For example, we detected recurrent conversions between the human β- and δ-globin genes.
This frequent sharing could be explained by recurrent conversions from the donor sequences in the human population, as an alternative to point mutations alone.
However, only one recurrent gene conversion event was observed in the study, but the same can apply to the effect of gene conversions on the genetic linkage.
Our sequence analysis discovered evidence of recurrent gene conversion within the intron and HEG following horizontal transfer.
For example, the plethora of Hb Winnipeg observed in the French population may indicate recurrent gene conversion events.
These mutational events are likely the product of recurrent gene conversion between the ends of organelle chromosomes and appear to occur more frequently in organelle DNAs that harbor large amounts of silent-site diversity.
These data indicate that the high sequence similarity and close relationship between mtrA-1 and mtrA-2 paralogs are maintained by recurrent gene conversion events, favoring the concerted evolution model (Scenario A, Figure 4A).
Since c.833T does not reside within an obvious mutational hotspot, we surmise that the three pathogenic and comparatively prevalent c.[833C; −] chromosomes may have originated by recurrent gene conversion employing the common nonpathogenic c.[833C; 844_845ins68] chromosomes as templates.
Our results rather suggest that recurrent gene conversion is probably limited to a relatively short region, with much higher conservation in the immediate sub-telomeric region and a gradient of sequence divergence.
Several studies have already pointed out a highly conserved duplication in the subtelomeric region of chromosomes r11-r12 and orthologous regions of s5-s8 and b4, this conservation being due to recurrent gene conversion events (Jacquemin et al. 2009, 2011).
