RAM pathway mutants are attenuated for virulence, and can only cause disease if they revert to wild type in a mouse model.

<p><b>A.</b> Survival of mice infection with wild type strain G (<i>n</i> = 9), <i>mob2</i> mutant DM09 (<i>n</i> = 10) and complemented strain AI255 (<i>n</i> = 9). <b>B.</b> Colony forming units measured from brain and lung tissue of mice when sacrificed. For the wild type and complemented strain, three mice were used. For the <i>mob2</i> mutant, all ten mice were examined. Four (#1–#4) that caused disease symptoms were sacrificed. The other six were sacrificed at day 70. Three had cleared the infection (not on graph), while three had the fungal burdens indicated. <b>C.</b> Cell morphology and <i>MOB2</i> chromatograms and sequences from strains isolated from mice infected with the <i>mob2</i> mutant strain (bar = 50 µm). The <i>mob2</i> mutant carries the g-a mutation that impairs splicing. Strains from mice #4 and 5 have a reversion mutation, while strains from mice #7 and #10 are pseudohyphal and maintain the original mutation. Sequence data from additional strains is provided as <a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1002936#ppat.1002936.s003" target="_blank">dataset S3</a>.