Electrophoretic mobility shift assay studies and qPCR analyses in the wild-type L. monocytogenes Y-27632 supplier and the deletion mutant L. monocytogenes ∆glnR revealed that the transcriptional regulator GlnR is directly involved in temperature- and nitrogen source-dependent regulation of the respective genes. Glutamine, a metabolite known to influence GlnR activity, seems
unlikely to be the (sole) intracellular signal mediating this temperature-and nitrogen source-dependent metabolic adaptation. “
“Arsenic is a toxic metalloid that is widely distributed in the environment, and its toxicity has been demonstrated in several models. However, the mechanism of arsenic toxicity still remains unclear. In this study, the toxic effects of sodium arsenite (1–7 mM)
on yeast cells were investigated. The experimental results showed that sodium arsenite inhibited yeast cell growth, and the inhibitory effect of cell growth (OD600 nm values) was positively correlated with arsenite concentrations. Sodium arsenite caused loss of cell viability Panobinostat in a concentration- and duration-dependent manner in yeast cells. However, arsenite-caused cell viability loss was blocked by either antioxidants (200 U mL−1 CAT and 0.5 mM AsA) or Ca2+ antagonists (0.5 mM LaCl3 and 0.5 mM EGTA). We also found intracellular reactive oxygen species (ROS) and Ca2+ levels increased significantly in yeast cells after exposure to 3 mM and 7 mM sodium arsenite for 6 h compared with the control. These results indicated that high concentrations of arsenite-induced yeast cell killing was associated with elevated levels of intracellular ROS and Ca2+. “
“A transformation system for Moorella thermoacetica ATCC39073 was developed using thermostable kanamycin resistant gene (kanR) derived from the plasmid pJH1 that Streptococcus faecalis harbored. When kanR with its native promoter was introduced into uracil auxotrophic Aprepitant mutant of M. thermoacetica ATCC39073 together with a gene to complement the uracil auxotrophy as a selection marker, it did not give kanamycin resistance due to poor transcription level of kanR.
However, the use of glyceraldehyde-3-phosphate dehydrogenase promoter cloned from M. thermoacetica ATCC39073 significantly improved transcription level of kanR and resulted in the cell growth in the presence of more than 150 μg mL−1 kanamycin. It was also demonstrated that kanR with G3PD promoter can be used as a selection marker for transformation of wild-type strain of M. thermoacetica ATCC39073. “
“Bacterial adaptation to changing environments can be achieved through the acquisition of genetic novelty by accumulation of mutations and recombination of laterally transferred genes into the genome, but the mismatch repair (MMR) system strongly inhibits both these types of genetic changes. As mutation and recombination do occur in bacteria, it is of interest to understand how genetic novelty may be achieved in the presence of MMR.