English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Deletion of single genes from expanded gene families in bacterial genomes often does not elicit a phenotype thus implying redundancy or functional non-essentiality of paralogous genes. The molecular mechanisms that facilitate evolutionary maintenance of such paralogs despite selective pressures against redundancy remain mostly unexplored. Here, we investigate the evolutionary, genetic, and functional interaction between the  Helicobacter pylori  cysteine-rich paralogs  hcpG  and  hcpC  in the context of  H. pylori  infection of cultured mammalian cells. We find that in natural  H. pylori  populations both  hcpG  and  hcpC  are maintained by positive selection in a dual genetic relationship that switches from  complete redundancy  during early infection, whereby  ΔhcpC  or  ΔhcpG  mutants themselves show no growth defect but a significant growth defect is seen in the  ΔhcpC,ΔhcpG  double mutant, to  quantitative redundancy  during late infection wherein the growth defect of the  ΔhcpC  mutant is exacerbated in the  ΔhcpC,ΔhcpG double  mutant although  the ΔhcpG  mutant itself shows no defect. Moreover, during early infection both  hcpG  and  hcpC  are essential for optimal translocation of the  H. pylori  HspB/GroEL chaperone, but during middle-to-late infection  hcpC  alone is necessary and sufficient for HspB/GroEL translocation thereby revealing the lack of functional compensation among paralogs. We propose that evolution of context-dependent differences in the nature of genetic redundancy, and function, between  hcpG  and  hcpC  may facilitate their maintenance in  H. pylori  genomes, and confer robustness to  H. pylori  growth during infection of cultured mammalian cells.

Robustness of Helicobacter pylori Infection Conferred by Context-Variable Redundancy among Cysteine-Rich Paralogs