Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0348321 (Haemophilus)
 15,372 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasmid RSF0885, which conferred ampicillin resistance, transformed competent Haemophilus influenzae cells with low efficiency (maximum, less than 0.01%). As judged by competition experiments and uptake of radioactivity, plasmid RSF0885 deoxyribonucleic acid was taken up into competent H. influenzae cells several orders of magnitude less efficiently than H. influenzae chromosomal deoxyribonucleic acid. Plasmid RSF0885 transformed cells with even lower efficiency than could be accounted for by the low uptake. Transformation was not affected by rec-1 and rec-2 mutations in the recipient, and strains cured of the plasmid did not show increased transformation. Plasmid molecules cut once with a restriction enzyme that made blunt ends did not transform. Transformation was favored by the closed circular form of the plasmid.
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PMID:Transformation of Haemophilus influenzae by plasmid RSF0885. 697 75

The plasmid pNov2, carrying a cloned chromosomal marker conferring resistance to at least 2.5 micrograms of novobiocin per ml, was constructed with a new Haemophilus influenzae cloning vehicle, pDM2. The novobiocin marker of pNov2 was not normally expressed, but in Rec+ cells approximately one in 10(4) cells in a culture of a transformant became novobiocin resistant, a frequency about four orders of magnitude higher than the spontaneous mutation frequency. Variants of such cells that had lost the plasmid were also novobiocin resistant. Since Rec- cultures bearing pNov2 showed novobiocin resistance only at the normal mutation frequency, we concluded that the Rec+ novobiocin-resistant transformants arose because of a rare recombination between plasmid and chromosome in which the chromosome acquired the novobiocin marker from the plasmid. Evidence is presented that novobiocin sensitivity is dominant over this particular novobiocin resistance marker.
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PMID:Novobiocin resistance marker in Haemophilus influenzae that is not expressed on a plasmid. 698 Aug 79

Porcine reproductive and respiratory syndrome (PRRS) was first known as blue-eared pig disease in the United Kingdom and the causative agent as 'Lelystad virus'. The disease is characterised by very variable clinical signs, including reproductive failure and respiratory disease. The respiratory syndrome is often associated with severe infection with secondary bacterial agents including Pasteurella multocida, Haemophilus parasuis and Streptococcus suis. However, some seropositive herds show no clinical signs of disease. The secondary infections may be facilitated by the destruction of circulating lymphocytes, by the destruction of the mucociliary clearance system and, most importantly, by a large reduction in the numbers of alveolar macrophages. The clinical syndrome observed in a herd may therefore depend in part upon the other diseases present.
Vet Rec 1995 Jan 14
PMID:Porcine reproductive and respiratory syndrome: clinical disease, pathology and immunosuppression. 770 69

DNA sequencing, RNA mapping, and protein expression experiments revealed the presence of a gene, tfoX+, encoding a 24.9-kDa polypeptide, that is transcribed divergently from a common promoter region with the Haemophilus influenzae rec-1+ gene. H. influenzae strains mutant for tfoX failed to bind transforming DNA and were transformation deficient. Primer extension experiments utilizing in vivo total RNA from precompetent and competent H. influenzae cells demonstrated that transcription of tfoX+ increased immediately upon competence induction, suggesting that tfoX+ is an early competence gene. Similar experiments showed that the expression of the late competence-specific gene, com101A+, was tfoX+ dependent. Moreover, expression of plasmid-borne tfoX+ in H. influenzae resulted in constitutive competence. The addition of cyclic adenosine monophosphate (cAMP) to strains carrying a tfoX::lacZ operon fusion resulted in an immediate increase in beta-galactosidase activity that correlated with an increase in genetic transformability. Collectively, our results suggest that TfoX may play a key role in the development of genetic competence by regulating the expression of late competence-specific genes.
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PMID:Identification of a DNA transformation gene required for com101A+ expression and supertransformer phenotype in Haemophilus influenzae. 772 7

An outbreak of infections with non-encapsulated Haemophilus influenzae, resistant to ampicillin, chloramphenicol, sulphonamide and tetracycline involved 13 elderly patients and three nurses on acute admission and care of the elderly wards. Thirty-two isolates were found to be indistinguishable on analysis of biotype, antibiogram, serotype and major outer membrane proteins (MOMP). Plasmids could not be identified in the original isolates but after mating with a Rec A H. influenzae recipient, the resultant transconjugates were found to harbour either a 72 kilobase pair (kB) plasmid coding for resistance to chloramphenicol, ampicillin, sulphonamide and tetracycline or a 65 kB plasmid coding for resistance to chloramphenicol, ampicillin and sulphonamide. Both plasmids yielded virtually indistinguishable restriction digest patterns. This suggests that the tetracycline resistance gene (Tc gene) is a non-essential component of one basic plasmid responsible for the multiple antibiotic resistances seen in the strains recovered during the outbreak. This illustrates the value of plasmid profiles to compare strains of non-encapsulated H. influenzae, and suggests that plasmid restriction enzyme analysis is critical.
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PMID:A nosocomial outbreak due to non-encapsulated Haemophilus influenzae: analysis of plasmids coding for antibiotic resistance. 791 59

The sxy-1 mutation of Haemophilus influenzae causes a 100- to 1,000-fold increase in spontaneous natural competence. We have used mapping and sequencing to identify this mutation as a G-to-A transition in an open reading frame adjacent to the rec-1 locus. This mutation substitutes valine for isoleucine at amino acid 19 of the protein specified by this gene (now named sxy). A multicopy plasmid containing the wild-type sxy gene confers constitutive competence on wild-type cells. Cells carrying this plasmid exhibit, in all stages of growth, DNA uptake levels and transformation frequencies as high those normally seen only after full induction of competence by starvation; deletion of part of the sxy gene from the plasmid abolishes this effect. In contrast, a transposon insertion in sxy entirely prevents both DNA uptake and transformation, indicating that sxy encodes a function essential for competence. These findings suggest that sxy may act as a positive regulator of competence. However, because cells carrying the transposon-inactivated sxy::Tn allele grow slowly under conditions that do not induce competence, sxy may also have a role in noncompetent cells.
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PMID:The Haemophilus influenzae sxy-1 mutation is in a newly identified gene essential for competence. 796 36

The nucleotide sequence of a 4243-bp PstI fragment containing the rec-2 gene of Haemophilus influenzae was determined. The amino acid (aa) sequences of four putative proteins were deduced from the corresponding open reading frames (ORFs). The 2400-bp ORF2 accounted for rec-2, based on the sequences of DNA fragments that contained rec-2::mini-Tn10 mutations. The rec-2 gene encoded a putative 800-aa protein with a M(r) of 90,561. Sequence analysis suggested that the rec-2 product contained nine highly probable integral membrane-spanning segments. Database searches showed that rec-2 was homologous to the comE-ORF3 gene of Bacillus subtilis. This hypothesis is consistent with the known involvement of both of these genes in the passage of transforming DNA through the competent-cell envelope. Although the sequences of the other three ORFs were incomplete, sufficient data were available to allow inferences about their homologies to other genes. ORF4, which overlapped ORF1, was homologous to the Escherichia coli dnaK suppressor gene, dksA, and therefore was named dsh-1 (dnaK suppressor homolog). Mutations in dsh-1 and its putative promoter region caused a mild sensitivity to UV light, but did not affect DNA recombination. ORF3, located downstream from rec-2, was homologous to msbA, an essential gene of E. coli with extensive similarity to the ATP-dependent translocators. ORF3 was named msh-1 (msbA homolog). Mutations in msh-1 had no effects on genetic transformation. The close juxtaposition of rec-2 and msh-1 implied that the expression of msh-1 could be linked to the translation of the rec-2 ORF.
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PMID:Sequence of the rec-2 locus of Haemophilus influenzae: homologies to comE-ORF3 of Bacillus subtilis and msbA of Escherichia coli. 806 12

The Haemophilus influenzae rec-1+ protein plays a central role in DNA metabolism, participating in general homologous recombination, recombinational (postreplication) DNA repair, and prophage induction. Although many H. influenzae rec-1 mutants have been phenotypically characterized, little is known about the rec-1+ gene at the molecular level. In this study, we present the genetic organization of the rec-1+ locus, the DNA sequence of rec-1+, and studies of the transcriptional regulation of rec-1+ during cellular assault by DNA-damaging agents and during the induction of competence for genetic transformation. Although little is known about promoter structure in H. influenzae, we identified a potential rec-1+ promoter that is identical in 11 of 12 positions to the bacterial sigma 70-dependent promoter consensus sequence. Results from a primer extension analysis revealed that the start site of rec-1+ transcription is centered 6 nucleotides downstream of this promoter. We identified potential DNA binding sites in the rec-1+ gene for LexA, integration host factor, and cyclic AMP receptor protein. We obtained evidence that at least one of the proposed cyclic AMP receptor protein binding sites is active in modulating rec-1+ transcription. This finding makes rec-1+ control circuitry novel among recA+ homologs. Two H. influenzae DNA uptake sequences that may function as a transcription termination signal were identified in inverted orientations at the end of the rec-1+ coding sequence. In addition, we report the first use of the Escherichia coli lacZ operon fusion technique in H. influenzae to study the transcriptional control of rec-1+. Our results indicate that rec-1+ is transcriptionally induced about threefold during DNA-damaging events. Furthermore, we show that rec-1+ can substitute for recA+ in E. coli to modulate SOS induction of dinB1 expression. Surprisingly, although 5% of the H. influenzae genome is in the form of single-stranded DNA during competence for genetic transformation, an event that could be a potent SOS-inducing signal, we failed to detect significant changes in rec-1+ transcription during the induction of genetic competence.
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PMID:Structural organization, nucleotide sequence, and regulation of the Haemophilus influenzae rec-1+ gene. 822 74

Antibiotic resistance in Haemophilus influenzae has been associated with the presence of large, chromosomally integrated, conjugative plasmids. The plasmids of 10 beta-lactamase-positive, ampicillin-resistant strains, two from the UK and eight from Greece, were investigated. Plasmids were detected and isolated after transfer to a rec-deficient recipient. Purified whole plasmid was used as probe. In addition a 12 kb PstI fragment containing the putative point of recircularization in one plasmid, p1056, was cloned and used as a probe. All plasmids shared a high degree of sequence homology suggesting that plasmids of diverse geographical origin are highly related. All plasmids also shared sequence homology with the 12 kb PstI fragment containing the point of recircularization, suggesting that the sequences involved in excision and recircularization are conserved.
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PMID:A molecular analysis of Greek and UK Haemophilus influenzae conjugative resistance plasmids. 909 78

We previously showed that dprA is required for efficient processing of linear DNA during cellular transformation in Haemophilus influenzae. In this study the transcriptional regulation of dprA and two downstream genes, dprB and dprC, is examined. We demonstrate by Northern blot analysis that the dprABC genes are transcriptionally coregulated and competence inducible. We used primer extension analysis to map the transcriptional start site of dprA and of rec-2, another transformation gene involved in DNA processing. Based upon these results, we were able to identify a 26-bp dyad symmetry element immediately upstream of the -35 regions of the predicted promoters of dprA, rec-2, and two other transformation genes, comA and pilA. Finally, using transcriptional fusions of dprA to the Escherichia coli lacZ gene, we show that expression of dprA::lacZ requires tfoX and that the presence of multiple copies of tfoX abolishes the temporal regulation of dprA, resulting in its constitutive expression.
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PMID:The Haemophilus influenzae dprABC genes constitute a competence-inducible operon that requires the product of the tfoX (sxy) gene for transcriptional activation. 924 70


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