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Table 2 Genes inferred as uniquely essential in Shigella

From: Combining Shigella Tn-seq data with gold-standard E. coli gene deletion data suggests rare transitions between essential and non-essential gene functionality

Gene(s) Function [49] Support for Different Physiological Roles in E. coli and Shigella
lysS aminoacyl tRNA synthetase, tRNA modification The lysU functional homologue is absent in Shigella [45]
proABC proline biosynthesis The active proline transporter putP is absent from Shigella [46]. The cryptic transporter proY may be silent, as observed in Salmonella [47], possibly necessitating proline biosynthesis
acetate kinase
pyruvate dehydrogenase
pyruvate kinase
All affect acetate accumulation [66] and utilization [23], which is required for robust growth (Shigella lacks the acetyl CoA synthetase present in E. coli K12 [67])
rfbA, rfbF, rfbG, rfc, and rfbI sugar nucleotide biosynthesis for LPS All except rfbA lack E. coli K12 orthologues, as this locus has been replaced by the laterally transferred wbb locus [48]
cysM cysteine synthase B ORFs in cysteine synthase A also depleted for inserts; 4 out of 5 sulfate ABC transporters depleted for inserts (see main text)
tufB elongation factor EF-Tu tufB and lepA (next entry) both are involved in translation elongation; the other ORF involved, tufA, is depleted for inserts (see main text)
lepA elongation factor 4 See above
spr murein DD-endopeptidase None known
rsxB soxR-reducing complex None known
  1. These genes were inferred as essential in Shigella, but have orthologous E. coli deletion genotypes that exhibit robust growth (greater than 0.75 OD600 after 22 h growth in LB). The genes in the rfb operon have no orthologues in E. coli K12 (see main text)