BMC Genomics 2009, 10(Suppl 2):S4 http://www.biomedcentral.com/1471-2164/10/S2/S4 Table 2: Changes in specific target gene expression in response to sub-MIC of antibiotics GeneID Product Name 1244738 1244702 1244823 1245164 1243991 30S ribosomal protein S4 30S ribosomal protein S7 DNA gyrase subunit B Recombinase A PonC Locus rpsD rpS7 gyrB recA ponC AMX* ns 1.11 ns ns -0.55 CTC* -0.82 -0.93 1.36 ns -0.56 ENR* 1.29 1.69 1.45 9.96 -0.62 COG(s) COG0522J COG0049J COG0187L COG0468L COG4953M *Ratio of treatment/control normalized intensities. ns: no significant change in gene expression with sub-MIC of antibiotic. RecA protein expression results in the cleavage of LexA repressor, thus removing the LexA mediated repression of DNA repair genes like uvrD. Expression of both recA and lexA genes increased in response to ENR (Table 1). Expres- sion of recN was increased, which also relieves LexA repression [23-25]. Genes involved in fine-tuning the actions of RecA, namely recX and uvrD, also had increased expression. Expression of primosome genes (dnaJ and iFFnuigmreuasrrpeaot4ne/sneittroateenreosflpooxnasceinrevigsuulaltiozerdneintwPaotrhkwinayPS.tmuudlitoocida Fumarate/nitrate response regulator network in P. multocida in response to enrofloxacin visualized in Pathway Studio. P. multocida sub-MIC ENR response was marked by significant changes in fnr response regulated genes. Red nodes are genes with increased expression and green nodes are genes with decreased expression. The rest of the interacting nodes are shown in gray. These nodes had no significant changes in expression or were orthologs from additional gram-negative species in the molecular interaction database in Pathway Studio. dnaK) that encode enzymes required for re-starting the stalled replication fork and other replicative enzymes like DNA polymerase III increased with ENR. It is reported that beta lactam mediated cell killing involves SOS response through SulA and DpiBA two com- ponent system [26]. Based on the genome annotation of Pm70 [6], all the components of this regulon are not present. There was no induction of the expression of recA or lexA with AMX (Additional file 3, supplemental figure 2). The expression profile of SOS response genes remained either unchanged or showed decreased expres- sion, which indicates that sub-MIC AMX does not activate SOS response in P. multocida. Excluding the increased expression of lexA and gyrB, CTC (Additional file 3, sup- plemental figure 3) also did not activate SOS response. DE virulence genes Productive infection by bacterial pathogens relies on the expression of virulence factors that have wide ranging functions like competence, adherence, capsule synthesis and export, evading host immune responses etc. Tran- scription profiling of the response of a bovine P. multocida isolate (L386) to MIC of eight different antibiotics identi- fied mostly reduced virulence gene expression [12]. In the current study, transcription profiling of the P. multocida response to AMX, CTC and ENR identified significant changes in the expression of known and putative viru- lence genes. AMX and CTC reduced the expression of ompA, a known virulence factor of P. multocida involved in binding to host cells [27] (Table 4). AMX and CTC decreased expression of the gene encoding detoxifying enzyme superoxide dismutase, which is one of the viru- lence genes identified in the P. multocida L386 study [12]. Additional virulence factors (based on L386 study) which had reduced expression in Pm70 are: clpB protease with AMX, capsule transport protein hexA with all three antibi- otics, PM1714 regulator with AMX and CTC, capsule bio- synthesis genes phyA and hyaE with AMX and CTC, phyB with CTC, and tight adherence gene tadB with AMX. Expression of dnaK, which is required for virulence in a number of bacterial pathogens [26], was decreased by CTC. Page 6 of 10 (page number not for citation purposes)