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)

Strains of Haemophilus influenzae that carry a defective prophage are more sensitive to heat than is a strain that does not, even in the presence of a rec-1 mutation, which normally renders prophage noninducible. The prophage of HP1c1, a nondefective phage, does not affect the heat sensitivity.
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PMID:Heat sensitivity of Haemophilus influenzae containing defective prophage. 30 42

Twenty-nine strains of Haemophilus influenzae highly resistant to ampicillin, chloramphenicol, or tetracycline were examined for the presence of plasmids. Agarose gel electrophoresis of ethanol-precipitated cell extracts revealed large plasmids in 11 strains, of which 7 were conjugative. Plasmid transfer by conjugation between isogenic strains was quite efficient, but transfer between different serotypes was nearly always much more inefficient. Type I or II restriction enzymes do not appear to be barriers to this transfer. Encapsulated cells can be both efficient donors and recipients. Small plasmids were seen in three strains, but only two of the three are resistance factors (RSF0885, pUB703). Thus, in 17 isolates antibiotic resistance genes are believed to be located in the bacterial chromosome. Most of these resistances could be transferred by genetic transformation into the widely used Rd strain. In some cases transfer of chromosomal resistance into conjugative plasmids was observed in both rec+ and rec host cells. Since transfer by conjugation seems to be the more efficient process, it is puzzling that in the majority of the 29 isolates studied resistance genes appeared to be in the chromosome.
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PMID:Plasmid transfer in Haemophilus influenzae. 31 93

A blood or yeast dependent pleomorphic Gram-negative bacillus was isolated from the pneumonic lung of a suckled calf which died suddenly. The organism was biochemically similar to American strains of Haemophilus somnus and was shown to be serologically similar by rapid slide agglutination, tube agglutination and micro-complement fixation tests. The possible importance of this organism in disease syndromes in cattle in the United Kingdom is discussed.
Vet Rec 1977 Feb 12
PMID:The isolation of Haemophilus somnus following sudden deaths in suckler calves in Scotland. 84 71

Deoxyribonucleic acid (DNA), pulse labeled after ultraviolet irradiation of excision-defective mutants of Haemophilus influenzae, is of lower single strand molecular weight than that of unirradiated cells but approaches the size of DNA from unirradiated cells upon further incubation in growth medium. This gap-filling process is controlled by the rec-1 gene. Gap-filling occurs normally in a temperature-sensitive DNA synthesis mutant at the restrictive temperature showing that normal semiconservative DNA synthesis is not necessary for gap-filling. To test for recombinational events after irradiation, the DNA synthesized after irradiation was radioactively labeled for a short time in medium containing 5-bromodeoxyuridine followed by incubation for various times in non-radioactive, 5-bromodeoxyuridine-containing medium. The DNA was denatured and analyzed isopycnically. The labeled DNA was initially "heavy," but later shifted toward lighter densities. This shift occurred in the temperature-sensitive DNA synthesis mutant at the restrictive temperature and in the recombination-defective mutant rec-2, but was not seen in the rec-1 mutant. The density shift can be interpreted as evidence that rather extensive exchanges occurred between parental DNA and the DNA made after irradiation. These results suggest that such exchanges are important for gap-filling in H. influenzae.
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PMID:Mechanism of gap-filling during postreplication repair of ultraviolet damage in Haemophilus influenzae. 108 Jul 60

Three Rec- mutants of Haemophilus influenzae have been studied with respect to their transformability, ultraviolet and mitomycin C sensitivities, spontaneous and ultraviolet-induced deoxyribonucleic acid breakdown, inducibility of lysogens, and the linkage of the three mutations to a streptomycin resistance marker. The data indicate that the three mutations cause the same phenotypic changes, and that they are all on the same gene. Transformability of the mutants is different when two different media are used for competence development, although transformability with the two competence methods is not different in a Rec- strain that is mutant at another gene.
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PMID:Similarity in properties and mapping of three Rec mutants of Haemophilus influenzae. 108 39

Evidence is presented indicating that a donor DNA processing step of the Haemophilus influenzae transformation pathway is blocked in the Com-101 mutant. Additional data are presented suggesting that, as in the Rec-2 strain, the donor DNA remains associated with the H. influenzae envelope.
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PMID:Donor DNA processing is blocked by a mutation in the com101A locus of Haemophilus influenzae. 157 4

A plasmid containing a 13.3-kb insert (pER194) was isolated from an EcoRI genomic library of Haemophilus influenzae on the basis of its ability to increase the transformability of the transformation-deficient mutants Com-78 and Com-101. The plasmid failed to increase the transformability of the Rec-1 and Rec-2 mutants, indicating that the mutations producing the Com-78 and Com-101 phenotypes are distinct from those giving rise to the Rec-1 and Rec-2 phenotypes. The physical mapping of the cloned fragment on the H. influenzae chromosome was found to be consistent with the genetic mapping of the Com-101 trait. A 2.8-kb EcoRI-BglII subfragment, representing one end of the 13.3-kb clone, was found to increase the transformation frequency of the Com-78 and Com-101 mutants when supplied in trans, indicating that the subfragment carries one or more loci required for chromosomal transformation. The corresponding region of the Com-101 chromosome was determined by hybridization analysis to contain a 0.3-kb insertion, suggesting that the Com-101 strain may contain an insertion mutation at this locus. A 3.0-kb EcoRI-MluI subfragment, representing the other end of the 13.3-kb EcoRI fragment, was found to increase the transformation frequency of the Com-101 mutant but not of the Com-78 mutant, suggesting that the Com-101 phenotype results from a complex genotype involving mutations at two or more transformation-related loci. This conclusion is consistent with data indicating that the Com-101 trait can be genetically separated into at least two components.
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PMID:Molecular cloning of two linked loci that increase the transformability of transformation-deficient mutants of Haemophilus influenzae. 164 18

A Haemophilus influenzae strain carrying a competence-enhancing mutation (sxy-1) was selected by transformation of a mutagenized culture in exponential growth at low cell density, where spontaneous competence is very rare. Under these conditions, sxy-1 cells spontaneously transformed 100 to 1,000 times more efficiently than wild-type cells. Moreover, sxy-1 cells responded to all known competence-inducing treatments with further increases in transformation frequency. At high cell densities, sxy-1 cells spontaneously developed the level of competence reached by wild-type cells only after maximal induction by transfer to starvation medium. The sxy-1 mutation appears to act early in the sequence of events leading to competence; it increased the competence of cells carrying the early-acting transformation-defective (Tfo-) mutation tfo-98 by as large a factor as it did the competence of wild-type cells, but it had no effect when combined with another early-acting Tfo- mutation (tfo-87) or with the late-acting Tfo- mutation rec-2.
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PMID:sxy-1, a Haemophilus influenzae mutation causing greatly enhanced spontaneous competence. 165 15

Genes for Haemophilus influenzae type b capsule expression are duplicated to form a potentially unstable structure, cap, of directly-repeated chromosomal regions of approximately 17 kb. Capsule-deficient mutants arise in a two-stage process, initiated by rec-dependent reduction of this region from two copies to one. This recombinational event is usually lethal, only about 1/200 surviving to form slow-growing colonies of organisms that continue to synthesize polysaccharide but are defective in its export. A variety of secondary 'rescue' mutations within cap can occur to reduce polysaccharide synthesis and restore normal organism appearance and colony morphology.
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PMID:Capsulation gene loss and 'rescue' mutations during the Cap+ to Cap- transition in Haemophilus influenzae type b. 178 4

A collection of transposon mutants of Haemophilus influenzae was constructed by additive transformation with mutagenized chromosomal DNA. A rec-2::miniTn10 km mutation was cloned from a transformation-defective member of the mutant collection, followed by the reconstruction of the wild-type rec-2 locus by recombination to create pDM62. Southern blots showed that the commonly studied Rec-2 mutant, Rd(DB117)rec-, contained either a large deletion or a substitution that removed part of rec-2 locus. A collection of transposon mutations in pDM62 was used to characterize the rec-2 locus by complementation. A corresponding collection of mutants was also constructed. A single segment was required to complement the transformation defect in Rd(DB117)rec-. All of the transformation-defective transposon mutants failed to translocate donor DNA into then cell, in agreement with previous studies of Rd(DB117)rec-.
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PMID:Cloning of the rec-2 locus of Haemophilus influenzae. 254 31


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