| Budget Amount *help |
¥2,500,000 (Direct Cost: ¥2,500,000)
Fiscal Year 2001: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2000: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1999: ¥900,000 (Direct Cost: ¥900,000)
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| Research Abstract |
In Enterohemorrhagic Exchericia coli, Shiga toxin is produced by lysogenic prophages. We have isolated the prophage VT2-Sa that is responsible for production of Shiga toxin type 2 protein, and determined the complete nucleotide sequence of this phage DNA. The entire DNA sequence consisted of 60942 bp, exhibiting a marked similarity to that of 933W phage genome. However, several differences were observed in the immunity and replication regions, where cI, cII, cIII, N, cro, O, and P genes were present : Predicted amino acid sequences of N, cI, cro, O and P in the VT2-Sa genome did not show significant similarity to the counterparts of the 933W genome ; however its cI showed higher similarity to λ ; further O and P closely resembled those of phage HK022.These observations suggest that the various degrees of hoology observed in the immunity and replication regions of VT2-Sa could have resulted from frequent recombination events among the lambdoid phages, and that these regions play a key role as a functional unit for phage propagation in competition with other lambdoid phages.
Antimicrobial agent nolfloxacin is recommended for medical treatment of O157 infection. However, we found that nolfloxacin induce the shiga toxin production, resulting in hemolytic-uremic syndrome. In addition, the increase of shiga toxin production was inhibited by recA mutation, indicating that the shiga toxin production is concomitant with the clavage of cI repressor protein by the activated recA protein.
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