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. 2013 Apr;79(7):2480–2483. doi: 10.1128/AEM.03111-12

Table 1.

Luminescence-up mutants

Disrupted gene (ORF) Independent mutant(s)a Putative functionb
arcA (VF2120) SLV41 Regulator, redox-responsive TCRS
arcB (VF2122) NL3, SLV41, SLV19, NL5, SLV36, NL6, SLV33 Sensor, redox-responsive TCRS
acnB (VF2158) NRc Aconitase (TCA cycle enzyme)
topA (VF1051) EMH12, EMH13 Topoisomerase I (relieves negative supercoils)
lonA (VF2352) SLV32, SLV39, EMH6 ATP-dependent protease
pstA (VF1984) SLV10 High-affinity phosphate transport
pstC (VF1985) SLV30 High-affinity phosphate transport
hns (VF1631) SLV15 Nucleoid-associated DNA-binding protein, global repressor
tRNAMet (VFIRNA222) EMH7 Methionine tRNA
tRNAThr (VFIRNA003) NL4 Threonine tRNA
tfoY (VF1573) NL1, EMH9 Regulator of transformation competence
phoQ (VF1397) SLV16, SLV43, EMH3 Sensor, Mg2+-responsive TCRS
guaB (VF0637) EMH5 Inositol-5-monophosphate dehydrogenase (purine metabolism)
ainS (VF1037) NR Octanoyl homoserine lactone synthase
a

Mutants previously identified as brighter than wild type in culture (12). Underlining indicates the representative strain for each locus reported here.

b

TCRS, two-component regulatory system; TCA, tricarboxylic acid.

c

NR, not reported, either due to a high rate of suppressor mutations (acnB mutants) or because symbiotic phenotypes were previously published (ainS mutants).