The cheY gene (HP1067) encodes a response regulator of a two-component signal transduction system regulating chemotaxis [84]. CheY does not act as a transcriptional activator. Instead, when activated, it interacts directly with the flagellar motor-switch complex, causing a clockwise rotation of the flagella that results in cell tumbling. Intra-hspEAsia divergence was very small for cheY (Table 6 and Figure 8C (a)). It would be interesting to see whether this divergence is related to differences in chemotaxis. Electron transfer

Seven genes in Table GSK2126458 cell line 6, fixQ, fixS, frxA, hypD, hydE, pgl and nuoF, are related to electron transfer. Aerobic respiration in H. pylori has been analyzed experimentally and by genome sequences. A cb-type cytochrome INK 128 nmr c oxidase is the sole terminal oxidase present in H. pylori [87]. FixQ (= CcoQ) is a component of the oxidase. The fixS gene likely encodes the cation transport

subunit of the oxidase [34]. It has been proposed that FixS plays a role in the uptake and metabolism of copper required for oxidase assembly [87]. Aerobic respiration results in production of toxic superoxide at this terminal oxidase, which is involved in bacterial death [88]. The frxA gene, NAD(P)H-flavin oxidoreductase, is involved in redox of flavins, which are important electron transfer mediators [89]. Reduced flavins reduce ferric complexes or iron proteins with low redox potential. FrxA is one of the enzymes that make H. pylori sensitive to metronidazole [90]. H. pylori is capable of hydrogen oxidation [87]. HypD is involved in maturation of the [NiFe] H2-uptake hydrogenase, and catalyzes insertion and cyanation of the iron center [91]. The hydE gene is also necessary for the hydrogenase activity [92]. The pgl gene (HP1102) encodes a 6-phosphogluconolactonase, which catalyzes the second step of the phosphopentose

pathway. This phase of the phosphopentose pathway generates reducing power in the form of NADPH and is important in other organisms in defense against reactive oxygen species and oxidative from stress response [93, 94]. Intra-hspEAsia divergence was very small for fixQ (Figure 8C (b), Table 5 and Table 6). Translation Four genes in Table 6, miaA, tilS, def, and prmA, are important for translation. MiaA and TilS affects translation fidelity [95–97]. MiaA isopentenyl-tRNA transferase modifies the tRNAs that read codons starting with U to minimize peptidyl-tRNA slippage in translation. TilS, the tRNA(Ile2) lysidine synthetase, modifies check details cytidine to lysidine (2-lysyl-cytidine) at the first anticodon of tRNA(Ile2), thereby switching tRNA(Ile2) from a methionine-specific to an isoleucine-specific tRNA. Def removes a formyl group from the N-terminus of a nascent polypeptide and is a potential drug target [98].