Figure 7

MAP upregulates double strand break repair and translesion synthesis to resist the host immune response in MAC-T cells. MAP responds to nitric oxide production inside MAC-T cells by upregulating a universal stress response gene, MAP3179c, which binds onto MAP DNA. In order to overcome NO, MAP upregulates MAP4216 which causes a reducing environment inside the cell and subsequently turns on antibiotic resistant genes (MAP1798, MAP2674c, and MAP3296c. MAP2835c, a hydrolase, is involved in cell wall division and double strand break repair commences to correct any deleterious effects created by NO. NO may also cause irreparable damage to DNA bases; therefore, MAP also employs translesion synthesis to continue replication. This may also cause insertion mutations; the impact of this is currently unknown.