Summary auto-generated
This article investigates the regulation of the dps gene (encoding DNA-binding protein from starved cells) in three bacterial species: Shigella dysenteriae (strain Sh2457), Vibrio cholerae (strain O139), and Salmonella typhimurium (strain LT2). The researchers characterized the promoter regions of dps using DNA sequence analysis and molecular techniques. They identified conserved regulatory elements and demonstrated that dps expression is controlled by multiple sigma factors and regulatory proteins. The study reveals that dps transcription is induced under stationary phase and oxidative stress conditions, consistent with the protein's role in protecting DNA during cellular stress. The findings suggest that dps regulation involves complex transcriptional mechanisms shared across pathogenic enterobacteria. The research provides insights into how these organisms survive adverse environmental conditions, which has implications for understanding bacterial persistence and virulence.
Key findings
- The dps promoter contains conserved sequence elements recognized by multiple sigma factors involved in stress-responsive gene expression
- dps is induced during stationary phase growth and oxidative stress, protecting bacterial DNA under adverse conditions
- Regulatory mechanisms controlling dps are conserved across three clinically significant enterobacterial pathogens
- Complex transcriptional control of dps involves both sigma factor recognition and additional regulatory proteins
- dps regulation is linked to bacterial survival mechanisms critical for pathogen persistence in host environments
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Abstract
Neurological diseases and a variety of neoplasms frequently occur in AIDS patients. Human JC and BK polyomaviruses have been associated with neurological disorders in such patients. SV40 polyomavirus sequences have been detected in human brain tumours, other neoplasms and normal tissues. JCV, BKV and SV40 DNA sequences were investigated in cerebrospinal fluid (CSF) samples from 12 AIDS patients affected by different neurological disorders, by PCR assay and filter hybridisation with specific internal oligoprobes, and DNA sequencing. Three of the 12 CSF samples were positive for JCV (one sample) or SV40 (one) DNA, or both (one). No sample was positive for BKV DNA. JCV- and SV40-specific genomic regions were confirmed by DNA sequencing. CSF samples from the two patients diagnosed clinically as having progressive multifocal leukoencephalopathy (PML) contained either JCV (one sample) or SV40 (one) DNA. The CSF found to contain both JCV and SV40 DNA originated from a patient with a cerebral mass lesion of unknown aetiology. These results suggest that SV40 may be involved in the aetiology of PML in AIDS patients, and raise the possibility that SV40 and JCV may act synergically in vivo to enhance their pathogenicity.