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Biomedical subjects

J D Griffith

Publications and source records attributed to J D Griffith.

At least 55 records · Page 3Linked to original sources

A domain of the gene 4 helicase/primase of bacteriophage T7 required for the formation of an active hexamer.

The bacteriophage T7 gene 4 protein, like a number of helicases, is believed to function as a hexamer. The amino acid sequence of the T7 gene 4 protein from residue 475 to 491 is conserved in the homologous proteins of the related phages T3 and SP6. In addition, part of this region is conserved in DNA helicases such as Escherichia coli DnaB protein and phage T4 gp41. Mutations within this region of the T7 gene 4 protein can reduce the ability of the protein to form hexamers. The His475-->Ala and Asp485-->Gly mutant proteins show decreases in nucleotide hydrolysis, single-stranded DNA binding, double-stranded DNA unwinding, and primer synthesis in proportion to their ability to form hexamers. The mutation Arg487-->Ala has little effect on oligomerization, but nucleotide hydrolysis by this mutant protein is inhibited by single-stranded DNA, and it has a higher affinity for dTTP, suggesting that this protein is defective in the protein-protein interactions required for efficient nucleotide hydrolysis and translocation on single-stranded DNA. Gene 4 protein can form hexamers in the absence of a nucleotide, but dTTP increases hexamer formation, as does dTDP, to a lesser extent, demonstrating that the protein self-association affinity is influenced by the nucleotide bound. Together, the data demonstrate that this region of the gene 4 protein is important for the protein-protein contacts necessary for both hexamer formation and the interactions between the subunits of the hexamer required for coordinated nucleotide hydrolysis, translocation on single-stranded DNA, and unwinding of double-stranded DNA. The fact that the gene 4 proteins form dimers, but not monomers, even while hexamer formation is severely diminished by some of the mutations, suggests that the proteins associate in a manner with two separate and distinct protein-protein interfaces.

Amino Acid Sequence↗

A multimerizing transcription factor of sea urchin embryos capable of looping DNA.

SpGCF1 is a recently cloned sea urchin transcription factor that recognizes target sites in several different sea urchin genes. We find that in gel-shift experiments this factor is able to multimerize. A quantitative simulation of the gel-shift results suggests that SpGCF1 molecules that are bound to DNA target sites may also bind to one another, thus associating several DNA probe molecules. SpGCF1 might therefore be able to loop DNA molecules bearing its target sites at distant locations. We demonstrate this prediction by electron microscopy, and using the well-characterized cis-regulatory domain of the CyIIIa cytoskeletal actin gene, we show that the loop conformations predicted from the known SpGCF1 target site locations are actually formed in vitro. We speculate that the multimerization of this factor in vivo may function to bring distant regions of extended regulatory domains into immediate proximity so that they can interact with one another.

Actins↗

Visualization of TBP oligomers binding and bending the HIV-1 and adeno promoters.

The binding of the 28 kDa yeast TATA binding protein (yTBP) to the HIV and adeno major late promoters has been examined by electron microscopy (EM). Three different EM preparative methods were employed: direct mounting and shadowcasting of fixed samples, cryofixation and freeze-drying followed by shadowcasting, and negative staining of unfixed samples. Excellent agreement among the three methods was obtained. With ten yTBP monomers/DNA fragment, up to 25% of the DNA molecules contained easily distinguished protein particles at the TATA box and, less frequently, smaller particles were observed. Non-specific binding to DNA ends was common. The mass of the easily distinguished particles measured 63(+/- 5) kDa (cryofixation and shadowcasting) and 48(+/- 6) kDa (negative staining) indicating TBP dimerization. With 22 and 44 yTBP monomers/DNA, yTBP polymerization produced DNA-protein rods 9 nm wide and 20 to 30 nm long, frequently with two DNA strands exiting one end. Bending analysis revealed that yTBP dimers bend the DNA about the TATA box by 80 to 90 degrees. Although these protein ratios are relatively high, the structures formed demonstrate the propensity of yTBP to engage in protein-protein interactions.

Adenoviridae↗

Coaxially stacked RNA helices in the catalytic center of the Tetrahymena ribozyme.

Coaxial stacking of helical elements is a determinant of three-dimensional structure in RNA. In the catalytic center of the Tetrahymena group I intron, helices P4 and P6 are part of a tertiary structural domain that folds independently of the remainder of the intron. When P4 and P6 were fused with a phosphodiester linkage, the resulting RNA retained the detailed tertiary interactions characteristic of the native P4-P6 domain and even required lower magnesium ion concentrations for folding. These results indicate that P4 and P6 are coaxial in the P4-P6 domain and, therefore, in the native ribozyme. Helix fusion could provide a general method for identifying pairs of coaxially stacked helices in biological RNA molecules.

Animals↗

Preferential nucleosome assembly at DNA triplet repeats from the myotonic dystrophy gene.

The expansion of CTG repeats in DNA occurs in or near genes involved in several human diseases, including myotonic dystrophy and Huntington's disease. Nucleosomes, the basic structural element of chromosomes, consist of 146 base pairs of DNA coiled about an octamer of histone proteins and mediate general transcriptional repression. Electron microscopy was used to examine in vitro the nucleosome assembly of DNA containing repeating CTG triplets. The efficiency of nucleosome formation increased with expanded triplet blocks, suggesting that such blocks may repress transcription through the creation of stable nucleosomes.

DNA↗

Human immunodeficiency virus type 1 may preferentially integrate into chromatin occupied by L1Hs repetitive elements.

Human DNA flanking sites of eight human immunodeficiency virus type 1 (HIV-1) proviral integrations have been analyzed in isolates derived both from integrations in an infected individual and from tissue culture. Sequence analysis encompassing 80-3000 bp of human DNA on one or both sides of the site of integration revealed that seven of the eight HIV-1 proviruses had integrated directly into or within one nucleosome's distance from an L1Hs or Alu repetitive element. To compare this with the frequency at which human L1 or Alu elements sharing > or = 70% identity with L1Hs and Alu consensus sequences would be encountered at random, > 200 bp from each of 82 individual anonymously cloned segments of human DNA were sequenced: L1Hs elements were encountered in 8.5% of the 82 clones and Alu elements were encountered in 13.4+ by using these homology windows. From these data it appears that HIV-1 integrates into or near L1Hs elements with an approximately 6-fold higher frequency than would be expected if HIV-1 integration events were distributed uniformly throughout the genome. A cumulative binomial probability test shows that there is a 0.26% chance that one would arrive at these figures by chance and puts the data well within a 99% confidence interval. We propose that sites of L1Hs and Alu insertions originally occurred in regions of chromatin that were more easily accessible to the retroposon machinery and that these regions are now acting as preferred integration sites for HIV-1.

Base Sequence↗

Visualization of a tertiary structural domain of the Tetrahymena group I intron by electron microscopy.

The P4-P6 domain RNA of the group I intron of Tetrahymena thermophila has previously been shown by chemical probing to be an independently folding domain of the intron's tertiary structure. To directly visualize this tertiary structure, the P4-P6 domain and two folding defective mutants were prepared for high-resolution electron microscopy using tungsten shadowcasting. In the presence of Mg2+, the P4-P6 domain predominantly consists of compact molecules, while the two mutant RNAs are nearly all rod-like molecules. The measured length of the rod-like molecules is 64 (+/- 6) bp, which agrees closely with the length expected for molecules containing secondary structure only. In the absence of Mg2+, the P4-P6 domain contains threefold or tenfold fewer compact structures (depending on the mounting procedures) than in the presence of Mg2+. These results provide direct evidence for the overall shape of the tertiary structure proposed on the basis of biochemical experiment, and they confirm the Mg2+ dependence of tertiary folding. An equilibrium between the extended (rod-like) and the compact structures is suggested, with the concentration of bound Mg2+ and different mounting methods influencing the direction of the equilibrium. The entire group I ribozyme (L-21 Sca I RNA) was also examined by electron microscopy in the presence of Mg2+, and was revealed to have a compact shape. These studies present a direct demonstration of long-range interactions in a catalytic RNA molecule.

Animals↗

Two mutant RecA proteins possessing pH-dependent strand exchange activity exhibit pH-dependent presynaptic filament formation.

In previous studies it was shown that the mutant RecA proteins, [G160N]RecA and [H163A]RecA, are unable to catalyze ATP-dependent DNA strand exchanges at pH 7.5, but are active at pH 6.0 to 6.8. Here, we have used electron microscopy to follow the assembly of these mutant proteins onto single-stranded DNA at pH 7.5 and pH 6.2. In the absence of ATP, the filaments formed by the mutant proteins were similar to those formed by the wild-type protein, at both pH 7.5 and pH 6.2. In the presence of ATP, however, the filaments formed by the wild-type protein at pH 7.5 were extended and were stable in the presence of saturating SSB protein, whereas the filaments formed by the mutant proteins were shorter and unstable in the presence of SSB protein. At pH 6.2, in contrast, the filaments formed by the mutant proteins in the presence of ATP were of the same contour length as the wild-type RecA protein filaments and were stable in the presence of SSB protein. In the presence of the non-hydrolyzable ATP analog, ATP gamma S, and SSB protein, the mutant proteins formed full-length filaments at pH 7.5 that had a helical periodicity identical with that of the wild-type filaments (and characteristic of the strand exchange-active open conformational state); if SSB protein was omitted, the mutant protein filaments still exhibited the open helical periodicity, but were shorter and of highly variable length, presumably because of an improper threading of the ssDNA into the mutant filament. To account for these results, we propose that: (1) the mutant proteins are unable to isomerize efficiently to the open conformational state at pH 7.5 in the presence of ATP, but are able to do so in the presence of ATP gamma S; this indicates that the mechanistic defect is related to ATP hydrolysis rather than ATP binding; and (2) the mutant proteins are able to isomerize to the open conformational state in the presence of ATP at pH 6.2, indicating that protonation of the mutant filaments is sufficient to relieve the mechanistic deficiency.

Adenosine Triphosphate↗

A cluster of strong topoisomerase II cleavage sites is located near an integrated human immunodeficiency virus.

The Human Immunodeficiency Virus (HIV) integrates into host cellular DNA as a double strand DNA molecule. Here a previously studied HIV isolate was examined for binding and cleavage by topoisomerase II in vitro within the 5' LTR region and human flanking DNA. A cluster of strong binding and cleavage sites in the human sequences was located approximately 850 bp upstream from the integration site. This region maps to a locus consisting of a complex repeating element, and alternating purine/pyrimidine sequences. Topoisomerase II binding and cleavage sites were also located within the HIV 5' LTR, in particular a site overlying the DNA sequence coding for TAR, another inverted repeat element in the DNA.

Base Sequence↗

Cotinine concentrations in semen, urine, and blood of smokers and nonsmokers.

Cotinine levels in the semen, urine, and blood of 88 male smokers and nonsmokers, aged 18 to 35, were analyzed via radioimmunoassay. Detectable cotinine levels were found in all three body fluids, and cotinine levels in all three fluids were highly correlated. Cotinine levels in semen and blood were of similar magnitude; cotinine levels in urine were an order of magnitude or more higher. In all three fluids, cotinine levels increased with an increase in cigarette smoke exposure.

Adolescent↗

Early stages in RecA protein-catalyzed pairing. Analysis of coaggregate formation and non-homologous DNA contacts.

RecA protein will catalyze the in vitro pairing of homologous DNA molecules. To further explore the events involved in the search for homology, we have applied a nitrocellulose filter binding assay to follow pairing, and a sedimentation assay to follow the generation of aggregates (termed coaggregates) formed between RecA-complexed single-stranded (ss) DNA and double stranded (ds) DNA. Electron microscopy (EM) was used to visualize the structures involved. RecA protein promoted the pairing of circular M13 ssDNA and linear M13mp7 dsDNA efficiently in the absence of coaggregates. Indeed, pairing of homologous ss- and dsDNAs involved coaggregate formation only if the dsDNA was circular. For DNAs containing only a few hundred base-pairs of homology, for example pUC7 dsDNA and M13mp7 ssDNA, pairing and joint formation was observed if the dsDNA was superhelical but not if it was topologically relaxed or linear with the homology internal to an end of the dsDNA. The effect of non-covalently attached heterologous dsDNA on the RecA-promoted joining of M13 ssDNA and linear M13mp7 dsDNA (with non-M13 sequences at both ends) was found to depend on the topology and concentration of the heterologous DNA. A tenfold excess of superhelical pBR322 DNA strongly inhibited pairing. However, addition of relaxed or linear pBR322 DNA to the pairing reaction had little effect. As seen by EM, superhelical pBR322 DNA inhibited joint formation by excluding the homologous dsDNA form the coaggregates. EM also revealed heterologous DNA interactions presumably involved in the search for homology. Here the use of EM has provided a direct visualization of the form and architecture of coaggregates revealing a dense interweaving of presynaptic filaments and dsDNA.

Catalysis↗

Characterization of DNA-binding and strand-exchange stimulation properties of y-RPA, a yeast single-strand-DNA-binding protein.

Single-stranded DNA binding proteins (SSBs) have been isolated from many organisms, including Escherichia coli, Saccharomyces cerevisiae and humans. Characterization of these proteins suggests they are required for DNA replication and are active in homologous recombination. As an initial step towards understanding the role of the eukaryotic SSBs in DNA replication and recombination, we examined the DNA binding and strand exchange stimulation properties of the S. cerevisiae single-strand binding protein y-RPA (yeast replication protein A). y-RPA was found to bind to single-stranded DNA (ssDNA) as a 115,000 M(r) heterotrimer containing 70,000, 36,000 and 14,000 M(r) subunits. It saturated ssDNA at a stoichiometry of one heterotrimer per 90 to 100 nucleotides and binding occurred with high affinity (K omega greater than 10(9) M-1) and co-operativity (omega = 10,000 to 100,000). Electron microscopic analysis revealed that y-RPA binding was highly co-operative and that the ssDNA present in y-RPA-ssDNA complexes was compacted fourfold, arranged into nucleosome-like structures, and was free of secondary structure. y-RPA was also tested for its ability to stimulate the yeast Sepl and E. coli RecA strand-exchange proteins. In an assay that measures the pairing of circular ssDNA with homologous linear duplex DNA, y-RPA stimulated the strand-exchange activity of Sepl approximately threefold and the activity of RecA protein to the same extent as did E. coli SSB. Maximal stimulation of Sepl occurred at a stoichiometry of one y-RPA heterotrimer per 95 nucleotides of ssDNA. y-RPA stimulated RecA and Sepl mediated strand exchange reactions in a manner similar to that observed for the stimulation of RecA by E. coli SSB; in both of these reactions, y-RPA inhibited the aggregation of ssDNA and promoted the co-aggregation of single-stranded and double-stranded linear DNA. These results demonstrate that the E. coli and yeast SSBs display similar DNA-binding properties and support a model in which y-RPA functions as an E. coli SSB-like protein in yeast.

DNA, Single-Stranded↗

Purification and characterization of the bacteriophage T7 gene 2.5 protein. A single-stranded DNA-binding protein.

Bacteriophage T7 gene 2.5 protein has been purified to homogeneity from cells overexpressing its gene. Native gene 2.5 protein consists of a dimer of two identical subunits of molecular weight 25,562. Gene 2.5 protein binds specifically to single-stranded DNA with a stoichiometry of approximately 7 nucleotides bound per monomer of gene 2.5 protein; binding appears to be noncooperative. Electron microscopic analysis shows that gene 2.5 protein is able to disrupt the secondary structure of single-stranded DNA. The single-stranded DNA is extended into a chain of gene 2.5 protein dimers bound along the DNA. In fluorescence quenching and nitrocellulose filter binding assays, the binding constants of gene 2.5 protein to single-stranded DNA are 1.2 x 10(6) M-1 and 3.8 x 10(6) M-1, respectively. Escherichia coli single-stranded DNA-binding protein and phage T4 gene 32 protein bind to single-stranded DNA more tightly by a factor of 25. Fluorescence spectroscopy suggests that tyrosine residue(s), but not tryptophan residues, on gene 2.5 protein interacts with single-stranded DNA.

Adenosine Triphosphate↗

DNA adduct formation by 12 chemicals with populations potentially suitable for molecular epidemiological studies.

DNA adduct formation, route of absorption, metabolism and chemistry of 12 hazardous chemicals are reviewed. Methods for adduct detection are also reviewed and approaches to sensitivity and specificity are identified. The selection of these 12 chemicals from the Environmental Protection Agency list of genotoxic chemicals was based on the availability of information and on the availability of populations potentially suitable for molecular epidemiological study. The 12 chemicals include ethylene oxide, styrene, vinyl chloride, epichlorohydrin, propylene oxide, 4,4'-methylenebis-2-chloroaniline, benzidine, benzidine dyes (Direct Blue 6, Direct Black 38 and Direct Brown 95), acrylonitrile and benzyl chloride. While some of these chemicals (styrene and benzyl chloride, possibly Direct Blue 6) give rise to unique DNA adducts, others do not. Potentially confounding factors include mixed exposures in the work place, as well the formation of common DNA adducts. Additional research needs are identified.

Animals↗

HMf, a histone-related protein from the hyperthermophilic archaeon Methanothermus fervidus, binds preferentially to DNA containing phased tracts of adenines.

HMf, a histone-related protein from Methanothermus fervidus, was found to bind preferentially to a DNA that is intrinsically bent as a result of the presence of phased oligo(dA) tracts. The intergenic regions in M. fervidus DNA are A+T rich and frequently contain oligo(dA) tracts, some of which may have the size and phasing required to create a net bending in one direction. The binding of HMf to bent DNA could play a direct role in gene expression and stabilization of the genome of this organism.

Archaeal Proteins↗

Phased adenine tracts in double-stranded RNA do not induce sequence-directed bending.

Tracts of four to six adenines phased with the DNA helix produce a sequence-directed bending of the helix axis. Here, using gel electrophoresis and electron microscopy (EM), we have asked whether a similar motif will induce bending in a duplex RNA helix. Single-stranded RNAs were transcribed either from short synthetic DNA templates or from Crithidia fasciculata kinetoplast bent DNA, and the complementary single-stranded RNAs were annealed to produce duplex RNA molecules containing blocks of four to six adenines. Electrophoresis on polyacrylamide gels revealed no retardation of the RNAs containing phased blocks of adenines relative to duplex RNAs lacking such blocks. Examination by EM showed most of the molecules to be straight or only slightly bent. Thus, in contrast to DNA duplexes, phased adenine tracts do not induce sequence-directed bending in double-stranded RNA. Analysis of the distribution of molecule shapes for the highly bent C. fasciculata DNA showed that the adenine blocks do not act cooperatively to induce DNA bending and that the molecules must equilibrate between a spectrum of bent shapes.

Animals↗

Drosophila topoisomerase II-DNA interactions are affected by DNA structure.

The binding of purified Drosophila topoisomerase II to the highly bent DNA segments from the SV40 terminus of replication and C. fasciculata kinetoplast minicircle DNA (kDNA) was examined using electron microscopy (EM). The probability of finding topoisomerase II positioned at or near the bent SV40 terminus and Crithidia fasciculata kDNA was two- and threefold higher, respectively, than along the unbent pBR325 DNA into which the elements had been cloned. Closer examination demonstrated that the enzyme bound preferentially to the junction between the bent and non-bent sequences. Using gel electrophoresis, a cluster of strong sodium dodecyl sulfate-induced topoisomerase II cleavage sites was mapped to the SV40 terminus DNA, and two weak cleavage sites to the C. fasciculata kDNA. As determined by EM, Drosophila topoisomerase II foreshortened the apparent length of DNA by only 15 base-pairs when bound, arguing that it does not wrap DNA around itself. When bound to pBR325 containing the C. fasciculata kDNA and the SV40 terminus, topoisomerase II often produced DNA loops. The size distribution was that predicted from the known probability of any two points along linear DNA colliding. In vitro mapping of topoisomerase II on DNA whose ends were blocked by avidin protein revealed that binding is enhanced at sites located near a blocked end as compared to a free end. These observations may contribute towards establishing a framework for understanding topoisomerase II-DNA interactions.

Animals↗

Intercalators promote the binding of RecA protein to double-stranded DNA.

Ethidium bromide, acridine orange, 4'-(9-acridinylamino)methanesulfon-o-anisidide (o-AMSA), and m-AMSA induce the rapid binding of RecA protein to double-stranded (ds) DNA. The filaments formed appear to retain the drug and are 12.8 nm in diameter with an 8.0-nm pitch. Two classes of drugs have been distinguished: (i) those that bind to RecA protein and induce assembly at low relative concentrations (e.g., ethidium bromide) and (ii) those that do not appear to interact directly with RecA protein and must be present at relatively high drug concentrations to stimulate assembly (e.g., m-AMSA). Ethidium bromide, acridine orange, and quinacrine inhibit RecA protein binding to single-stranded DNA. Addition of ATP to the drug-induced filaments causes the protein to rapidly dissociate from dsDNA, and protein binding to dsDNA diminishes upon extended exposure to room light. We suggest that the structure of the drug-induced filaments may be more typical of the complex that initiates RecA protein assembly along DNA rather than the product of extensive polymerization as induced by adenosine 5'-[gamma-thio]triphosphate.

Coliphages↗