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The ionizing radiation (IR) dose that yields 20% survival ([D.sub.20]) of Shewanella oneidensis MR-1 is lower by factors of 20 and 200 than those for Escherichia coli and Deinococcus radiodurans, respectively. Transcriptome analysis was used to identify the genes of MR-1 responding to 40 Gy ([D.sub.20]). We observed the induction of 170 genes and repression of 87 genes in MR-1 during a 1-h recovery period after irradiation. The genomic response of MR-1 to IR is very similar to its response to UV radiation (254 nm), which included induction of systems involved in DNA repair and prophage synthesis and the absence of differential regulation of tricarboxylic acid cycle activity, which occurs in IR-irradiated D. radiodurans. Furthermore, strong induction of genes encoding antioxidant enzymes in MR-1 was observed. DNA damage may not be the principal cause of high sensitivity to IR, considering that MR-1 carries genes encoding a complex set of DNA repair systems and 40 Gy IR induces less than one double-strand break in its genome. Instead, a combination of oxidative stress, protein damage, and prophage-mediated cell lysis during irradiation and recovery might underlie this organism's great sensitivity to IR.

Research has been conducted on the Deinococcus radiodurans RecA protein important for the radiation resistance of this organism. The cloning of this protein and its expression in Escherichia coli have been carried out and the results indicate the existence of the sharp contrast between D. radiodurans and E. coli RecA proteins.

Results demonstrate that the genome sequence of Clostridium acetobutylicum accounts for majority of the genes involved in solvent-production. It consists of a 3.94-megabase chromosome and a 192-kilobase megaplasmid and exhibits both genome conservation and organization to that displayed by Bacillus subtilis.

The ability of Deinococcus radiodurans R1 to repair severe damage to its DNA, without mutagenesis or lethality, is dependent on recA. The process of recombinational DNA repair during the first few hours is distinct from that occurring over the next 24 hours. Initially, the repair occurs to the same degree in both MD424 recA(super +) and MD431 recA cells. At a later stage, DNA fragments in the former continue to enlarge while the process stops in the latter. This suggests the presence of a different mode of repair at early times rather than one that is solely recA-dependent.

Expression of the Shigella (S) flexneri recA gene in recA-defective Deinococcus (D) radiodurans does not result in the alleviation of the D. radiodurans recA phenotype. The absence of phenotype complementation despite S. flexneri accumulation in D radiodurans indicates a fundamental difference in the mode of action of the S. flexneri RecA protein and that of D. radiodurans RecA, making them unable to function when introduced into the the other species.

The resistance of the bacterium Deinococcus radiodurans to ionizing radiation may be the result of a process of chromosomal recombination that is dependent upon the recA gene and mediated by DNA double-strand breaks. Following irradiation of chromosomes in the cells, which causes DNA fragmentation, there may have been up to 175 crossovers per chromosome being repaired. Details of the recombination processes are discussed.

Experimental studies of DNA repair in Deinococcus radiodurans show that cell repair of plasmid DNA damaged by high irradiation is similar to that of chromosomal DNA repair. There is extensive recombination among plasmids during repair, the study of which serves as a model for understanding the repair mechanisms in the chromosome. The capacity of the D. radiodurans to withstand high doses of radiation aids these studies.

Gene mutations and plasmid construction studies reveal that the gene recA, belonging to the genus family of Deinococcus radiodurans R1, repairs plasmid DNA damages due to ionizing radiation exposure by a mechanism homologous to chromosomal DNA repair. All viable cells retain a heterologous plasmid without drug selection. Plasmid repair is pronounced in recA cells.

The ionizing radiation (IR) dose that yields 20% survival (D20) of Shewanella oneidensis MR-1 is lower by factors of 20 and 200 than those for Escherichia coli and Deinococcus radiodurans, respectively. Transcriptome analysis was used to identify the genes of MR-1 responding to 40 Gy (D20). We observed the induction of 170 genes and repression of 87 genes in MR-1 during a 1-h recovery period after irradiation. The genomic response of MR-1 to IR is very similar to its response to UV radiation (254 nm), which included induction of systems involved in DNA repair and prophage synthesis and the absence of differential regulation of tricarboxylic acid cycle activity, which occurs in IR-irradiated D. radiodurans. Furthermore, strong induction of genes encoding antioxidant enzymes in MR-1 was observed. DNA damage may not be the principal cause of high sensitivity to IR, considering that MR-1 carries genes encoding a complex set of DNA repair systems and 40 Gy IR induces less than one double-strand break in its genome. Instead, a combination of oxidative stress, protein damage, and prophage-mediated cell lysis during irradiation and recovery might underlie this organism's great sensitivity to IR. [ABSTRACT FROM AUTHOR]

Describes the characteristics of RecA protein from bacterium Deinococcus radiodurans. Importance of RecA protein in radiation resistance of D. radiodurans; Utilization of D. radiodurans in bioremediation of radioactive wastes; Role of RecA protein in the hydrolysis of adenosine triphosphate.