4.4 Article

Acinetobacter baumannii RecA Protein in Repair of DNA Damage, Antimicrobial Resistance, General Stress Response, and Virulence

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JOURNAL OF BACTERIOLOGY
卷 193, 期 15, 页码 3740-3747

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AMER SOC MICROBIOLOGY
DOI: 10.1128/JB.00389-11

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资金

  1. Spanish Network for Research on Infectious Diseases-REIPI (Instituto de Salud Carlos III) [RD06/0008/0025, RD006/0008/0011]
  2. Fondo de Investigaciones Sanitarias [PI061368, PI081368, PS09/00687]
  3. SERGAS [PS07/90]
  4. Xunta de Galicia [07CSA050916PR]
  5. MICINN [BFU2008-01078]
  6. Generalitat de Catalunya [2009SGR1106]
  7. Instituto de Salud Carlos III (ISCIII, Madrid)
  8. Conselleria de Economia e Industria, Xunta de Galicia
  9. Instituto de Salud Carlos III, through the Spanish Network for Research in Infectious Diseases (REIPI) [RD06/0008]
  10. Spanish Society of Infectious Diseases and Clinical Microbiology (SEIMC)
  11. Xunta de Galicia through the Direccion Xeral de I+D+i. C
  12. Generalitat de Catalunya
  13. ISCIII
  14. Fundacao para a Ciencia e a Tecnologia from the Ministerio da Ciencia, Tecnologia e Ensino Superior (Portugal)

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RecA is the major enzyme involved in homologous recombination and plays a central role in SOS mutagenesis. In Acinetobacter spp., including Acinetobacter baumannii, a multidrug-resistant bacterium responsible for nosocomial infections worldwide, DNA repair responses differ in many ways from those of other bacterial species. In this work, the function of A. baumannii RecA was examined by constructing a recA mutant. Alteration of this single gene had a pleiotropic effect, showing the involvement of RecA in DNA damage repair and consequently in cellular protection against stresses induced by DNA damaging agents, several classes of antibiotics, and oxidative agents. In addition, the absence of RecA decreased survival in response to both heat shock and desiccation. Virulence assays in vitro (with macrophages) and in vivo (using a mouse model) similarly implicated RecA in the pathogenicity of A. baumannii. Thus, the data strongly suggest a protective role for RecA in the bacterium and indicate that inactivation of the protein can contribute to a combined therapeutic approach to controlling A. baumannii infections.

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