Lyme borreliosis is rapidly emerging in the United Kingdom, with over 1000 cases per annum now reported. Lyme borreliosis is caused by the Borrelia burgdorferi sensu lato (s.l.) group of spirochetes, which are transmitted by ixodid ticks. In the United Kingdom, Ixodes ricinus is recognized as the principal vector of the spirochetes, and this tick species is widely distributed across the country. However, as yet, it is unclear whether the distribution of B. burgdorferi essentially mirrors that of its vector, or if there are marked differences between the 2. The aim of this survey was to investigate the prevalence of B. burgdorferi in I. ricinus populations across northern England, north Wales, and the Scottish Border region. We surveyed for questing I. ricinus nymphs and adults at 17 sites, encountering ticks at 12. At 8 sites, large numbers (>160) ticks were collected, and at 3 of these sites B. burgdorferi infection prevalence was significantly higher (>7.5%) than the other 5 (<1.0%). Habitat type was associated with B. burgdorferi prevalence, with ticks from deciduous and mixed woodland being significantly more likely to be infected than those from other habitat types. Identification of infecting Borrelia species indicated that Borrelia valaisiana was the most common and widespread species encountered. B. garinii was common at sites where infection prevalence was high, and B. afzelii was also occasionally encountered at these sites. The survey revealed a surprisingly uneven distribution of B. burgdorferi s.l. across the region, thereby indicating that the presence of ticks does not necessarily mean the presence of the pathogen. Indeed, the spirochete appears to be absent or very rare at some sites where ticks are abundant.

Highlights d Wild Prunus germplasm is collected from the high altitudes of the Himalayas d SINE retrotransposons expand in the genomes of three Tibetan Prunus species d UV response and phenylpropanoid metabolism associate with high-altitude adaptation d Specific SINE insertions change the expression of altituderelated genes

In peach orchards, birds severely damage flowers during blossom season, decreasing the fruit yield potential. However, the wild peach species Prunus mira shows intraspecific variations of bird damage, indicating that some of the wild trees have developed strategies to avert bird foraging. Motivated by this observation, we formulated the present study to identify the potential flower metabolites mediating the bird’s selective feeding behavior in P. mira flowers. The birds’ preferred (FG) and avoided (BFT) flowers were collected from wild P. mira trees at three different locations, and their metabolite contents were detected, quantified, and compared. The widely-targeted metabolomics approach was employed to detect a diverse set of 603 compounds, predominantly, organic acids, amino acid derivatives, nucleotide and its derivatives, and flavones. By quantitatively comparing the metabolite contents between FG and BFT, three candidate metabolites, including Eriodictiol 6-C-hexoside 8-C-hexoside-O-hexoside, Luteolin O-hexosyl-O-hexosyl-O-hexoside, and Salvianolic acid A, were differentially accumulated and showed the same pattern across the three sampling locations. Distinctly, Salvianolic acid A was abundantly accumulated in FG but absent in BFT, implying that it may be the potential metabolite attracting birds in some P. mira flowers. Overall, this study sheds light on the diversity of the floral metabolome in P. mira and suggests that the bird’s selective feeding behavior may be mediated by variations in floral metabolite contents.

BackgroundFlesh color is one of the most important traits for the commercial value of peach fruit. To unravel the underlying regulatory network in Prunus mira, we performed an integrated analysis of the transcriptome and metabolome of 3 fruit types with various flesh pigmentations (milk-white, yellow and blood) at 3 developmental stages (pit-hardening, cell enlargement and fruit ripening).ResultsTranscriptome analysis showed that an intense transcriptional adjustment is required for the transition from the pit-hardening to the cell enlargement stage. In contrast, few genes were differentially expressed (DEGs) from the cell enlargement to the fruit ripening stage and importantly, the 3 fruits displayed diverse transcriptional activities, indicating that difference in fruit flesh pigmentations mainly occurred during the ripening stage. We further investigated the DEGs between pairs of fruit types during the ripening stage and identified 563 DEGs representing the ‘core transcriptome’ associated with major differentiations between the 3 fruit types, including flesh pigmentation. Meanwhile, we analyzed the metabolome, particularly, at the ripening stage and uncovered 40 differential metabolites (‘core metabolome’) between the 3 fruit types including 5 anthocyanins, which may be the key molecules associated with flesh coloration. Finally, we constructed the regulatory network depicting the interactions between anthocyanins and important transcripts involved in fruit flesh coloration.ConclusionsThe major metabolites and transcripts involved in fruit flesh coloration in P. mira were unraveled in this study providing valuable information which will undoubtedly assist in breeding towards improved fruit quality in peach.

Bartonella quintana has been considered to be specifically adapted to humans. Our isolation of the organism from 2 of 36 captive rhesus macaques in China and finding antibodies against B. quintana in 12 of 33 indicates that the reservoir hosts of B. quintana may include primates other than humans.

AIM:To investigate whether hepatitis B virus (HBV) infection activates DNA damage response and DNA repair cofactors inhibit HBV infection and replication. METHODS: Human hepatocyte cell line HL7702 was studied. Immunoblotting was performed to test the expression of ataxia telangiectasia-mutated (ATM)-Rad3-related protein (ATR), p21 and the level of phosphorylation of Chk1, p53, H2AX, ATM in HBVinfected or non-infected-cells. Special short RNAi oligos was transfected to induce transient ATR knockdown in HL7702. ATR-ATM chemical inhibitors caffeine (CF) and theophylline (TP), or Chk1 inhibitor 7-hydroxystaurosporine (UCN01) was studied to determine whether they suppress cellular DNA damage response and MG132 inhibits proteasome. RESULTS: The ATR checkpoint pathway, responding to single-strand breaks in DNA, was activated in response to HBV infection. ATR knockdown cells decreased the HBV DNA yields, implying that HBV infection and replication could activate and exploit the activated DNA damage response. CF/TP or UCN01 reduced the HBV DNA yield by 70% and 80%, respectively. HBV abrogated the ATR-dependent DNA damage signaling pathway by degrading p21, and introduction of the p21 protein before HBV infection reduced the HBV DNA yield. Consistent with this result, p21 accumulation after MG132 treatment also sharply decreased the HBV DNA yield. CONCLUSION: HBV infection can be treated with therapeutic approaches targeting host cell proteins by inhibiting a cellular gene required for HBV replication or by restoring a response abrogated by HBV, thus providing a potential approach to the prevention and treatment of HBV infection.

Klebsiella pneumoniae (K. pneumoniae) is a frequent pathogen causing nosocomial infections and outbreaks. We developed a multiple cross displacement amplification (MCDA) assay for the detection of K. pneumoniae, which can get the positive results within 40 minutes’ isothermal amplification. Gold-nanoparticle lateral flow biosensor (LFB) and colorimetric indicators were used for the rapid readouts of MCDA amplification. The detection limit of this assay was 100 fg per reaction at 65°C, which was confirmed to be the optimal amplification temperature according to the real time turbidimeters. For specificity, all of the 30 clinical-source K. pneumoniae strains were positive for the MCDA, and all of the non-K. pneumoniae strains belonging to 31 different species were negative for this MCDA assay. To evaluate the practical applicability of this method, we assessed its detection limit for K. pneumoniae strains in sputum samples (24 CFU per reaction), and DNA templates of 100 sputum samples further underwent the MCDA-LFB tests. All of the sputum samples being positive for K. pneumoniae (30/100) with the culture method were successfully identified with the MCDA assay, the detection power of which was higher than that of polymerase chain reaction (PCR) (25/100). Thus, the MCDA test for K. pneumoniae combined with the gold nanoparticle LFB as the results readout scheme, are simple, specific, and sensitive methods for the rapid diagnosis of K. pneumoniae in clinical samples.

apoptosis. Research on cell survival changes upon radiation following HBV infection showed that survival of UV-treated host cells was greatly increased by HBV infection, owing to the reduced apoptosis. INTRODUCTIONEukar yotic cells employ multiple strategies of checkpoint signaling and DNA repair mechanisms to monitor and repair damaged DNA [1][2][3][4][5] . There are two branches of the checkpoint response pathway, ataxia telangiectasia-mutated (ATM) pathway and ATM-Rad3-related (ATR) pathway. The major difference between ATM and ATR is the type of DNA damage to which each responds. For example, ATM responds to ionizing radiation (IR) and other agents that cause double-strand breaks (DSBs) in DNA. ATR responds to ultraviolet radiation (UV) radiation and other agents that induce the accumulation of stalled replication forks and subsequent single-stranded breaks (SSBs) in DNA. The DSBs are recognized by the Mre11-Rad50-Nbs1 complex, which recruits and activates ATM kinase [6] . The SSBs are coated METHODS:We incubated HL7702 hepatocytes with HBV-positive serum, mimicking a natural HBV infection process. We used immunoblotting to evaluate protein expression levels in HBV-infected cells or in non-infected cells; immunofluorescence to show ATR foci ands Chk1 phosphorylation foci formation; flow cytometry to analyze the cell cycle and apoptosis; ultraviolet (UV) radiation and ionizing radiation (IR)-treated cells to mimic DNA damage; and Trypan blue staining to count the viable cells. RESULTS: We found that HBV infection induced an increased steady state of ATR protein and increased phosphorylation of multiple downstream targets including Chk1, p53 and H2AX. In contrast to ATR and its target, the phosphorylated form of ATM at Ser-1981 and its downstream substrate Chk2 phosphorylation at Thr-68 did not visibly increase upon infection. However, the level of Mre11 and p21 were reduced beginning at 0.5 h after HBV-positive serum addition. Also, HBV infection led to transient cell cycle arrest in the S and the G2 phases without accompanying increased