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The level of genetic variability that maximises the fitness of population varies with the degree of its adaptation to the environment. It is low when environment is stable and high when environment is unstable and hostile. Since environmental conditions are changing, the adaptation is never permanent. Consequently, because the genetic variability in bacteria is first generated by mutagenesis, it could be expected that populations with high mutation rates would have better chance for successful evolution. Indeed, bacteria with elevated mutation rates are frequently found among natural isolates. Experimental observations and theoretical calculations suggest that there must be positive selection for higher mutation rate in spite of the fact that majority of newly generated mutations are deleterious or lethal. Mutator alleles rise to a high frequency through their association with the favourable mutations they generate that counterbalance the load of deleterious mutations. However, when adaptation is achieved, the load of deleterious mutations counterselects high-mutation rates. Therefore, evolution of bacterial populations may happen through alternating periods of high and low mutation rates that provide a remarkable potential for the fine tuning of the rates of generation of genetic variability in the function on the adaptation to environmental conditions.

The nuclear cytoplasmic interaction hypothesis (NCI) states that in a newly formed allopolyploid genetic instabilities are induced giving rise to altered paternal genome structure and chromosomal translocations. The hypothesis predicts that plants emerging from a “bottleneck of sterility” are stable, with increased fertility, fixed for particular translocations that are “species-specific”, and have a degraded paternal genome. We investigate this hypothesis in the allopolyploids Nicotiana tabacum (tobacco), N . rustica and N. arentsii. Each of these natural allopolyploids have a similar chromosome complement, 2n = 4x = 48. We review the cytological data available for these species. From those studies using genomic in situ hybridisation (GISH) we found evidence in support of NCI only in N . tabacum . To our surprise there is also supporting evidence in the form of structurally similar translocations in a synthetic tobacco line that is only three generations old. These data suggest that the mechanisms of genetic change act early and fast. However in the synthetic material no translocation resolvable by GISH had gone to fixation. Nevertheless the presence of translocations does support the argument that in natural tobacco at least the genomic restructuring that occurred after polyploidy may have facilitated the establishment and stabilisation of the polyploid genome.

The cyclin-dependent kinases play an essential role in the timing of cell division and repair, furthermore a high incidence of genetic alterations of CDKs or deregulation of CDK inhibitors have been observed in several cancers. These arguments make of CDC28 of Saccharomyces cerevisiae yeast a very attractive model to study CDK regulation mechanisms. We observed certain gene mutations, including cdc28-srm [G20S], affect cell cycle progression, maintenance of different genetic structures (Devin, 1990), checkpoint-control (Li, 1997) and increase cell radiosensitivity (Koltovaya, 1998). A cdc28 -srm mutation is not a temperature-sensitive mutation and differs from known cdc28 -ts mutations, since it shows the evident phenotypic manifestations at 30°C. The mutation is on the third glycine site in the conserved sequence GxGxxG of the G-rich loop, whose position is opposite to the activation T-loop. Despite its established importance, the role of the G-loop is still unclear. The crystal structure of the human CDK2 served as model for the catalytic core of other CDKs, including CDC28. Nanoseconds long molecular dynamics trajectories of the CDK2/ATP complex were analysed. The MD simulations of corresponded substitution CDK2-G16S in conserved G-loop shows this amino acid importance and the induced conformational change in CDK2 structure, resulting in the ATP removal from G-loop and in new amino acids rearrangement in the T-loop.

The bacterium Deinococcus radiodurans is highly resistant to the effects of ionizing radiation, (IR). Cultures of Deinococcus survive exposure to IR doses of 5,000 Gray (Gy) with no lethality. At 5,000 Gy, several hundred double strand breaks are introduced into the genome. Recovery from this DNA damage occurs in two phases, one independent of RecA protein and one that requires RecA. A number of proteins are induced in Deinococcus in response to exposure to ionizing radiation, and many of those most highly expressed are novel proteins. A variety of Deinococcus proteins involved in genome reconstitution are now under biochemical investigation. Many of these proteins exhibit unusual properties, but a complete explanation for the radiation resistance of Deinococcus is not yet available.