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PubMed1983

Temperate phage induction and filament formation in Vibrio cholerae by furazolidone.

Furazolidone a synthetic nitrofuran used in the treatment of cholera, was found to cause prophage induction and filament formation in Vibrio cholerae. Maximum induction of phage beta was obtained at a drug concentration of 0.5 microgram/ml. Neither induction of prophage nor filamentation took place if the drug treatment was carried out in the presence of 2.5 micrograms/ml chloramphenicol, indicating a requirement for de novo protein synthesis. Our results strongly suggest the existence of "SOS" type functions in Vibrio cholerae.

Chloramphenicol↗
PubMed1986

Control of gene expression in the P2-related temperate coliphages. IV. Concerning the late control gene and control of its transcription.

In this paper we have sequenced four amber mutants and thereby confirmed the gene D (CP65) and gene B (CP67) assignments made in the accompanying paper (Kalionis et al., 1986). We have also studied, by gel electrophoresis, the transcription patterns of gene B in vivo. In a lysogen, gene B is present on a short transcript under autogenous (negative) control. Upon prophage induction, this transcript is amplified, but later in the cycle gene B is present on a larger transcript that originates in the late region. We have detected two copies of an inverted repeat in the promoter region of the B gene that we predict is recognized by the B protein. One arm of this repeat is associated with three of four P2 late promoters, downstream from the start point of transcription. The repeat is not present in the promoter region of P2 ogr. We describe the considerable homology in amino acid sequence seen with the late control proteins 186 gpB, P4 gp delta and P2 gpOgr, and present a working model for control of late gene transcription.

Amino Acid Sequence↗
PubMed1988

Control of gene expression in the P2-related temperate coliphages. V. The use of sequence analysis of 186 Vir mutants to indicate presumptive repressor binding sites.

The prophage of coliphage 186 produces a repressor protein that is required for maintenance of lysogeny and that renders lysogenic cells immune to superinfection by 186. The repressor is likely to be a DNA-binding protein that prevents transcription of the 186 early-lytic genes from promoter pR. To identify the binding site of the repressor, we have isolated virulent mutants that are able to form plaques in the presence of repressor and determined their DNA sequences around pR. The mutants all have mutations in an inverted repeat within pR, and we predict that this repeat is the primary binding site of the repressor. Many of the mutants have second mutations near pR, which allow them to form plaques in the presence of higher concentrations of repressor. The sequences containing these "secondary" mutations show no homology with the putative repressor-binding site, and the role of these mutations in virulence is not clear.

Base Sequence↗
PubMed1982

Necrotizing fasciitis-a disease of temperate and warm climates.

Necrotizing fasciitis is a distinct clinical entity. It is usually due to Streptococcus pyogenes but may occasionally be caused by Staphylococcus aureus. It needs to be considered in relationship to other infections due to Streptococcus pyogenes, in which the clinical disease that occurs may be associated with the depth of inoculation of the coccus. Mild cases have been identified that are self-limiting as well as serious cases which would have succumbed without surgical debridement. It is likely that some cases of necrotic tropical ulcer are due to necrotizing fasciitis.

Fasciitis↗