Recombination start or end point were not observed exactly, but i

Recombination start or end point were not observed exactly, but Caspase inhibition instead in an interval [mi;Mi] (with Mi = ∞ if the beginning or end is out of the sequenced region). We assume a geometric length of recombination with mean δ on both sides of the mutation conferring resistance to rifampicin. Model comparisons using the BIC found no evidence for a difference between the lengths on the two sides, and no support for a more complex negative binomial distribution which has an additional parameter compared to the geometric distribution. The likelihood

of N observations is therefore equal to: (2) The effect of gene knock-outs on the lengths of import was evaluated using the BIC where one hypothesis is that δ remains the same and the other hypothesis is that δ changes. Let p denote the probability of occurrence of ISR in a clone. The number m of clones selleck containing ISR amongst n clones is thus distributed as Binomial(n,p). A Jeffrey’s prior was assumed on p PD0332991 solubility dmso (i.e. Beta (½,½)). We assessed whether the probability of ISR was identical between two recipient/donor combinations (m 1,n 1 and m 2,n 2) using the Bayes Factor: (3) where B(.,.) denotes the Euler Beta function. Acknowledgements The authors thank Christine Josenhans for plasmid pCJ535 and

valuable discussions, Martin Blaser for plasmid pUvrDKm and Kerstin Ellrott, Jessika Schulze, Birgit Brenneke and Friederike Kops for excellent technical assistance.

This work was supported by funding under the Sixth Research Framework Programme of the European Union, project INCA (LSHC-CT-2005-018704) and by grant SFB 900/A1 from the German Research Foundation. C.M. received a Ph.D. stipend from the German Academic Exchange Service (DAAD) and the Wilhelm Hirte Foundation. S.K. and J.K. received Ph.D. stipends CYTH4 from the German Research Foundation (DFG) within the frameworks of GRK 745 and IRTG 1273, respectively, as well as support through the Hannover Biomedical Research School (HBRS). Publication charges for this article were supported by the German Research Foundation in the framework of the program “Open Access Publishing”. Electronic supplementary material Additional file 1: Figure S1. Growth curves (OD600) of H. pylori strains 26695, 26695uvrA, 26695uvrB, 26695uvrC, 26695uvrD and complemented mutant strains. (PDF 24 KB) Additional file 2: Figure S2. Nucleotide sequence alignment of the 1663 bp fragment of the rpoB gene used to determine import length. Sequences are shown for strains 26695, J99 and J99R3. The sequences were aligned using CLC Sequence Viewer v6.6.1 and the point mutation (A1618T) that confers Rif resistance is labeled. (PDF 219 KB) Additional file 3: Figure S3. Amino acid sequence alignments of the four NER components, UvrA, UvrB, UvrC and UvrD. The primary sequences from H. pylori 26695, C. jejuni NCTC11168, E. coli K12 and S.

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