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Query: UNIPROT:P06889 (
Mol
)
630,302
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The complementation pattern of twelve rudimentary mutations have been analyzed at two different levels. When analyzed on the basis of complementation for a wing abnormality the mutations can be divided into three groups, each of which is believed to affect the activity of one of the first three enzymes of
pyrimidine
synthesis (Norby, 1973; Jarry and Falk, 1974; Rawls and Fristrom, 1975). However, when the mutants are analyzed for complementation on the basis of a second phenotype,
pyrimidine
auxotrophy, the distinction between two of these three groups is not evident. The disparity in the two patterns probably reflects a different threshold of gene activity required for the detection of an auxotrophic phenotype as compared to that at which a wing abnormality is detectable. The biochemical basis of these results is interpreted in light of recent data suggesting that at least the first two enzymes of
pyrimidine
synthesis are contained within a single multifunctional protein complex (Soderholm et al., 1975).
Mol
Gen Genet 1976 Oct 18
PMID:Pyrimidine auxotrophy and the complementation map of the rudimentary locus of Drosophila melanogaster. 82 17
The DNA polymerase of Ustilago maydis is stimulated by a DNA binding protein from the same organism. Analysis of this stimulation shows that there is an increase in affinity for both substrates of the reaction. The apparent Km for deoxynucleoside triphosphates is decreased 3 fold, and that for denatured DNA by 4 fold. In both cases the maximum velocity (Vmax) is increased 1.2 to 1.4 fold. It is suggested that the variability in the affinity of the enzyme for deoxynucleoside triphosphates mediated by the binding protein may provide the basis for the UV sensitivity of
pyrimidine
auxotrophs in this organism.
Mol
Gen Genet 1976 May 07
PMID:The influence of DNA binding protein on the substrate affinities of DNA polymerase from Ustilago maydis: one polymerase implicated in both DNA replication and repair. 93 54
In terms of the mechanical model of molecules, a calculation has been carried out of possible positions and binding energies of 1-methyl uracyl in the contact region of the ribonuclease S active site. In the most preferential orientation, 1-methyl uracyl forms hydrogen bonds C(2)=O(uracyl)...H-N(Thr-45), N-H...Ogamma (Thr-45), C(4)=O... ...H-Ogamma (Ser-123). The base position found (atom coordinates are given) is in complete qualitative agreement with the position of the uracyl in UpcA bound to ribonuclease S as revealed by X-ray analysis. The influence studied of methyl substitution in positions 3 and 5 of the
pyrimidine
cycle on the base orientation within the protein field. It has been shown that the formation of hydrogen bonds with Thr-45 and Ser-123 is not prerequisite for productive fixation of the phosphoribosyl nucleotide moiety in the catalytic region of the enzyme active site.
Mol
Biol (Mosk)
PMID:[A theoretical analysis of the binding of methyl derivatives of uracil at the contact portion of the active center of ribonuclease S]. 94 May 57
Genetic recombination induced by structural damage in DNA molecules was investigated in E. coli K12 (lambda) lysogens infected with genetically marked phage lambda. Photoproducts were induced in the phage DNA before infection by exposing them either to 313 nm light in the presence of acetophenone or to 254 nm light. To test the role of the replication of the damaged phage DNA on the frequency of the induced recombination, both heteroimmune and homimmune crosses were performed. First, samples of a heteroimmune phage lambda imm434 P80 exposed to these treatments were allowed to infect cells lysogenic for prophage lambda cI857 P3. Phage DNA replication and maturation took place, and the resulting progeny phages were assayed for the frequency of P+ recombinants. Recombination was less frequent in infected cells exposed to visible light and in wild type cells able to perform excision repair than in excision-defective lysogens. Therefore, much of the induced recombination can be attributed to the
pyrimidine
dimers in the phage DNA, the only photoproducts known to be dissociated by photoreactivating enzyme. Second, in homoimmune crosses, samples of similarly treated homoimmune lambda P3 phages were allowed to infect lysogens carrying lambda cI857 P80. Replication of the phage DNA containing ultraviolet photoproducts was repressed by lambda immunity, and was further blocked by the lack of the P gene product needed for replication. The lysogens were purified and scored for both colony forming ability and for P+ recombinant prophages. The 254 nm photoproducts increased the frequency of recombination in these homimmune crosses, even though phage DNA replication was blocked. Irradiation with 313 nm light and acetophenone M, which produces dimers and unknown photoproducts, was not as effective per dimer as the 254 nm light. It is concluded from these results that certain unidentified 254 nm photoproducts can cause recombination even in the absence of DNA replication. They are not
pyrimidine
dimers, as they are not susceptible to excision repair or photoreactivation. In contrast,
pyrimidine
dimers appear to cause recombination only when the DNA containing them undergoes replication.
Mol
Gen Genet 1976 Jul 23
PMID:Genetic exchanges caused by ultraviolet photoproducts in phage lambda DNA molecules: the role of DNA replication. 95
The nucleotide composition, relative concentration of
pyrimidine
clusters, and the degree of methylation of the mitochondrial and nuclear DNA's of various vertebrates and the protozoan Crithidia oncopelti have been studied. With respect to the relative concentration of GC pairs, the mtDNA of animals (bull, rat) does not differ from the corresponding nDNA. The relative concentration of GC pairs in the mtDNA of certain fish and birds is 1.5-2.5 mole% higher than in the respective nDNA. The kinetoplast DNA of the protozoan C. oncopelti (where the relative concentration of the GC pairs is 42.9 mole %) differs very sharply in composition from the nDNA (where the relative concentration of GC pairs is 51.3 mole %). The mtDNA's and kDNA's studied are distinguished from the respective nDNA'S by a lower degree of clustering of
pyrimidine
nucleotides. The proportion of mono- and dipyrimidine fragments in the mtDNA and kDNA is 30 mole %, while in the nDNA it does not exceed 23 mole %. The relative concentration of long
pyrimidine
clusters (hexapyrimidine clusters of larger) in the mtDNA is smaller than in the nDNA by a factor of 2-5. The low degree of clustering of the
pyrimidine
nucleotides is apparently characteristic of all the known mtDNA's and may support the fact that they have a single type of organization and are of a single origin. All the vertebrate mtDNA's studied contain 5-methylcytosine as a minor base (1.5-3.15 mole %), and their level of methylation is 1.5-2 times greater than that in the respective nDNA's. It has been shown that animals display species specificity with respect to the 5-methylcytosine content in the mtDNA. Its distribution among the
pyrimidine
clusters in the bovine heart mtDNA differs substantially from that in the nDNA. This suggests that the methylation specificities of nuclear and mitochondrial DNA are different. A DNA methylase, which effects the in vitro methylation of cytosine residues both in the homologous mtDNA and in different heterologous DNA's, has been found in rat liver and bovine heart mitochondria. The specificity of the in vitro methylation of the cytosine residues in the same heterologous Escherichia coli B DNA by the nuclear and mitochondrial enzymes is different: The mitochondrial enzyme methylates predominantly in monopyrimidine fragments, and the nuclear enzyme methylates mostly in di- and tripyrimidine fragments. They, therefore, recognize different nucleotide sequences.
Mol
Biol (Mosk)
PMID:Structure of animal mitochondrial DNA: nucleotide composition, pyrimidine clusters, and methylation character. 102 50
113
pyrimidine
auxotrophs, unable to synthesise UMP have been selected in Aspergillus nidulans. These mutants can be classified by complementation into eight groups, and genetic analysis has shown that five loci are involved. One complex locus consists of the mutually complementing pyrA, pyrB and pyrC groups, as well as the cis-dominant pyrN group, members of which do not complement with members of the A, B or C groups. pyrA mutants have been shown to lack CPSase-ur, pyrB and pyrC mutants have been shown to lack ACTase, and pyrN to lack both these enzymes. This locus appears to code for products which form an enzyme aggregate. The four simple loci, as well as the complex loci have been located genetically, and distinguished from one another on the basis of accumulation of
pyrimidine
precursors in vivo. The synthesis of ACTase has been shown to subject to end-product repression.
Mol
Gen Genet 1975 Jun 19
PMID:Pyrimidine biosynthesis in Aspergillus nidulans: isolation and preliminary characterisation of auxotrophic mutants. 110 32
The photoreversibility of UV-induced mutations to Trp+ in strain Escherichia coli WP2 uvrA trp (unable to excise
pyrimidine
dimers) was lost at different rates during incubation in different media. In Casamino acids medium after a short initial lag, photoreversibility was lost over about one generation time; in minimal medium with tryptophan, photoreversibility persisted for more than two generations; in Casamino acids medium with pantoyl lactone photoreversibility was lost extremely slowly. The rate of loss of photoreversibility was unaffected by UV dose in either Casamino acids medium or in minimal medium. The same eventual number of induced mutants was obtained when cells were incubated for two generations in any of the three media before being transferred to selective plates supplemented with Casamino acids. Thus in each the proportion of cells capable of giving rise to a mutant was the same and only the rate at which these cells did so during post-irradiation growth varied, suggesting that there might be a specific fraction of
pyrimidine
dimers at a given site capable of initiating a mutagenic repair event, and that the size of this fraction is dose dependent. Segregation experiments have shown that error-prone repair appears to occur once only and is not repeated in subsequent replication cycles, in contrast to (presumed error-free) recombination repair. The results are discussed in the light of current models of UV mutagenesis.
Mol
Gen Genet 1975 Oct 03
PMID:Mutagenic DNA repair in Escherichia coli. II. Factors affecting loss of photoreversibility of UV induced mutations. 110 95
Measurements of UV sensitivity of wildtype cells (wt) and UV senistive mutants of E. coli and P. mirabilis suggest that the increased sensitivity of P. mirabilis (wt) is due either to incomplete repair of DNA lesions or to additive lethality probably as a result of UV induction of defective phage(s) present in P. mitabilis (Taubeneck, 1967). Direct estimates of the rate of
pyrimidine
dimer excision and a comparison of the UV reactivation capacity of E. coli and P. mirabilis for the temperate phages lambda and pi 1, respectively, support this conclusion.
Mol
Gen Genet 1975 Nov 24
PMID:DNA repair in Proteus mirabilis. III.Survival, dimer excision, and UV reactivation in comparison with Escherichia coli K12. 110 8
We have examined lexA1 uvrA6 and recF143 uvrBdelta derivatives of Escherichia coli K-12 for post-replication repair and DNA synthesis after UV irradiation. Compared to corresponding lex+ rec+ strains, we found that the lexA and recF cells were defective in (1) converting short DNA segments synthesized after irradiation to DNA of normal size; (2) synthesizing high molecular weight DNA after irradiation; (3) transferring
pyrimidine
dimers from irradiated DNA into unirradiated daughter strands. Our results support the hypothesis that after UV irradiation the formation of large DNA molecules in excision-deficient cells of E.coli depends directly or indirectly upon joining short DNA segments into longer strands, concomitant with the transfer of DNA from irradiated tamplates into unirradiated daughter strands. This process appears to require the activity of lexA and recF genes.
Mol
Gen Genet 1975 Dec 01
PMID:The effect of lexA and recF mutations on post-replication repair and DNA synthesis in Escherichia coli K-12. 110 15
The 1 P+f phage, a virulent mutant of the moderate P+ phage for Bac. brevis var. G.-B., consists of a hexagonal head (90x90 nm) and a long non-contractile tail (340 nm). This phage is characterized by a relatively long latent period (90-110 min) and a low yield (40-50 particles per cell). The 1P+f phage is quite stable at pH values from 1 to 11, insensitive to osmotic shock, treatment with chloroform and acridine orange. The sensitivity of the phage to thermal treatment and UV-radiation has been studied. The nucleic acid of the P+f phage is double-stranded DNA of AT-type (GC equals 34.5 mole %) which contains 5-methylcytosine (0.18 mole %) and N6-methyladenine (0.32 mole%). The level of methylation of cytosine and adenine residues in DNA of the 1 P+f phage does not depend on the host studied (Bac. brevis, P- and S variants). The specificity of methylation of cytosine residues in the S and P- cells appears to be the same. DNA of the 1 P+f phage strongly differs from DNA of the host in nucleotide composition (GC equals 45.7 mole %). Nevertheless, phage DNA is very similar to DNA from Bac. subtilis in the character of
pyrimidine
distribution (the amount of different
pyrimidine
isopliths). This may testify to a somewhat common character of the nucleotide sequence organization in DNA of the phage and its host.
Mol
Biol (Mosk)
PMID:[Some properties of 1 P+f bacteriophage for Bacillus brevis var. G.-B and its nucleic acid]. 121 2
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