Morphological changes leading to aerial mycelium formation and sporulation in the mycelial bacterium Streptomyces coelicolor rely on establishing distinct patterns of gene expression in separate regions of the colony. σH was identified previously as one of three paralogous sigma factors associated with stress responses in S. coelicolor. Here, we show that sigH and the upstream gene prsH (encoding a putative antisigma factor of σH) form an operon transcribed from two developmentally regulated promoters, sigHp1 and sigHp2. While sigHp1 activity is confined to the early phase of growth, transcription of sigHp2 is dramatically induced at the time of aerial hyphae formation. Localization of sigHp2 activity using a transcriptional fusion to the green fluorescent protein reporter gene (sigHp2–egfp) showed that sigHp2 transcription is spatially restricted to sporulating aerial hyphae in wild‐type S. coelicolor. However, analysis of mutants unable to form aerial hyphae (bld mutants) showed that sigHp2 transcription and σH protein levels are dramatically upregulated in a bldD mutant, and that the sigHp2–egfp fusion was expressed ectopically in the substrate mycelium in the bldD background. Finally, a protein possessing sigHp2 promoter‐binding activity was purified to homogeneity from crude mycelial extracts of S. coelicolor and shown to be BldD. The BldD binding site in the sigHp2 promoter was defined by DNase I footprinting. These data show that expression of σH is subject to temporal and spatial regulation during colony development, that this tissue‐specific regulation is mediated directly by the developmental transcription factor BldD and suggest that stress and developmental programmes may be intimately connected in Streptomyces morphogenesis.
Extracellular Gram negative bacteria were found to be commonly associated to the oesophageal bulb of Ceratitis capitata with Klebsiella oxytoca and Enterobacter agglomerans as the most common species. All the isolates tested in vitro, except one, were sensitive to the antibacterial material present on the medfly laid egg surface.
In a 1-year period (January to December 1984), Aeromonas strains were isolated from feces of 21 of 561 (3.7%) children with gastroenteritis and from 12 of 576 (2.1%) children without intestinal disturbances (controls). The difference between the two isolation rates was not significant (X2 = 2.2; P > 0.05). In five cases of illness other intestinal pathogens were isolated together with Aeromonas in the same stool sample. A total of 39 Aeromonas strains were detected since in some cases aeromonads with different biochemical characteristics were obtained from the same stool sample. Of the 39 Aeromonas isolates, 6 strains (5 from patients) were Aeromonas hydrophila, 5 strains (3 from patients) were Aeromonas sobria, and 26 strains (18 from patients) were Aeromonas caviae; 2 strains isolated from controls did not ferment sucrose and were considered a distinct group of Aeromonas. We found no significant difference between the prevalence of each of these species from patients and the prevalence from controls. We found no significant difference in the prevalence of enterotoxinproducing strains (suckling mouse model), cytotoxin-producing strains (HEp-2 cell model), or hemolysinproducing strains (rabbit erythrocyte model) between patients and controls. In our geographical region there is no evidence that Aeromonas species are primary intestinal pathogens in children.
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