Among the 70 family bacterial factors, group 2 factors have similar promoter recognition specificity to group 1 (principal) factors and express and function under specific environmental and physiological conditions. In general, the cyanobacterial genome encodes more than four group 2 factors, and the unicellular Synechococcus elongatus PCC 7942 (Synechococcus) has five group 2 factors (RpoD2-6). In this study, we analyzed expression of group 2 factors of Synechococcus at both mRNA and protein levels, and we showed that the rpoD3 expression was activated only by high light (1,500 mol photons m ؊2 s ؊1 ) among the various stress conditions examined. After high light shift, rpoD3 mRNA accumulated transiently within the first 5 min and diminished subsequently, whereas RpoD3 protein increased gradually during the first several hours. We also found that the rpoD3 deletion mutant rapidly lost viability under the same conditions. Analysis of the rpoD3 promoter structure revealed the presence of an HLR1 (high light-responsive element 1) sequence, which was suggested to be responsible
SummaryThe chromosome of the cyanobacterium Synechococcus sp. PCC7942 contains at least one group 1 (rpoD1) and three group 2 (rpoD2, rpoD3 and rpoD4) sigma factor genes. In this study, we have analysed the structure of rpoD3 and rpoD4 and have shown that these genes are dispensable for growth at normal physiological conditions. An RNA polymerase core enzyme of the cyanobacterial strain was puri®ed, reconstituted with the recombinant sigma factors (the rpoD1, rpoD3 and rpoD4 gene products), and the resultant holoenzymes were examined in vitro for transcription speci®city. All of the holoenzymes recognized canonical promoters of Escherichia coli as well as cyanobacterial rrnA, cpcB1A1 P1a and rpoD1 promoters, although the three holoenzymes had some preference for speci®c promoters. These results suggest that group 1 as well as group 2 sigma factors of cyanobacteria may direct transcription initiation from the eubacterial consensus-type promoters containing the Pribnow À10 element, and we postulate that speci®city crosstalk is a common characteristic among eubacterial group 1 and group 2 sigma factors. Phylogenetic analyses revealed that most group 2 sigma factors were positioned in one of four distinct clusters. The implication of the phylogenetic tree is also discussed in this paper.
Cross-allergenicity between five cereal grains including rice, wheat, corn, Japanese millet (Panicum crus-galli L. var. frumentaceum Trin.) and Italian millet (Setaria italica Beauv. var. germanica schrad.) was examined by radioallergosorbent test (RAST) and RAST inhibition assay. There were significant close correlations between every combinations of RAST values for the five cereal grain extracts. RAST inhibition assay of each extract against RAST discs coupled with other cereal grain extracts indicated marked cross-reactivity of IgE binding between these cereal grain extracts. Rice protein 16KD (RP16KD) was shown to be one of major allergens in rice grain extracts by immunoblotting analysis, histamine release assay from human leukocytes and RAST inhibition. Next, the involvement of RP16KD in the cross-allergenicity between these cereals was investigated. RAST values for RP16KD significantly correlated with that for Italian millet as well as rice but not with those for corn and wheat. There was a trend of positive correlation between RAST values for RP16KD and Japanese millet. In the RAST inhibition assay using sera with positive RAST for these five cereal grain extracts and RP16KD, RP16KD inhibited IgE binding to these all cereal discs in a dose-dependent manner. Similarly, all of the five cereal grain extracts showed an effective decrease in IgE binding to the RP16KD disc. These results indicated possible participation of IgE binding structure on RP16KD in cross-allergenicity between these cereal grain extracts in the Poaceae family.
Paclitaxel-induced painful peripheral neuropathy is a major doselimiting factor. Recently, it has been reported that macrophages accumulated in the dorsal root ganglion of paclitaxel-treated rats, and their activation is suggested to contribute to generation and development of the neuropathy. However, the mechanism for macrophage activation is still unknown. In this study, to explore candidate genes involved in the mechanism for macrophage activation in the dorsal root ganglion of paclitaxel-treated rats, we developed model rats for paclitaxel-induced neuropathic pain and performed a microarray assay to analyze the changes of gene expressions in the dorsal root ganglion. Among the genes with changed expression levels, we focused on matrix metalloproteinase-3 (MMP-3, stromelysin-1) and CD163, a macrophage marker. By reverse transcription-polymerase chain reaction, the expression levels of MMP-3 and CD163 were markedly up-regulated in paclitaxel-treated dorsal root ganglion. As a result of immunohistochemical study, large ganglion neurons, but neither Schwann cells nor macrophages, predominantly expressed MMP-3. This MMP-3 up-regulation occurred prior to macrophage accumulation in the dorsal root ganglion. In addition, recombinant MMP-3 led to the activation of RAW264 macrophages in vitro. Taken together, the up-regulation of MMP-3 and following macrophage activation caused in the dorsal root ganglion might be a significant event to trigger a series of reactions developing paclitaxel-induced peripheral neuropathic pain. (Cancer Sci 2008; 99: 1618-1625) P aclitaxel is an antineoplastic agent used clinically to treat nonsmall-cell lung cancer and ovarian cancer.(1,2) Paclitaxel suppresses microtubule dynamics, causing mitotic arrest in dividing cells.(3) On the other hand, painful peripheral neuropathy is a major dose-limiting factor in clinical cancer chemotherapy with paclitaxel. (4,5) Although the administration of glutamine and acetyl-L-carnitine has been reported to relieve paclitaxel-induced neuropathic pain as symptomatic treatment, (6,7) its effectiveness shows large interindividual variation. To develop a specific treatment, the molecular mechanisms underlying paclitaxelinduced neuropathy should be explored.It has been assumed that paclitaxel-induced neuropathy is generally due to effects on axonal microtubules.(8) Paclitaxelinduced neuropathy is characterized by an ascending distal paresthesia and dysesthesia in a 'glove and stocking' distribution. (5,8) Blocking of axonal transport due to paclitaxel-induced disruption of microtubule dynamics, which seems to be a reasonable mechanism, has been observed in vitro.(9) Nerve biopsies from patients with taxane-induced neuropathy have shown evidence of a loss of large diameter afferents.(10) In contrast, it has been reported that administration of low dose of paclitaxel caused neuropathic pain without any change of axonal morphology. (11) Additively, in vitro, axonal transport was not impaired in DRG neurons exposed to paclitaxel at chemotherapeutic doses. (12) ...
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