identifier.funder | http://dx.doi.org/10.13039/501100000780 | es_ES |
dc.identifier.funder | http://dx.doi.org/10.13039/501100002341 | es_ES |
dc.identifier.pmid | 26138485 | - |
dc.type.coar | http://purl.org/coar/resource_type/c_6501 | es_ES |
item.openairetype | artículo | - |
item.cerifentitytype | Publications | - |
item.grantfulltext | open | - |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
item.fulltext | With Fulltext | - |
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Salas M Bacteriophage GIL01.pdf | 13,77 MB | Adobe PDF | Visualizar/Abrir |
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