Fine-tuning cellular levels of DprA ensures transformant fitness in the human pathogen Streptococcus pneumoniae.

Calum Johnston (1) , Isabelle I. Mortier (1) , Vanessa Khemici (1, 2) , Patrice P. Polard (1)

1 LMGM - Laboratoire de microbiologie et génétique moléculaires - UMR5100
2 UNIGE - Université de Genève = University of Geneva

Natural genetic transformation is a widespread mechanism of horizontal gene transfer. It involves the inter-nalization of exogenous DNA as single strands and chromosomal integration via homologous recombi-nation, promoting acquisition of new genetic traits. Transformation occurs during a distinct physiological state called competence. In Streptococcus pneumo-niae, competence is controlled by ComDE, a two-component system induced by an exported peptide pheromone. DprA is universal among transformable species, strongly induced during pneumococcal competence, and crucial for pneumococcal transformation. Pneumococcal DprA plays three crucial roles in transformation and competence. Firstly, DprA protects internalized DNA from degradation. Secondly, DprA loads the homologous recombinase RecA onto transforming DNA to promote transformation. Finally, DprA interacts with the response regulator ComE to shut-off competence. Here, we explored the effect of altering the cellular levels of DprA on these three roles. High cellular levels of DprA were not required for the primary role of DprA as a transformation-dedicated recombinase loader or for protection of transforming DNA. In contrast, full expression of dprA was required for optimal competence shut-off and trans-formant fitness. High cellular levels of DprA thus ensure the fitness of pneumococcal transformants by mediating competence shut-off. This promotes survival and propagation of transformants, maximizing pneumococcal adaptive potential.

Domaines: Bactériologie; Biochimie, Biologie Moléculaire

Calum Johnston, Isabelle I. Mortier, Vanessa Khemici, Patrice P. Polard. Fine-tuning cellular levels of DprA ensures transformant fitness in the human pathogen Streptococcus pneumoniae.. Molecular Microbiology, 2018, 109 (5), pp.663-675. ⟨10.1111/mmi.14068⟩. ⟨hal-02367975⟩