Light Response of Pseudomonas putida KT2440 Mediated by Class II LitR, a Photosensor Homolog.

Pseudomonas putida KT2440 retains three homologs (PplR1 to PplR3) of the LitR/CarH family, an adenosyl B12-dependent light-sensitive MerR family transcriptional regulator. Transcriptome analysis revealed the existence of a number of photoinducible genes, including pplR1, phrB (encoding DNA photolyase), ufaM (furan-containing fatty acid synthase), folE (GTP cyclohydrolase I), cryB (cryptochrome-like protein), and multiple genes without annotated/known function. Transcriptional analysis by quantitative reverse transcription-PCR with knockout mutants of pplR1 to pplR3 showed that a triple knockout completely abolished the light-inducible transcription in P. putida, which indicates the occurrence of ternary regulation of PplR proteins. A DNase I footprint assay showed that PplR1 protein specifically binds to the promoter regions of light-inducible genes, suggesting a consensus PplR1-binding direct repeat, 5'-T(G/A)TACAN12TGTA(C/T)A-3'. The disruption of B12 biosynthesis cluster did not affect the light-inducible transcription; however, disruption of ppSB1-LOV (where LOV indicates "light, oxygen, or voltage") and ppSB2-LOV, encoding blue light photoreceptors adjacently located to pplR3 and pplR2, respectively, led to the complete loss of light-inducible transcription. Overall, the results suggest that the three PplRs and two PpSB-LOVs cooperatively regulate the light-inducible gene expression. The wide distribution of the pplR/ppSB-LOV cognate pair homologs in Pseudomonas spp. and related bacteria suggests that the response and adaptation to light are similarly regulated in the group of nonphototrophic bacteria.IMPORTANCE The LitR/CarH family is a new group of photosensor homologous to MerR-type transcriptional regulators. Proteins of this family are distributed to various nonphototrophic bacteria and grouped into at least five classes (I to V). Pseudomonas putida retaining three class II LitR proteins exhibited a genome-wide response to light. All three paralogs were functional and mediated photodependent activation of promoters directing the transcription of light-induced genes or operons. Two LOV (light, oxygen, or voltage) domain proteins, adjacently encoded by two litR genes, were also essential for the photodependent transcriptional control. Despite the difference in light-sensing mechanisms, the DNA binding consensus of class II LitR [T(G/A)TA(C/T)A] was the same as that of class I. This is the first study showing the actual involvement of class II LitR in light-induced transcription.

Outbreak of Salmonella Braenderup infection originating in boxed lunches in Japan in 2008.

There have been only 2 reports of a large-scale foodborne outbreak arising from Salmonella enterica serotype Braenderup infection worldwide. On August 9, 2008, an outbreak originating in boxed lunches occurred in Okayama, Japan. We conducted a cohort study of 786 people who received boxed lunches from a particular catering company and collected 644 questionnaires (response rate:82%). Cases were defined as those presenting with diarrhea (≧4 times in 24h) or fever (≧38℃) between 12 am on August 8 and 12 am on August 14. We identified 176 cases (women/men:39/137);younger children (aged＜10 years) appeared to more frequently suffer severe symptoms. Three food items were significantly associated with higher risk of illness;tamagotoji (soft egg with mixed vegetables and meat) (relative risk (RR):11.74, 95% confidence interval (CI):2.98-46.24), pork cooked in soy sauce (RR:3.17, 95% CI:1.24-8.10), and vinegared food (RR:4.13, 95% CI:1.60-10.63). Among them, only the RR of tamagotoji was higher when we employed a stricter case definition. Salmonella Braenderup was isolated from 5 of 9 sampled cases and 6 food handlers. It is likely that unpasteurized liquid eggs contaminated by Salmonella Braenderup and used in tamagotoji caused this outbreak.