Meyer M, Stenzel U, Hofreiter M: Parallel tagged sequencing GDC 0449 on the 454 platform. Nat Protoc 2008, 3:267–278.PubMedCrossRef 39. Excoffier L, Laval G, Schneider S: Arlequin (version 3.0): an integrated software package for population genetics data analysis. Evol Bioinform 2005,

1:47–50. 40. Clarke KR: Non-parametric multivariate analysis of changes in community structure. Aust J Ecol 1993, 18:117–143.CrossRef 41. Opgen-Rhein R, Strimmer K: From correlation to causation networks: a simple approximate learning algorithm and its application to high-dimensional plant gene expression data. BMC Syst Biol 2007, 1:37.PubMedCrossRef 42. Nawrocki EP, Kolbe DL, Eddy SR: Infernal 1.0: inference of RNA alignments. Bioinformatics 2009, 25:1335–1337.PubMedCrossRef 43. Price MN, Dehal PS, Arkin AP: FastTree: computing large minimum evolution trees with profiles instead of a distance matrix. CX-5461 supplier Mol Biol Evol 2009, 26:1641–1650.PubMedCrossRef 44. Kembel SW, Cowan PD, Helmus MR, Cornwell WK, Morlon H, Ackerly DD, Blomberg SP, Webb CO: Picante: R tools for integrating phylogenies and ecology. Bioinformatics 2010, 26:1463–1464.PubMedCrossRef 45. Smoot ME, Ono K, Ruscheinski J, Wang PL, Ideker T: Cytoscape 2.8: new features for data integration and network visualization.

Bioinformatics 2011, 27:431–432.PubMedCrossRef 46. Ludwig W, Strunk O, Westram R, Richter L, Meier H, Yadhukumar , Buchner A, Lai T, Steppi S, Jobb G, et al.: ARB: a software environment for sequence data. Nucleic Acids Res 2004, 32:1363–1371.PubMedCrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions MS designed the study. CA, RMG, MH, and AF collected the samples. DQ carried out the laboratory work. JL, IN, ML, and HPH analyzed the data. MS, JL, and HPH wrote the manuscript. All authors read and approved the final manuscript (with the exception of IN, who read and approved a preliminary version).”
“Background Porphyromonas gingivalis Protein kinase N1 is one of the most important etiologic

agents involved in chronic periodontitis (CP), an infectious and multifactorial disease that leads to the destruction of the periodontium. During the infective process, bacteria acquire nutrients to survive and multiply at the site of infection. Heme, one of these nutrients, is an iron-dependent cofactor of many indispensable enzymes and proteins. P. gingivalis acquires heme from host heme-binding proteins through proteolysis and transports heme into the HSP inhibitor bacterial cell using outer membrane receptors [1]. A previously characterized heme uptake system in P. gingivalis utilizes two proteins: HmuY, which scavenges heme from host hemoproteins, and HmuR [2–4], which transports the nutrient across bacterial cell membranes. These proteins are virulent factors, yet they can be antigenic and immunogenic as well, potentially affecting a host’s immune system with respect to stability and resistance. HmuY is a membrane-associated lipoprotein identified in P.