SummaryErwinia carotovora produces the b b b b -lactam antibiotic, carbapenem, in response to a quorum sensing signalling molecule, N-(3-oxohexanoyl)-L -homoserine lactone (OHHL). We have mapped the OHHL-dependent promoter upstream of the first of the biosynthetic genes, carA . We have also analysed the effect on this promoter of the known genetic regulators of carbapenem expression, carR , carI (encoding homologues of LuxR and LuxI respectively) and hor (encoding a SlyA/MarR-like transcriptional regulator). We describe a previously unknown promoter located within the carA-H operon. This promoter does not respond to CarR and is required for quorum sensing-independent expression of the carbapenem resistance determinants encoded by the carFG genes. We have mapped the carR , carI and hor transcription start points, shown that CarR is positively autoregulated in the presence of OHHL, and have demonstrated negative feedback affecting transcription of carI . In addition, various environmental and physiological factors were shown to impinge on the transcription of the car biosynthetic genes. The nature of the carbon source and the temperature of growth influence carbapenem production by modulating the level of the OHHL signalling molecule, and thereby physiologically fine-tune the quorum sensing regulatory system.

20089 Background: Association of glutathione-S-transferase M1 (GSTM1) polymorphisms and cancer has been demonstrated. Especially the deletion polymorphism of GSTM1 has been related to risk for lung cancer in some studies. We thus investigated the frequency of GSTM1-null genotype in lung cancer patients and healthy individuals from the Lake District in Turkey. Methods: Cases were recruited among patients with clinically and histologically confirmed diagnosis of lung cancer patients from the Lake District. Controls were selected among the nonsmoking healthy blood donors applied to hospital in same region. DNA samples were extracted from whole blood using proteinaz K (20 mg/mL) digestion in lysis buffer (10 mM Tris-HCl, 400 mM NaCl, 2 mM EDTA, % 10 SDS). Homozygous deletion of the GSTM1 gene was determined by PCR using the primers E4F: 5′-CTGCCCTACTTGATTGATGGG-3′, E5R: 5′-CTGGATTGTAGCAGATCATGC-3′, corresponding to exons 4 and 5 of the GSTM1 gene. PCR products were analyzed by 1% agarose gel electrophoresis and UV transilluminator was then used to evaluate the product content. Individuals carrying the GSTM1 gene were identified by the presence of a 273 bp DNA fragment. Results: The study comprised 30 patients and 30 controls. The frequency of GSTM1-null genotype was found to be (n = 14) 46.7% in lung cancer patients and (n = 5) 16.6% in controls. The difference was statistically significant (Fisher’s chi square test: 4.80, P: 0.0251). Conclusion: We found an increased incidence of GSTM1-null genotype among lung cancer patients, indicating that the GSTM1 absence is associated with a slightly increased lung cancer risk in people from the Lake District in Turkey. No significant financial relationships to disclose.