Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The Host Factor required for in vitro coliphage Q beta RNA replication, a heat-stable RNA binding protein present in uninfected Escherichia coli, has been detected by both immunological and functional tests in Acinetobacter calcoaceticus, Klebsiella pneumoniae, Pseudomonas aeruginosa and Pseudomonas putida. It was not detectable by these criteria in Bacillus stearothermophilus, Bacillus subtilis, Caulobacter crescentus, Micrococcus lysodeikticus, Rhodopseudomonas capsulata or Saccharomyces cerevisiae. In Escherichia coli the Host Factor protein has been shown to be associated with ribosomes. It is demonstrated here that this association is specific for the 30S ribosomal subunit.
Mol Gen Genet 1977 May 20
PMID:Host factor for coliphage Q beta RNA replication: presence in procaryotes and association with the 30S ribosomal subunit in Escherichia coli. 32 1

Mutants of Klebsiella aerogenes W70 that metabolize the uncommon pentose D-arabinose were isolated. These mutants were found to be either constitutive or indicible by D-arabinose for the synthesis of enzymes in the L-fucose pathway. Such mutants could then utilize L-fucose isomerase to convert the structurally similar D-arabinose molecule to D-ribulose. D-Ribulose is an intermediate and the inducer of an existing ribitol pathway and could thus be metabolized. In those D-arabinose-positive mutants where the ribitol pathway was blocked by mutation, D-ribulose could alternatively be metabolized by using the remaining L-fucose pathway enzymes. When the two D-arabinose catabolic routes were compared, catabolism of D-arabinose via the ribitol pathway was found to be more efficient. Catabolism of D-arabinose using the L-fucose pathway permitted D-ribulose to escape into the media and produced an unmetabolizable end product, L-glycolic acid. A comparison of growth using constitutive versus inducible control of the borrowed L-fucose isomerase did not reveal an advantage for one control type over the other. Several differences were observed, however, when we determined the degree to which these control mutations perturbed the normal functioning of the L-fucose and associated pathways. Growth of the constitutive mutant was impaired with L-fucose as substrate. The inducible-control mutant had altered growth characteristics on ribitol and L-rhamnose.
J Mol Evol 1977 Nov 25
PMID:A comparison of alternate metabolic strategies for the utilization of D-arabinose. 33 26

A series of mutants defective in nitrogen fixation (nif) were isolated in Klebsiella pneumoniae strain M5a1. The nif mutations were either located on plasmid pRD1 or on the K. pneumoniae chromosome. A total of 37 plasmid mutants and 28 chromosomal mutants were employed in complementation tests using the acetylene reduction technique. Most mutants could be assigned to one of seven nif cistrons: nifA, nifB, nifD, nifE, nifF, nifH, and nifK. Complementation analysis of two nif deletion mutants confirmed transductional evidence that these strains carry nifB-A-F deletions. One deletion mutant had, in contrast to previous transductional analysis, a functional nifK cistron and presumably is deleted for nifB-A-F-E. Examination of the biochemical phenotype of several mutants suggests that the nifA product has a regulatory function, and nifK, nifD and nifH are most probably the structural genes for nitrogenase.
Mol Gen Genet 1977 Nov 29
PMID:Complementation analysis of Klebsiella pneumoniae mutants defective in nitrogen fixation. 34 Sep 23

Three new genes nifM, nifI and nifN have been mapped in the nif gene cluster of Klebsiella pneumoniae and a fourth gene nifJ has been confirmed as being a separate cistron. Polar nif mutations were obtained by transposition of Tn7 to plasmid pRD1, and of Tn5 and Tn10 to plasmid pMF100, a derivative of pRD1. Complementation analysis of the nif::Tn mutants led to the identification of at least six transcriptional units: nifB; nifA; nifJ; nifH, nifD and nifK; nifE and nifI; nifN, nifM and nifF. Biochemical and genetic evidence suggest that the three genes nifH, nifD and nifK, which are probably the structural genes for nitrogenase, belong to the same operon and are transcribed from nifH to nifK. A polypeptide with a molecular weight of approximately 120,000 is presumed to be the nifJ product.
Mol Gen Genet 1978 Sep 20
PMID:Polarity of mutations induced by insertion of transposons Tn5, Tn7 and Tn10 into the nif gene cluster of Klebsiella pneumoniae. 36 60

Polar mutations were obtained by integration of bacteriophage Mu c+ or Mu cts DNA into the Klebsiella pneumoniae nif genes located on plasmid pCE1, a derivative of pRD1. In addition, nif deletions were isolated from nif::Mu cts plasmids. Complementation data allowed the characterization of twelve nif cistrons, nine corresponding to previously identified genes. Polar effect of Mu DNA insertions suggested the existence of at least six transcription units: 1) nif K, nif D and nif H--2)nif A and nif L--3) nif E and a new gene--4) nif B--5) nif F--6) nif J. Nif K, nif D and nif H, which are most probably the structural genes for nitrogenase, seem to belong to the same operon transcribed from nif H to nif K. This was confirmed by SDS gel autoradiography of pulse labelled proteins. Moreover it was possible to identify, on the autoradiograms, a polypeptide which likely is the product of nif J and whose biosynthesis is under the control of nif A.
Mol Gen Genet 1978 Oct 04
PMID:Genetic and biochemical analysis of mutants induced by bacteriophage Mu DNA integration into Klebsiella pneumoniae nitrogen fixation genes. 36 77

A HindIII (17.0 kb) and an EcoR1 restriction fragment (6.9 kb) of Klebsiella pneumoniae nif DNA were cloned on two small amplifiable plasmids, pCM1 and pSA30 respectively. These plasmids between them carry 14 of the 15 known Klebsiella nif genes. The operon for the three structural genes for nitrogenase, nifpHDK, is carried on pSA30: four and five of the remaining six operons are on pCRA37 and pCM1 respectively. All of the nif genes were assigned to endonuclease restriction fragments of DNA using the Southern blotting technique (Southern, 1975) with total DNA of nif insertion mutants and radioactive plasmid DNA which contained cloned nif DNA sequences. Their locations were consistent with the genetic map of nif genes. The estimated size of the nif gene cluster was 24 kb.
Mol Gen Genet 1979 Jul 02
PMID:Overlapping sequences of Klebsiella pneumoniae nifDNA cloned and characterized. 38 62

When Klebsiella aerogenes was grown in continuous culture with xylitol. an unnatural pentitol, as the growth limiting substrate, the structural gene which codes for ribitol dehydrogenase, an enzyme which gratuitously catalyzes the oxidation of xylitol to D-xylulose, was duplicated. It appears that the duplication mechansim only duplicates the gene which is subjected to selective pressure and not any of the other closely linked genes. The degree to which the ribitol dehydrogenase gene is duplicated does not appear to be strictly correlated with the ability to grow faster on xylitol. Duplication mutants do, in fact, grow faster than their parent strain, but when challenged to grow at even higher growth rates there is a catabolic repression of enzyme activity. Thus a situation is created in which a structural gene is duplicated in response to selective pressure; these mutants can grow faster on the new substrate, but faster growth results in a "silencing" of a portion of the genes by catabolite repression.
J Mol Evol 1977 Apr 29
PMID:Growth of Klebsiella aerogenes on xylitol: implications for bacterial enzyme evolution. 86 22

We describe here the isolation of a mutant derivative of the drug resistance factor R1 (Meynell and Datta, 1966) that carries a nonsense mutation in a gene determining resistance to penicillins. We have used this mutant R1 to isolate derivatives of Escherichia coli and Klebsiella pneumoniae that contain nonsense suppressors (Sup- strains) by screening penicillin-resistant revertants of strains containing the mutant R factor for the presence of such suppressors. This obviates the need to have known nonsense mutations in chromosomal genes. Theoretically, suppressor-containing derivatives of any bacterial species that can maintain and express R1 can be constructed.
Mol Gen Genet 1975 Jul 10
PMID:A method for isolating nonsense suppressors in enterobacteriaceae using an amber mutant of the drug resistance factor R1. 109 92

Many human diseases are associated with HLA class I, class II and class III antigens. It appears that the class III antigen disease associations can be explained by a direct defect operating at the level of either the class III gene or its gene product. The mechanism underlying class I and class II antigen disease associations is at present unknown. In this review we have considered thirty diseases which have been ranked according to their relative risk as defined by the frequency of a given HLA antigen in patient and control populations. The chronic inflammatory disorder, ankylosing spondylitis and its association with HLA B27 has been used as a model to study the HLA linked diseases. We have suggested that the disease may be caused by the Gram-negative microorganism Klebsiella which has antigenic similarity to HLA B27. It is proposed that some antibodies made against Klebsiella bind to HLA B27, thereby acting as autoantibodies leading to the pathological sequelae of chronic inflammatory arthritis. This is the crosstolerance hypothesis or molecular mimicry model and it has been compared to the receptor model. It is further suggested that the crosstolerance hypothesis can be utilised as a general theory to explain the association of other diseases with the class I and class II antigens, and offer a possible explanation for the polymorphism of HLA.
Mol Aspects Med 1992
PMID:HLA and disease. 128 96

A 6940 bp Klebsiella pneumoniae chromosomal DNA fragment, containing genes involved in pyrroloquinoline quinone (PQQ) biosynthesis, was sequenced. Six open reading frames, pqqA, pqqB, pqqC, pqqD, pqqE and pqqF were identified in the pqq operon, which coded for polypeptides of 2764 (23 amino acids), 33,464, 28,986, 10,436, 42,881 and 83,616 Da, respectively. The transcription startpoint was mapped by primer extension analysis, upstream of pqqA, and promoter boxes could be identified. The gene products of pqqB, pqqC, pqqE and pqqF were detected in maxi-cells and the molecular weights of the proteins corresponded with the molecular weights deduced from the nucleotide sequence. The gene products of pqqA, pqqB, pqqC, pqqD and pqqE show 49%-64% identity in amino acid sequence with those of pqqIV, pqqV, pqqI, pqqII and pqqIII respectively in the cloned pqq cluster of Acinetobacter calcoaceticus. The 84 kDa protein encoded by pqqF, which is not present in the cloned pqq cluster of A. calcoaceticus but which is essential for PQQ biosynthesis in K. pneumoniae and Escherichia coli, seems to belong to a family of proteases.
Mol Gen Genet 1992 Mar
PMID:Nucleotide sequence and structure of the Klebsiella pneumoniae pqq operon. 131 37


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