Beyond paralogs: The multiple layers of redundancy in bacterial pathogenesis

Soma Ghosh, Tamara J. O'Connor

Research output: Contribution to journalArticle

Abstract

Redundancy has been referred to as a state of no longer being needed or useful. Microbiologists often theorize that the only case of true redundancy in a haploid organism would be a recent gene duplication event, prior to divergence through selective pressure. However, a growing number of examples exist where an organism encodes two genes that appear to perform the same function. For example, many pathogens translocate multiple effector proteins into hosts. While disruption of individual effector genes does not result in a discernable phenotype, deleting genes in combination impairs pathogenesis: this has been described as redundancy. In many cases, this apparent redundancy could be due to limitations of laboratory models of pathogenesis that do not fully recapitulate the disease process. Alternatively, it is possible that the selective advantage achieved by this perceived redundancy is too subtle to be measured in the laboratory. Moreover, there are numerous possibilities for different types of redundancy. The most common and recognized form of redundancy is functional redundancy whereby two proteins have similar biochemical activities and substrate specificities allowing each one to compensate in the absence of the other. However, redundancy can also exist between seemingly unrelated proteins that manipulate the same or complementary host cell pathways. In this article, we outline 5 types of redundancy in pathogenesis: molecular, target, pathway, cellular process, and system redundancy that incorporate the biochemical activities, the host target specificities and the impact of effector function on the pathways and cellular process they modulate. For each type of redundancy, we provide examples from Legionella pathogenesis as this organism employs over 300 secreted virulence proteins and loss of individual proteins rarely impacts intracellular growth. We also discuss selective pressures that drive the maintenance of redundant mechanisms, the current methods used to resolve redundancy and features that distinguish between redundant and non-redundant virulence mechanisms.

Original languageEnglish (US)
Article number467
JournalFrontiers in cellular and infection microbiology
Volume7
Issue numberNOV
DOIs
StatePublished - Nov 15 2017

Fingerprint

Proteins
Virulence
Genes
Legionella
Gene Duplication
Host Specificity
Haploidy
Substrate Specificity
Maintenance
Phenotype
Growth

Keywords

  • Effector
  • Functional redundancy
  • Genetic redundancy
  • Legionella
  • Pathogenesis
  • Redundancy

ASJC Scopus subject areas

  • Microbiology
  • Immunology
  • Microbiology (medical)
  • Infectious Diseases

Cite this

Beyond paralogs : The multiple layers of redundancy in bacterial pathogenesis. / Ghosh, Soma; O'Connor, Tamara J.

In: Frontiers in cellular and infection microbiology, Vol. 7, No. NOV, 467, 15.11.2017.

Research output: Contribution to journalArticle

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