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Gene tandem amplifications are thought to drive bacterial evolution, but they are transient in the absence of selection, making their investigation challenging. Here, we analyze genomic sequences of  Staphylococcus aureus  USA300 isolates from the same geographical area to identify variations in gene copy number, which we confirm by long-read sequencing. We find several hotspots of variation, including the  csa1  cluster encoding lipoproteins known to be immunogenic. We also show that the  csa1  locus expands and contracts during bacterial growth in vitro and during systemic infection of mice, and recombination creates rapid heterogeneity in initially clonal cultures. Furthermore,  csa1  copy number variants differ in their immunostimulatory capacity, revealing a mechanism by which gene copy number variation can modulate the host immune response.

“Gene accordions” cause genotypic and phenotypic heterogeneity in clonal populations of Staphylococcus aureus