Bacterial Wilt (BW) is among the most devastating plant diseases in the world. This disease is caused by the soilborne plant pathogen Ralstonia solanacearum (Rs) and affects more than 200 plant species. In tomato, resistance to Rs is quantitative. No resistance genes to the US Rs strain K60 have been identified, and the molecular basis of resistance remains unclear. Transcriptomic analysis of resistant tomato roots showed that at 48 hours post inoculation with Rs K60, genes involved in auxin transport and signaling pathways are downregulated. Furthermore, a tomato mutant defective in auxin transport and signaling, known as diageotropica (dgt 1-1) has enhanced resistance to Rs K60. Rs K60 root vasculature colonization is delayed in dgt 1-1 compared to wild type. Treating wild type susceptible tomato plants with the auxin transport inhibitor naphthylphthalamic acid (NPA) enhances resistance to Rs K60 in a dose-dependent manner. Auxin acts antagonistically with the plant hormone salicylic acid (SA), and we found that dgt 1-1 has higher levels of SA and increased expression of SA-response genes. A strain of Rs that can degrade SA is partially virulent on dgt 1-1. Our research suggests that the DGT gene is required for susceptibility to Rs K60, and that proper auxin transport and signaling is important for susceptibility to Rs K60 in tomato plants. This may be due in part to interactions with the SA pathway. Understanding the role of DGT, auxin, and SA in defense responses to Rs in tomato is important for Solanaceae crop improvement.