Deletion of potD, encoding a putative spermidine-binding protein, results in a complex phenotype in Legionella pneumophila

Gheyath K. Nasrallah, Hany Abdelhady, Nicholas P. Tompkins, Kaitlyn R. Carson, Rafael A. Garduño

Research output: Contribution to journalArticlepeer-review

9 Citations (Scopus)

Abstract

L. pneumophila is an intracellular pathogen that replicates in a membrane-bound compartment known as the Legionella-containing vacuole (LCV). We previously observed that the polyamine spermidine, produced by host cells or added exogenously, enhances the intracellular growth of L. pneumophila. To study this enhancing effect and determine whether polyamines are used as nutrients, we deleted potD from L. pneumophila strain JR32. The gene potD encodes a spermidine-binding protein that in other bacteria is essential for the function of the PotABCD polyamine transporter. Deletion of potD did not affect L. pneumophila growth in vitro in the presence or absence of spermidine and putrescine, suggesting that PotD plays a redundant or no role in polyamine uptake. However, deletion of potD resulted in a puzzlingly complex phenotype that included defects in L. pneumophila's ability to form filaments, tolerate Na+, associate with macrophages and amoeba, recruit host vesicles to the LCV, and initiate intracellular growth. Moreover, the δpotD mutant was completely unable to grow in L929 cells treated with a pharmacological inhibitor of spermidine synthesis. These complex and disparate effects suggest that the L. pneumophila potD encodes either: (i) a multifunctional protein, (ii) a protein that interacts with, or regulates a, multifunctional protein, or (iii) a protein that contributes (directly or indirectly) to a regulatory network. Protein function studies with the L. pneumophila PotD protein are thus warranted.

Original languageEnglish
Pages (from-to)703-716
Number of pages14
JournalInternational Journal of Medical Microbiology
Volume304
Issue number5-6
DOIs
Publication statusPublished - Jul 2014

Bibliographical note

Funding Information:
This work was funded by a Discovery Grant to RAG from the Natural Sciences and Engineering Research Council (NSERC) of Canada and a start-up Grant to GKN from Qatar University.

ASJC Scopus Subject Areas

  • Microbiology
  • Microbiology (medical)
  • Infectious Diseases

PubMed: MeSH publication types

  • Journal Article
  • Research Support, Non-U.S. Gov't

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