Figure 7. Simplified model of stable maintenance of hcpC and hcpG in H. pylori populations.

The fate of a duplicate gene can be studied in three distinct phases beginning with fixation of the duplicate in the H. pylori population [42]. We propose that in the preduplication phase, hcpC is fixed in H. pylori populations; the fixation phase begins with the origin of hcpG. During the fixation phase, the duplicate copy escapes loss because of genetic drift and is fixed. This initiates the second phase, in which the duplicate accumulates fate-determining mutations. We suggest that multiple fate-determining mutations give rise to polymorphic hcpG variants. In the preservation phase, hcpC and hcpG are maintained subject to selection intensity for 1) dosage amplification in early infection or 2) functional divergence during late infection. Strains harboring pseudogenized hcpG or lacking hcpG altogether are postulated to reflect weak selection or competition among variants for occupation of specific biochemical niches, respectively. The dashed line in the preservation phase indicates cyclical duplication and loss events that may periodically give rise to hcpG alleles with new functional capacities; only well adapted hcpG variants survive whereas the others are pseudogenized. Black rectangles, hcpC; grey rectangle, duplicate copy; white rectangle, pseudogenized hcpG; Δ, hcpG deletion; colored rectangles, hcpG variants; sS, strong selection; wS, weak selection.