A genomic approach to understand interactions between Streptococcus pneumoniae and its bacteriophages

BMC Genomics

Research Article

Philippe Leprohon¹  Hélène Gingras¹  Marc Ouellette¹  Siham Ouennane²  Sylvain Moineau² 

[1] Centre de recherche en Infectiologie du Centre de Recherche du CHU de Québec, Université Laval, 2705 Boul. Laurier, G1V 4G2, Québec, QC, Canada,;Département de Microbiologie, Infectiologie et Immunologie, Faculté de Médecine, Université Laval, 1050, avenue de la Médecine, G1V 0A6, Québec, QC, Canada,;Département de Biochimie, Microbiologie et Bio-informatique and PROTEO, Faculté des Sciences et Génie, Université Laval, Québec, QC, Canada;Félix d’Hérelle Reference Center for Bacterial Viruses and GREB, Faculté de Médecine Dentaire, Université Laval, Québec, QC, Canada;

关键词: Streptococcus pneumoniae;    Bacteriophage;    Resistance;    Whole genome sequencing;    GntR regulator;   

DOI  :  10.1186/s12864-015-2134-8

 received in 2015-06-25, accepted in 2015-10-23,  发布年份 2015

来源: Springer

【 摘 要 】

BackgroundBacteriophage replication depends on bacterial proteins and inactivation of genes coding for such host factors should interfere with phage infection. To gain further insights into the interactions between S. pneumoniae and its pneumophages, we characterized S. pneumoniae mutants selected for resistance to the virulent phages SOCP or Dp-1.ResultsS. pneumoniae R6-SOCPR and R6-DP1R were highly resistant to the phage used for their selection and no cross-resistance between the two phages was detected. Adsorption of SOCP to R6-SOCPR was partly reduced whereas no difference in Dp-1 adsorption was noted on R6-DP1R. The replication of SOCP was completely inhibited in R6-SOCPR while Dp-1 was severely impaired in R6-DP1R. Genome sequencing identified 8 and 2 genes mutated in R6-SOCPR and R6-DP1R, respectively. Resistance reconstruction in phage-sensitive S. pneumoniae confirmed that mutations in a GntR-type regulator, in a glycerophosphoryl phosphodiesterase and in a Mur ligase were responsible for resistance to SOCP. The three mutations were additive to increase resistance to SOCP. In contrast, resistance to Dp-1 in R6-DP1R resulted from mutations in a unique gene coding for a type IV restriction endonuclease.ConclusionThe characterization of mutations conferring resistance to pneumophages highlighted that diverse host genes are involved in the replication of phages from different families.

【 授权许可】

CC BY   
© Leprohon et al. 2015