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)

The sequences in lambda DNA in and around six sites cut by Hph, a restriction enzyme isolated from Haemophilus parahaemolyticus, are compared. The enzyme produces a staggered cut around an AT or TA base pair, but the sequences immediately surroinding the cleavage sites bear no obvious relation to one another. Eight (in some cases nine) base pairs to one side of each cleavage site is the common sequence TCACC AGTGG. Two lines of evidence indicate that these bases constitute part or all of the Hph recognition site. First, mutations in this sequence prevent Hph cutting. Second, dimethylsulfate-mediated methylation of Gs and As in this site prevent cutting, whereas methylation of purines in the region between this sequence and the cleavage sites has no such effect. There is discernible 2-fold rotational symmetry neither in the common sequence nor around the cleavage sites.
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PMID:Novel properties of a restriction endonuclease isolated from Haemophilus parahaemolyticus. 106 Nov 31

A physical map of the bacteriophage M13 genome has been constructed on the basis of specific cleavage of M13 replicative form DNA by bacterial restriction endonucleases. The 13 fragments produced by the enzyme from Haemophilus aphirophilus (endonuclease R.Hap II) as well as the 10 fragments produced by the enzyme from Haemophilus aegyptius (endonuclease R.Hae III) have been ordered by analysis of partial digest products and by analysis of overlapping sets of fragments. In addition, the single site in M13 replicative form DNA cleaved by the restriction enzyme from Haemophilus influenzae Rd (endonuclease R.Hin dII) has been located more precisely. With this unique site as a reference point, the H. aphirophilus cleavage sites and the H. aegyptius cleavage sites have been localized on the map.
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PMID:Studies on bacteriophage M13 DNA. 1. A cleavage map of the M13 genome. 107 69

In Haemophilus influenzae strains only the type 1 of the restriction endonucleases have an in vivo effect on phage and bacterial transforming DNA. The type 2 of restriction endonucleases which act very efficiently in vitro are completely inactive in vivo. The reasons for this inactivity is unknown.
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PMID:Host specificity of DNA in Haemophilus influenzae: the in vivo action of the restriction endonucleases on phage and bacterial DNA. 108 Mar 42

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

A strain of Haemophilus influenzae, called hpm- inhibits the growth of phage HP1c1 but not S2. This inhibition is overcome by HP1c1ph mutants. Phage HP1c1 adsorbs normally to hpm- cells but only a small fraction of infected cells produce phage with a normal burst size or become lysogenic. When hpm- strains lysogenic for HP1c1 are induced, 100 percent of the cells yield phage. There is no degradation of phage DNA after infection of hpm- cells and HP1c1 can normally grow when its DNA is introduced into hpm- by transfection. The most probable explanation is that in hpm- cells the penetration of phage DNA is blocked. The hpm- property behaves as as unstable mutation.
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PMID:An Haemophilus influenzae mutant which inhibits the growth of HP1c1 phage. 108 Aug 31

Methylation of accessible DNA within chromatin by restriction modification methylases from Haemophilus influenzae was used to detect movement of histones along the DNA strand during chromatin manipulation. Methylation at different stages of chromatin preparation was followed by titration of the nucleoprotein with ploy(D-lysine), digestion of chromosomal proteins with pronase and analysis of the DNA-poly(D-lysine) complex in steep cesium chloride gradients. Comparison of the specific radioactivities in the peak fractions of the free DNA and the DNA-poly(D-lysine) complex, respectively, reveals that lateral movement of histones, relative to specific sites in the DNA marked by restriction methylases, occurs during manipulation and fragmentation of chromatin.
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PMID:Movement of histones in chromatin induced by shearing. 108 77

New mutation detection systems are described for Haemophilus influenzae. They involve two independently isolated proline auxotrophs which appear to be mutants at different sites in a proline locus (proB) that is very closely linked to a locus (thd) for thymidine requirement. One of the mutants, proB1, appears to revert to prototrophy only by mutations at the locus. The other, proB2, reverts both by mutation at the locus and by unlinked suppressors. The latter account for about 90% of the reversions induced by MNNG and by HZ. The close linkage of proB to thd was used to distinguish between true revertants and suppressors by a transformation test. A comparison was made between the mutation induction kinetics of the different classes of revertants and mutations to novobiocin resistance with MNNG and HZ. The very different induction kinetics for these two mutagens previously reported for the novobiocin resistance system were also found for the proline systems. There were some differences between the detection systems, however, in the frequency of induced mutation relative to the spontaneous frequency and, in one case, in the form of the induction curve. It is concluded that the major features of the induction curves reflect the amount of damage done to DNA and so are general for all systems, but that there are some features which are locus-or site-specific.
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PMID:Reversions of two proline-requiring auxotrophs of Haemophilus influenzae by n-methyl-n'-nitro-n-nitrosoguanidine and hydrazine. 108 55

Premutational damage induced in Haemophilus influenzae by hydrazine appears to be fixed as final mutation only at replication as judged by the transformation assay. Fixation at replication is independent of the rec1 gene, unlike the case with nitrosocarbaryl. Prior to replication premutational damage induced by hydrazine disappears by an unknown process that is not dependent on the presence of a pyrimidine dimer excision system nor on the rec1 gene. Hydrazine does not produce detectable single-strand breaks or alkali-labile sites in the treated DNA nor gaps in DNA newly synthesized after treatment. In these respects it also differs from nitroso compounds. It is concluded that hydrazine acts to produce and altered base, possibly N(4)-aminocytosine, that produces mutations by mispairing at replication rather than by error-prone repair.
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PMID:Fixation and loss of hydrazine-induced premutational damage in Haemophilus influenzae. 108 56

The rate of production of acid-soluble material during degradation of duplex DNA by Hemophilus influenzae ATP-dependent DNAse (Hind exonuclease V) has been shown to be directly dependent upon the Mg2+ concentration in the reaction mixture. At high concentrations of Mg2+ (5 to 20 mM), DNA degradation to acid-soluble products is rapid and the rate of ATP hydrolysis is slightly depressed. At low concentrations of Mg2+ (0.1 to 0.5 mM), the enzyme rapidly hydrolyzes ATP and converts up to 35% of linear duplex DNA to single-stranded material while degrading less than 0.2% of the DNA to acid-soluble products. We refer to this enzymatic production of single-stranded DNA as the "melting" activity. Under the conditions of our assay, the initial melting reaction is processive, lasting about 70s on phage T7 DNA. Using DNAs with several different lengths, we have established that the duration of the initial reaction is dependent upon DNA length, requiring approximately 1 s per 0.18 mum. The products of the initial reaction on phage T7 DNA are somewhat heterogeneous, consisting of short duplex fragments approximately 0.5 mum long, purely single-stranded products up to 7 mum long, and longer duplex fragments 3 to 11 mum in length, some of which have single-stranded tails. Nearly half of the single-stranded material remains linked to a duplex segment of DNA after the inital processive reaction. We propose that Hind exo V initiates attack at the DNA termini and then acts in a processive manner, migrating along the DNA molecule, converting some regions to single-stranded material by the combined action of the melting activity and limited phosphodiester cleavage, while leaving other regions double-stranded. At the completion of its processive movement through a single DNA molecule, it is released and then recycles onto either intact molecules or the partially degraded products, continuing in this manner until the DNA is finally reduced to oligonucleotides.
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PMID:Mechanism of DNA degradation by the ATP-dependent DNase from Hemophilus influenzae Rd. 108 72

Three temperature-sensitive mutants of the Haemophilus influenzae phage HP1c1 were tested for reversion to wild type (ts leads to ts+). Treatment with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) produced revertants at levels up to 0.1% of the total progeny phage from treated lysogens. Cells treated with MNNG after infection with whole ts phage produced progeny phage with similar reversion frequencies, but when the uninfected cells or the phage were treated alone no reversion was induced. Fixation of premutational lesions was shown to occur with no evidence for host-cell DNA synthesis, indicating that phage DNA synthesis may be responsible for fixation of mutation in phage DNA. Evidence is given which shows that prophage DNA replicating by the cells' replicating system after treatment and before induction, produces the same number of revertants per survivor as phage DNA which is replicated outside the host genome. Two of the phage mutants (ts1 and ts2) reverted at similar frequencies, while one of the mutants (ts3) exhibited a much lower induced reversion frequency.
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PMID:Mutation induction by MNNG in a bacteriophage of Haemophilus influenzae. 108 14


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