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Mycobacteriophage Fruitloop gp52 inactivates Wag31 (DivIVA) to prevent heterotypic superinfection

Ching-Chung Ko1, Graham F Hatfull1

  • 1Department of Biological Sciences, University of Pittsburgh, Pittsburgh, PA, 15260, USA.

Molecular Microbiology
|March 1, 2018
PubMed

Insights

Mycobacteriophage Fruitloop

Area of Science:

  • Microbiology
  • Virology
  • Molecular Biology

Background:

  • Bacteriophages (phages) and bacteria engage in complex co-evolutionary dynamics, with bacteria employing resistance mechanisms and phages adapting to overcome them or switch hosts.
  • Phages also compete with each other through mechanisms like prophage-mediated defense and superinfection exclusion, influencing viral population dynamics.
  • Bacteriophages possess numerous small genes of unknown function that may play roles in modulating host-phage and phage-phage interactions beyond essential lytic replication.

Purpose of the Study:

  • To identify and characterize phage-encoded proteins that modulate bacterial host-phage and phage-phage interactions.
  • To investigate the functional role of mycobacteriophage Fruitloop's gene 52 product, gp52, in bacterial interactions.
  • To determine the mechanism by which gp52 influences phage competition and bacterial host dependencies.

Main Methods:

  • Utilized cellular toxicity assays resulting from phage gene overexpression to identify functional phage proteins.
  • Investigated the interaction of mycobacteriophage Fruitloop's gp52 protein with essential bacterial proteins in Mycobacterium smegmatis.
  • Assessed the impact of gp52 expression on the lytic replication of other phages, specifically Subcluster B2 phages.

Main Results:

  • Overexpression of the 93-residue protein gp52 from mycobacteriophage Fruitloop caused cellular toxicity.
  • Fruitloop gp52 was found to interact with and inactivate Wag31 (DivIVA), a crucial protein for cell wall biosynthesis in Mycobacterium smegmatis.
  • Fruitloop gene 52, expressed early in lytic growth, is not essential for Fruitloop's own replication but inhibits the growth of related phages like Hedgerow and Rosebush.

Conclusions:

  • Mycobacteriophage Fruitloop's gp52 protein confers heterotypic superinfection exclusion by targeting the essential bacterial protein Wag31.
  • The phages Hedgerow and Rosebush are dependent on Wag31 for their replication, making them susceptible to inactivation by Fruitloop's gp52.
  • This study reveals a novel mechanism of phage-phage competition mediated by a phage protein targeting a host cell division protein.

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