Mycoplasma genitalium (MG) is an emerging sexually transmitted pathogen associated with reproductive tract disease in men and women. Despite the development of a robust antibody response, MG can persist for months to years, potentially increasing the risk for sexual transmission and serious upper reproductive tract infection in women. The molecular basis of MG pathogenesis is poorly understood, in part due to its fastidious nature, extremely small genome lacking known virulence genes, and the limited genetic tools available for molecular investigations. Nevertheless, previous studies have linked MG virulence to its unique terminal organelle, a complex structure that mediates adherence, motility, and cell division. The terminal organelle is composed of a complex array of unique proteins, including MgpB and MgpC which serve as major adhesins and are required for terminal organelle biogenesis. Remarkably, these two surface-exposed proteins also undergo phase and antigenic variation through a unique process of segmental recombination between discreet variable regions within mgpB and mgpC and multiple homologous archived sequences, termed MgPa repeats (MgPar). Our goal is to identify the molecular factors required to promote this genetic diversity, a mechanism which likely contributes to the ability of MG to adapt to different host conditions and maintain persistent infections. Recently, we have shown that RecA is required for mgpB/C gene variation and that this protein is expressed in several isoforms. We have now expanded these studies by showing that these RecA isoforms originate from different translational start sites and that specific recA upstream sequences regulate the expression ratio of these isoforms and mgpB/C-MgPar recombination. Together, these studies suggest the presence of novel regulatory mechanisms that may allow this genetically challenged organism to cause disease, evade the host immune response, and persist in infected individuals.