serve the plant defense reaction in flowers still attached to the living tree. E. amylovora expressed key E. amylovora hrp Expression Outruns Plant Defense genes for type III secretion, namely the pilin hrpA, the putative translocator hrpN and the effector dspA/E in a narrow time frame of 2448 hpi and in well-defined ratios under the control of the regulator hrpL. No hierarchy for the 
expression of these genes or for the encoded secreted proteins was found. This leads to a model where simultaneous expression of the type III components is required for successful infection. The bacterial presence as well as secreted HrpN is recognized by host cells, thus concomitant injection of effectors is necessary to counteract elicitation of defense responses. Interestingly, main expression of hrp genes coincided with a transient suppression in plant PR-1 expression at 24 hpi suggesting that E. amylovora quickly impacts the major SA-dependent plant defense pathway. This implies that co-transcription of E. amylovora structural genes with effectors of the type III secretion system is necessary to outrun plant defense. hrpL expression. A recA transcript numbers on single flowers plotted against relative expression of hrpL at indicated time points post inoculation. B The same transcript values are plotted against gyrA transcript numbers and gave virtually identical results. Supporting Information qPCR analyses and standard PCR. Acknowledgments We are grateful for the technical assistance and support provided in verification of plant expression results by Dr. F. Trognitz, Austrian Institute of Technology, Vienna, Austria. We also want to thank two anonymous reviewers for their valuable comments, which helped to improve this manuscript. ~~ Pseudomonas aeruginosa is an opportunistic pathogen associated with debilitating infections of immunocompromised individuals and individuals with cystic fibrosis and is characterized by an innate resistance to many antimicrobials and the ability to develop/acquire resistance. Significant contributors to this intrinsic and/or acquired multidrug resistance are several members of the RND family of multidrug efflux systems, particularly that encoded by the mexAB-oprM efflux operon. MexAB-OprM exhibits one of the broadest substrate profiles of the RND pumps in P. aeruginosa, accommodating a wide range of PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/22189475 clinically-relevant antimicrobials and biocides as well as a variety of non-clinical agents associated with quorum-sensing ). An important determinant of intrinsic multidrug resistance this efflux system contributes to acquired fluoroquinolone and b-lactam resistance in clinical isolates of P. aeruginosa. Expression of the mexAB-oprM operon is regulated by the product of a local repressor gene, mexR, occurring 871700-17-3 web upstream of the efflux genes and the target of mutation in MexAB-OprM- overexpressing multidrug-resistant nalB lab and clinical isolates. MexR acts to control mexAB-oprM expression from one of two promoters for this efflux operon, binding as a dimer to a site that also overlaps the mexR promoter and, so, effects negative autoregulation. Recent studies show that its ability to bind and so repress mexAB-oprM is governed by the redox status of the protein, MexR serving to regulate mexAB-oprM expression in responsive to oxidative stress. MexR repressor activity is also modulated by the product of the armR anti-MexR repressor gene, which binds to MexR and negatively impacts its ability to bind to the mexABoprM PI promoter re