Change in fitness caused by disruption of selected genes during PCP exposurea

GeneProductΔ fitnessb
(WWt, +PCPWWt, −PCP)
Δ fitnessb
(WΔpcpB, +PCPWΔpcpB, −PCP)
P valuec
pcpRPCP transcriptional activator0.16*0.50*4.8e−52
pcpBPCP hydroxylase−0.20*n/an/a
pcpDTCBQ reductase−0.25*-0.043.1e−23
pcpCTCHQ dehalogenase−0.25*0.07*1.2e−37
pcpADCHQ dioxygenase−0.32*0.013.0e−14
pcpEMaleylacetate reductase−0.29*0.014.4e−31
pcaJ3-Oxoacid CoA transferase, subunit B−0.30*0.012.0e−12
pcaI3-Oxoacid CoA transferase, subunit A−0.27*0.012.6e−08
pcaFBeta-ketoadipyl CoA thiolase−0.26*0.017.1e−08
pcaRIclR family transcriptional regulator−0.29*0.021.2e−36
sodASuperoxide dismutase−0.10*−0.029.8e−11
pntANAD(P)+ transhydrogenase, subunit A−0.21*0.022.0e−17
pntBNAD(P)+ transhydrogenase, subunit B−0.24*0.033.5e−34
zapEAFG1 family ATPase−0.16*0.001.2e−22
  • a Fitness values for all transposon integrants are listed in Data Set S1B. This table contains genes important during PCP degradation. Genes shown in bold type are upregulated after PCP exposure.

  • b Fitness (W) difference comparing the control and experimental (PCP-treated) conditions for each Tn-seq library. Significant fitness changes are those that cause a fitness difference of >0.05 and those for which P < 1.2e−5 (two-sample t test with a Bonferroni correction). Asterisks indicate significant differences.

  • c A two-sample t test was used to test for significant difference of disrupting a given gene between the PCP-treated wild-type and ΔpcpB Tn-seq libraries. n/a, not available.