Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.30.2 (endonuclease)
18,621 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A new temperate bacteriophage, rho11, isolated by J. Hoch, has been characterized. This new phage is very similar to the temperate phage phi3T in size (380 nm), host range, homoimmunity, DNA buoyant density (1.694 g/ml), antigenicity, and molecular weight (around 6.0 X 10(7)) as determined in gels. Like phi3T, rho11 converts thymine auxotrophs to prototrophy at high frequency (250 out of 250 tested). Phage rho11 differs from phi3T in plaque morphology and in the endonuclease R-EcoRI digest pattern. Sixteen of the 20 rho11 DNA fragments have migration patterns corresponding to those of the 21 fragments of phi3T. The close similarities yet clear differences between these phages suggest that the two phages have a common ancestor.
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PMID:New temperate bacteriophage for Bacillus subtilis, rho 11. 6 60

DNA from a temperate phage rho 11 and chromosomal DNA of Bacillus subtilis 168 were digested with endonuclease EcoRI and then ligated with T4 polynucleotide ligase. The ligated DNA fragments were used to transform a lysogenic strain, B. subtilis spoA12 lys21 hisA1 leuA8 p11, and Lys+, His+ or Leu+ transformants were selected. The cells of each type were then mixed, grown and treated with mitomycin C; the induced phages were tested for abilities abilities to form plaques and to tranduce the auxotrophic marker. Various types of plaque-forming or defective phages which transduce hisA or lys marker at considerably high frequencies were thus obtained.
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PMID:A method for construction of specialized transducing phage rho 11 of Bacillus subtilis. 10 55

Phage N-1 grown in Anabaena strain 7120 [N-1 . 7120] forms plaques on A. variabilis about 10(-7) to 10(-6) as efficiently as on Anabaena 7120. By manipulating different characteristics of the interaction between phage and host, it was possible to increase the relative efficiency of plaque formation to 0.38. Growth of A. variabilis at 40 degrees C for at least three generations resulted in an increase in the rate of phage adsorption and a 10-fold increase in the efficiency of plaque formation. The efficiency of plaque formation was further increased about 42-fold, with little or no further increase in rate of adsorption, in a variant strain. A. variabilis strain FD, isolated from a culture of A. variabilis which had grown for more than 30 generations at 40 degrees C. The low relative efficiency of plaque formation by N-1 . 7120 on A. variabilis could be partially accounted for if A. variabilis contains a deoxyribonucleic acid restriction endonuclease which is absent from Anabaena 7120. Indirect evidence for such an endonuclease included the following: (i) phage N-1 grown in A. variabilis (N-1 . Av) had approximately a 7 X 10(3)-fold higher relative efficiency of plaque formation on A. variabilis than had N-1 . 7120; and (ii) the efficiency of plaque formation by N-1 . 7120 on A. variabilis strain FD was increased by up to 146-fold after heating the latter organism at 51 degrees C.
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PMID:Characteristics of Anabaena variabilis influencing plaque formation by cyanophage N-1. 11 Jul 87

Seven early mutants, three late mutants, and one plaque morphology mutant of polyoma have been mapped by marker rescue using wild-type restriction endonuclease fragments. The early mutants map between 1.0 and 26.4 units from the Eco RI site, a region previously shown to correspond to the 3'-OH termainal half of "early" RNA (Kamen et al., 1974). The late mutants as well as the plaque morphology mutant map between 26.6 and 45.4 map units, a region previously shown to correspond to the 3'-OH terminal half of "late" RNA (Kamen et al., 1974). Analysis of the genotype of rescued virus demonstrated that the modification of the mutant DNA during marker rescue was limited to the region of the genome covered by the wild-type restriction endonuclease fragment tested.
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PMID:Construction of the genetic map of the polyoma genome. 17 24

Most humans in the United States have been infected with BK virus (BKV), a human papovavirus. Because BKV has oncogenic properties, we have investigated whether it may be a cause of human cancer. Basic principles of tumor virology imply that BKV-induced tumors should contain BKV DNA sequences. Therefore, we assayed (by molecular hybridization) DNA from human tumors and malignant cell lines for BKV DNA, using BKV [(32)P]DNA as probe. The BKV [(32)P]DNA was labeled in vitro (nick translation) to specific activities of 1 to 2 x 10(8) cpm/mug. The BKV DNA used to prepare our probes had the properties expected of authentic BKV genomes, including density of superhelical DNA, sedimentation velocity in alkaline and neutral sucrose gradients, production of one fragment by endonuclease EcoRI cleavage and four fragments by endonuclease Hin II + III cleavage and reassociation properties. From these studies we conclude that our BKV probes hybridized well, and represented bona fide BKV DNA. Using three different BKV [(32)P]DNA probes, i.e., from three distinct plaque isolates, we have analyzed DNA from BKV-transformed cells, normal human tissues, and a large number of human tumors. All human DNAs (cell lines, normal tissues, tumors) hybridized 5% with BKV DNA. Hybridization analysis of BKV-transformed hamster cell DNA indicated 5-6 copies of at least 88% of the BKV genome per cell. No BKV DNA sequences were detected (above the normal 5% hybridization to all human DNAs) in the following normal human tissues: 10 kidney (BKV is usually isolated from urine), 3 spleen, 13 lung, 23 colon, 2 rectum, 1 ileum, and 1 skin. No BKV-specific DNA was found in 166 tumors, including 5 carcinomas (Ca) of stomach, 3 Ca small intestine, 26 Ca colon, 9 Ca rectum, 31 Ca lung, 9 adenocarcinomas and 5 oat cell carcinomas of lung, 17 melanomas, 5 Ca prostate, 4 Ca bladder, 6 Wilms tumors, 4 hypernephromas, 15 Ca kidney, 7 brain tumors, 5 Hodgkin lymphomas, 10 lymphomas (immunosuppressed patients have a high incidence of lymphomas), 2 reticulum cell sarcomas (spleen), and 3 skin tumors. We have also analyzed 7 human malignant cell lines (melanoma, lung, rhabdomyosarcoma, and glioblastomas), including several clones of a lung melanoma line; no BKV DNA sequences were detected. Because our probes could detect one copy of BKV DNA if only 10% of the cells were tumor cells, our results are very strong evidence that the tumors we analyzed did not have a BKV etiology. The tumors we tested represent about 50% of all cancers in the United States; there is no evidence that BKV is involved in the etiology of these types of tumors.
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PMID:Analysis of human tumors and human malignant cell lines for BK virus-specific DNA sequences. 20 40

An unusual cytomegalovirus (CMV, strain Colburn) isolated from brain biopsy of a boy with clinical encephalopathy was studied for genetic relatedness to human and simian CMV. Cross-examination of the purified viral DNA by DNA-DNA reassociation kinetics analyses showed more than 90% homology between Colburn virus and simian CMV (strain GR2757) and a lack of detectable homology between Colburn virus and human CMV (strains AD-169 and TW-87). Restriction endonuclease analysis of Colburn DNA showed some similarity of the DNA fragment pattern with that of simian CMV DNA, although the DNA fragment patterns were not identical, and showed no similarity to that of human CMV DNA. The molecular size and density of viral DNA were close to those of simian CMV DNA. The antigenic study, as performed by complement fixation and neutralization tests, showed strong cross-reactivity of Colburn virus to simian GR2757 virus. One-way cross-reaction of Colburn virus to several human CMV isolates (AD-169, Davis, and Town) was detected by complement fixation; this one-way cross-reaction was not obvious in a plaque neutralization test. It was concluded that Colburn is a simian CMV-related virus.
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PMID:Genetic analysis of a cytomegalovirus-like agent isolated from human brain. 20 16

Analysis of restriction endonuclease cleavage sites within the inverted, repeated sequences in the joint region of the DNA of herpes simplex virus type 1 strain KOS revealed the presence of two types of sequence heterogeneity. The first was an insertion of 280 base pairs or multiples of 280 base pairs which was found in approximately half of all DNA molecules from every plaque-purified stock of virus. These insertions seemed to be tandem duplications of sequences which were present at the joint and correspond closely to the inverted terminal redunancy. The second type of heterogeneity was due to variable insertions and deletions which were present in some, but not all, plaque-purified virus stocks. Comparison of restriction fragments from the joint region with fragments from the termini indicated that in the simplest observed molecules of herpes simplex virus type 1 DNA, only one copy of the inverted terminal redundancy was present at the joint. A map of restriction endonuclease cleavage sites in the joint region is presented.
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PMID:Structure of the joint region and the termini of the DNA of herpes simplex virus type 1. 21 Dec 66

A plaque morphology mutant (pm-522) of human papovavirus BK, which was rescued from a human papovavirus BK-induced hamster pineocytoma, was characterized and compared with a cloned wild-type virus (wt-501). Mutant pm-522 formed turbid plaques and grew more slowly than wt-501 in human embryonic kidney (HEK) cells. The immunofluorescence assay revealed that more HEK cells underwent abortive infection with pm-522 than with wt-501. Whereas wt-501 induced brain tumors and osteosarcomas, but no insulinomas, in hamsters, pm-522 induced brain tumors and insulinomas. The DNA of pm-522 was found by electrophoresis and electron microscopy to have a deletion (85 +/- 15 base pairs) and an insertion (40 +/- 10 base pairs) between map coordinates 0.708 and 0.725 from the endonuclease EcoRI cleavage site. These results demonstrate the presence of a viable deletion human papovarivus BK mutant capable of inducing insulinomas in hamsters.
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PMID:Viable deletion mutant of human papovavirus BK that induces insulinomas in hamsters. 22 73

In the Escherichia coli lysogen HfrH73 described by Shimada et al. (1973), none of the enzymes coded for by the leucine operon is synthesized due to an insertion of phage lambda into cistron leuA. The orientation of lambda in the chromosome is ara leuDCB lambda JAN leuA. After heat induction of the lysogen, plaque-forming transducing phages of two types are formed at low frequency. One type (e.g., lambda pleu9) transduces leuD, leuC, and leuB strains to prototrophy. The other type (e.g., lambda pleu 13) transduces leuA strains to prototrophy. lambda pleu 13 forms lysogens at low frequency (about 0.2%) by integration into the leucine operon. These lysogens are unstable, segregating phage-sensitive clones at high frequency (about 1%). Phages carrying different portions of the leucine operon were formed by aberrant excision after heat induction of strain CV437 (leuA371 lambda pleu13). A phage carrying the entire leucine operon (lambda K2) was constructed by a cross between lambda pleu9 and lambda pleu13. An analysis of leucine-forming enzyme levels in strains lysogenized with lambdaK2 indicated that leuO and leuP are present and functional in lambda K2. leu-specific messenger ribonucleic acid from E. coli hybridizes to the heavy (r) strand of lambdaK2. The leucine operon of lambda G4 pleuABCD (an S7 derivative of lambda K2) exists intact on a 7.3 x 10(6)-dalton fragment (lambdaG4EcoRI-B) generated by cleavage with endonuclease EcoRI. Heteroduplexes formed between lambda G4 and lambda show a 5.4 x 10(6)-dalton piece of bacterial deoxyribonucleic acid (DNA) replacing a 4.5 x 10(6)-dalton piece of lambda DNA starting at 0.46 fractional unit on the map of lambda. Fragment lambda G4EcoRI-B has about 0.6 x 10(6) daltons of lambda DNA from the b2 region at one end and about 1.4 x 10(6) daltons of lambda DNA from the int region at the other end.
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PMID:Isolation and characterization of lambda pleu bacteriophages. 32 Jan 78

A plaque-forming lambdapolA phage was isolated from a population of transducing phage made in vitro from Escherichia coli DNA and a phage vector digested with restriction endonuclease HindIII. Amber mutations, in genes whose products are necessary for late protein synthesis (Q) and cell lysis (S), were crossed into the lambdapolA phage. Infection of either polA+ or polA- bacteria with this phage, under conditions permitting DNA replication but preventing phage production and lysis, elevated the levels of DNA polymerase I to between 75- and 100-fold that detected in a wild-type strain. The kinetics of enzyme production suggest that the polA gene is transcribed from its own promoter rather than from any of the well-characterized phage promoters. The fragment of E. coli DNA within the lambdapolA phage comprises approximately 5000 base pairs, sufficient to accommodate the polA gene and one, or two, coding sequences for smaller proteins.
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PMID:Isolation and characterization of a lambdapolA transducing phage. 34 Nov 64


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