Microbiology Monthly Newsletter for Microbiology at the Department of Cell & Molecular Biology Lundberg Laboratory, Göteborg University [ January 1999 ] [ February 1999 ] [ March 1999 ] [ April 1999 ] [ May 1999 ] [ June 1999 ] [ July-August 1999 ] [ September 1999 ] [ October 1999 ] May 1999 Scientific Contributions Could bacteria play havoc with radioactive waste disposal in subterranean repositories? This question is reviewed by Karsten Pedersen in a new publication on our paper display and a number of conclusions are drawn from work in a number of different subterranean research sites. First, it is clear that the likelihood of finding a bacterial biosphere in subterranean granite rock is very high. Thus, the bacteria are clearly there but what do they do and could it be harmful? One hypothesis put forward is that these biospheres may be hydrogen driven systems and that this primary energy source is generated and renewed through radiolysis, mineral reactions and/or volcanic activities. The primary carbon source, on the other hand, would be carbon dioxide, while phosphate is available in aspartite and nitrogen as nitrogen gas (thus, utilizable nitrogen needs to be provided by nitrogen fixation). If so, this would be an example of a biosphere that is totally independent on solar energy! And the limiting factor in these systems are suggested to be the availability of hydrogen. So, could the microbial activities in such a biosphere be a potential problem in waste disposal? Well, perhaps, since sulphide reducing bacteria are present in these biospheres and because these have the ability to corrode copper which is used in the canisters holding the radioactive waste such a potential problem should be considered. However, it is argued that other factors, such as the pH and the conditions and materials used in isolating the canisters make it unlikely, but not theoretically impossible, that bacterial activity could seriously harm such depositories. Why do some bacteria of a population survive while others die in stationary phase? A new review on our display summarizes recent data dealing with this question. The study of the mortality of bacteria and how they survive starvation-induced growth arrest has raised the question of whether the free radical hypothesis of aging is relevant also for explaining the progressive deterioration of growth arrested bacterial cells. This issue seems relevant in light of the well documented increase in the levels of oxidative stress defence proteins in bacteria starved for any of a variety of nutrients. Recent data support the idea that these oxidative stress defence proteins prevent stasis-related accumulation of oxidative damage of proteins and mutations of DNA in stationary phase cell. The results highlight the fact that many, or most, oxidative stress proteins are not solely emergency response proteins but mediate homeostatic regulation of reactive oxygen species produced by normal aerobic catabolism. Similar to eukaryotic mitochondria, most of the superoxide anions is generated at the NADH dehydrogenase and ubiquinone sites at least during "normal" aerobic conditions in bacteria. By extensive mutant analysis we are beginning to understand the tricks bacteria use to survive stasis. However, it is much less clear why a certain fraction of a wild-type bacterial population still dies during growth arrest. What’s the use of having enzyme isoforms doing the same job? The yeast Saccharomyces cerevisiae possesses three isoforms of an enzyme called pyruvate decarboxylase (Pdc). This enzyme catalyses the conversion of pyruvate to acetaldedyde and carbon dioxide during alcohol fermentation. The activity requires a cofactor, namely thiamine diphosphate. In a recent paper by Stefan Hohmann, Anders Blomberg, Joakim Norbeck and coworkers the regulation of PCD5, encoding the minor isoform of Pdc is elucidated. The authors demonstrate that this isoform is expressed under thiamine limitations and repressed by thiamine (or rather thiamine diphosphate) whereas the gene, PDC1, encoding the major isoform does not respond to fluctuations in thiamine levels. Moreover, PDC5 is strongly expressed in cells lacking functional Pdc1p and this expression is not due to reduced levels of thiamine in the PDC1 mutant. Finally something to think about "General questions never lead to more than limited answers. On the contrary, limited questions have often led to more and more general answers" Francois Jacob Have a great month!