Table 1.
S. typhimurium genes that are induced in vivo
| Strain | Gene* | Function | Role in pathogenesis | Parameters† |
|---|---|---|---|---|
| Regulatory genes | ||||
| MT1466 | phoP | Virulence regulator | Invasion/macrophage survival | 1BC |
| MT1731 | pmrB | Polymyxin resistance | Neutrophil survival | 8D |
| MT1396 | cadC | Cadaverine synthesis | Acid tolerance | 1A, C |
| MT1398 | iviXIII‡ | ChvD-like | Regulator induction | 1B; 99 min |
| MT1632/1633 | vacB‡/vacC | RNA processing | Post-transcriptional regulation | 1BC/1A; 95 min/9 min |
| RpoS-regulated genes | ||||
| MT1483 | spvB | Plasmid virulence | Systemic survival | 8C |
| MT1397 | cfa | Membrane modification | Stationary-phase survival | 1AC |
| MT1459 | otsA | Trehalose synthesis | Stationary-phase/osmoprotectant | 1A |
| Metabolic functions | ||||
| MT1562 | recD | Recombination/repair | Macrophage survival | 8D |
| MT1426 | hemA | Catalase cofactor | Peroxide resistance | 1C |
| MT1505 | entF | Enterobactin synthesis | Iron acquisition | 8D |
| MT1415 | fhuA | Iron transport | Iron uptake | 1A |
| MT1399 | cirA | Colicin I receptor | Catechol transport | 8D |
| MT1442/1443 | mgtA‡/mgtB‡ | Mg2+ transport | Mg2+ uptake | 8CD/8C |
| MT1498 | iviX‡ | Heavy metal transport | Cu2+ homeostasis | 8D; 11 min |
| MT1446 | ndk | Nucleotide balance | Alarmone synthesis | 1AC |
| Systemic adhesin- and invasin-like genes | ||||
| MT1461 | iviVI-A‡ | Tia/Hra1-like | Adhesion/invasion | 8C; 7 min |
| MT1461 | iviVI-B‡ | PfEMP1-like | Adhesion/invasion | 8C; 7 min |
| Mouse spleen and cultured macrophages | ||||
| MT1799 | iviXI‡ | Unknown | Macrophage survival | 8CD; 53 min |
| MT1501/1733 | iviXII | Unknown | Macrophage survival | 8D/1C; 9 min |
| MT1500 | iviXV | Unknown | Macrophage survival | 8CD; 9 min |
Listed are functions or attributes of ivi genes and their known or inferred roles in pathogenesis.
ivi fusions were cloned using a transductional method (11), and the first 200–400 base pairs were sequenced using an oligonucleotide primer that directs synthesis from the 5′ end of the selected promoterless gene (purA or cat) into the cloned fragment. Nucleotide and deduced amino acid sequences were compared with known data bases by using the fasta and blast programs of GCG (Madison, WI). All fusions listed are in the known coding sequence or in the predicted ORF of the gene indicated with the following exceptions: cfa, where the joint point is 23 bp before the ATG start codon, cirA, where the fusion joint point is 104 bp after the translational stop codon, and iviXV, where the coding sequence has not been identified although it has been recovered from three independent experiments (from the spleen after an i.p. infection and from two cultured macrophage selections). A
designation after the gene indicates that an insertion mutation in the coding sequence was isolated and assayed for a virulence defect in an LD50 study, 500-fold and >100-fold above the i.g. and i.p. LD50, respectively. None of these mutations conferred a virulence defect by this assay.
The numbers refer to the IVET vector used in the selection: 1 = pIVET1 (purA); 8 = pIVET8 (cat). The capital letters denote the route of delivery and the host tissue (BALB/c mice) from which the bacteria were recovered. A = i.g., small intestine; B = i.g., spleen; C = i.p., spleen; and D = cultured RAW 264.7 macrophages. Map positions in minutes are provided for ivi genes that have not been previously described in Salmonella. Map position on the Salmonella chromosome was determined by Mud-P22 transductional mapping (12).