Legionella pneumophila prevents proliferation of its natural host Acanthamoeba castellanii

• Published in: Scientific reports Vol. 6; no. 1; p. 36448
• Main Authors: Mengue, Luce, Régnacq, Matthieu, Aucher, Willy, Portier, Emilie, Héchard, Yann, Samba-Louaka, Ascel
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 02.11.2016; Nature Publishing Group
• Subjects: 13; 13/95; 14; 14/19; 38/109; 45; 45/90; 631/326/88; 631/80/641/151/1431; 96; Acanthamoeba castellanii - genetics; Acanthamoeba castellanii - growth & development; Acanthamoeba castellanii - microbiology; Amino Acid Sequence; Amoeba; Animals; Bacterial Proteins - genetics; Bacterial Proteins - metabolism; CDC28 Protein Kinase, S cerevisiae - deficiency; CDC28 Protein Kinase, S cerevisiae - genetics; Cell cycle; Cell Cycle Proteins - classification; Cell Cycle Proteins - genetics; Cell Cycle Proteins - metabolism; Cell division; Cell Size; Cyclin-dependent kinases; DNA Replication; Escherichia coli - physiology; Genes; Gram-negative bacteria; Humanities and Social Sciences; Humans; Legionella pneumophila - physiology; Life Sciences; Microscopy, Video; multidisciplinary; Mutagenesis; Phylogeny; Saccharomyces cerevisiae - growth & development; Saccharomyces cerevisiae - metabolism; Science; Sequence Alignment; Legionellosis
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/srep36448

Legionella pneumophila is a ubiquitous, pathogenic, Gram-negative bacterium responsible for legionellosis. Like many other amoeba-resistant microorganisms, L. pneumophila resists host clearance and multiplies inside the cell. Through its Dot/Icm type IV secretion system, the bacterium injects more than three hundred effectors that modulate host cell physiology in order to promote its own intracellular replication. Here we report that L. pneumophila prevents proliferation of its natural host Acanthamoeba castellanii . Infected amoebae could not undergo DNA replication and no cell division was observed. The Dot/Icm secretion system was necessary for L. pneumophila to prevent the eukaryotic proliferation. The absence of proliferation was associated with altered amoebal morphology and with a decrease of mRNA transcript levels of CDC2b, a putative regulator of the A. castellanii cell cycle. Complementation of CDC28 -deficient Saccharomyces cerevisiae by the CDC2b cDNA was sufficient to restore proliferation of CDC28 -deficient S. cerevisiae and suggests for the first time that CDC2b from A. castellanii could be functional and a bona fide cyclin-dependent kinase. Hence, our results reveal that L. pneumophila impairs proliferation of A. castellanii and this effect could involve the cell cycle protein CDC2b.