Binding of an HIV Rev peptide to Rev responsive element RNA induces formation of purine-purine base pairs

Biochemistry ◽  
1994 ◽  
Vol 33 (10) ◽  
pp. 2741-2747 ◽  
Author(s):  
John L. Battiste ◽  
Ruoying Tan ◽  
Alan D. Frankel ◽  
James R. Williamson
Keyword(s):  
Base Pairs ◽  
Purine Base ◽  
Responsive Element

Purine-purine base pairs and the origin of transversion-type mutation

2009 ◽  
Vol 12 (S4) ◽  
pp. 197-204
Author(s):  
Ramon Gardun̄to ◽  
Robert Rein ◽  
John T. Egan ◽  
Yves Coeckelenbergh ◽  
Robert D. Macelroy
Keyword(s):  
Base Pairs ◽  
Purine Base

scholarly journals Reverse Watson-Crick purine-purine base pairs — the Sharp-turn motif and other structural consequences in functional RNAs

2017 ◽  
Author(s):  
Abhinav Mittal ◽  
Antarip Halder ◽  
Sohini Bhattacharya ◽  
Dhananjay Bhattacharyya ◽  
Abhijit Mitra
Keyword(s):  
Structural Alignment ◽  
Bimodal Distribution ◽  
Base Pairs ◽  
Purine Base ◽  
Functional Roles ◽  
Nmr Structures ◽  
Sharp Turn ◽  
Interesting Class ◽  
Functional Rnas ◽  
Noncanonical Base Pairs

AbstractIdentification of static and/or dynamic roles of different noncanonical base pairs is essential for a comprehensive understanding of the sequence-structure-function space of RNA. In this context, reverse Watson-Crick purine-purine base pairs (A:A, G:G&A:GW:W Trans) constitute an interesting class of noncanonical base pairs in RNA due to their characteristic C1′–C1′ distance (highest among all base pairing geometries) and parallel local strand orientation. Structural alignment of the RNA stretches containing these W:W Trans base pairs with their corresponding homologous sites in a non-redundant set of RNA crystal structures show that, as expected, these base pairs are associated with specific structural folds or functional roles. Detailed analysis of these contexts further revealed a bimodal distribution in the local backbone geometry parameters associated with these base pairs. One mode, populated by both A:A and G:G W:W Trans pairs, manifests itself as a characteristic backbone fold. We call this fold a ‘Sharp-turn’ motif. The other mode is exclusively associated with A:A W:W Trans pairs involved in mediating higher order interactions. The same trend is also observed in available solution NMR structures. We have also characterized the importance of recurrent hydrogen bonding interactions between adenine and guanine in W:W Trans geometry. Quantum chemical calculations performed at M05-2X/6-31++(2d,2p) level explain how the characteristic electronic properties of these W:W Trans base pairs facilitate their occurrence in such exclusive structural folds that are important for RNA functionalities.

The novel double-folded structure of d(GCATGCATGC): a possible model for triplet-repeat sequences

2015 ◽  
Vol 71 (10) ◽  
pp. 2119-2126 ◽  
Author(s):  
Arunachalam Thirugnanasambandam ◽  
Selvam Karthik ◽  
Pradeep Kumar Mandal ◽  
Namasivayam Gautham
Keyword(s):  
Hydrogen Bonds ◽  
Dna Sequences ◽  
Single Strand ◽  
Triplet Repeat ◽  
The Novel ◽  
Base Pairs ◽  
Purine Base ◽  
Ion Interactions ◽  
Folded Structure ◽  
Triplet Repeat Sequences

The structure of the decadeoxyribonucleotide d(GCATGCATGC) is presented at a resolution of 1.8 Å. The decamer adopts a novel double-folded structure in which the direction of progression of the backbone changes at the two thymine residues. Intra-strand stacking interactions (including an interaction between the endocylic O atom of a ribose moiety and the adjacent purine base), hydrogen bonds and cobalt-ion interactions stabilize the double-folded structure of the single strand. Two such double-folded strands come together in the crystal to form a dimer. Inter-strand Watson–Crick hydrogen bonds form four base pairs. This portion of the decamer structure is similar to that observed in other previously reported oligonucleotide structures and has been dubbed a `bi-loop'. Both the double-folded single-strand structure, as well as the dimeric bi-loop structure, serve as starting points to construct models for triplet-repeat DNA sequences, which have been implicated in many human diseases.

IMPORTANCE OF CHARGE TRANSFER EXCITATIONS IN DNA ELECTRON SPECTRUM: A ZINDO SEMIEMPIRICAL QUANTUM-CHEMICAL STUDY

2004 ◽  
Vol 18 (16) ◽  
pp. 825-831 ◽  
Author(s):  
E. B. STARIKOV
Keyword(s):  
Charge Transfer ◽  
Quantum Chemical ◽  
Spectral Band ◽  
Quantum Chemical Study ◽  
Chemical Study ◽  
Molecular Orbitals ◽  
Base Pairs ◽  
Purine Base ◽  
Dna Conformations

Electron spectra of DNA model compounds, adenosine-thymidine and guanosine-cytidine nucleoside base pairs, as well as the relevant homogeneous stacked base pair steps in A-DNA and B-DNA conformations, were investigated using ZINDO semiempirical quantum-chemical method. This work confirms that, in DNA with intact Watson–Crick hydrogen bonding and base stacking, the highest occupied molecular orbitals (HOMO) are residing on purine base residues, whereas the lowest unoccupied molecular orbitals (LUMO) — on pyrimidine base residues. In general, the present results are satisfactorily comparable with the available experimental data. The role of charge transfer excitations in the polymer DNA 260 nm spectral band is discussed.

scholarly journals 7-Iodo-5-aza-7-deazaguanine ribonucleoside: crystal structure, physical properties, base-pair stability and functionalization

2020 ◽  
Vol 76 (5) ◽  
pp. 513-523
Author(s):  
Dasharath Kondhare ◽  
Simone Budow-Busse ◽  
Constantin Daniliuc ◽  
Frank Seela
Keyword(s):  
Base Pair ◽  
Crystal Packing ◽  
Donor Site ◽  
Proton Donor ◽  
Proton Acceptor ◽  
Acceptor Site ◽  
Base Pairs ◽  
Purine Base ◽  
Value Differences ◽  
Ribose Moiety

The positional change of nitrogen-7 of the RNA constituent guanosine to the bridgehead position-5 leads to the base-modified nucleoside 5-aza-7-deazaguanosine. Contrary to guanosine, this molecule cannot form Hoogsteen base pairs and the Watson–Crick proton donor site N3—H becomes a proton-acceptor site. This causes changes in nucleobase recognition in nucleic acids and has been used to construct stable `all-purine' DNA and DNA with silver-mediated base pairs. The present work reports the single-crystal X-ray structure of 7-iodo-5-aza-7-deazaguanosine, C10H12IN5O5 (1). The iodinated nucleoside shows an anti conformation at the glycosylic bond and an N conformation (O4′-endo) for the ribose moiety, with an antiperiplanar orientation of the 5′-hydroxy group. Crystal packing is controlled by interactions between nucleobase and sugar moieties. The 7-iodo substituent forms a contact to oxygen-2′ of the ribose moiety. Self-pairing of the nucleobases does not take place. A Hirshfeld surface analysis of 1 highlights the contacts of the nucleobase and sugar moiety (O—H...O and N—H...O). The concept of pK-value differences to evaluate base-pair stability was applied to purine–purine base pairing and stable base pairs were predicted for the construction of `all-purine' RNA. Furthermore, the 7-iodo substituent of 1 was functionalized with benzofuran to detect motional constraints by fluorescence spectroscopy.

trans-a2Pt(II) (a=NH3, CH3NH2) modified purine base pairs and triples: Hydrogen bonding between self-complementary pairs and triples and heterometal (Ag+) coordination leading to a 1 D helix

2000 ◽  
Vol 300-302 ◽  
pp. 339-352 ◽  
Author(s):  
Irene B. Rother ◽  
Eva Freisinger ◽  
Andrea Erxleben ◽  
Bernhard Lippert
Keyword(s):  
Hydrogen Bonding ◽  
Base Pairs ◽  
Purine Base

scholarly journals Binding of quinomycin antibiotic UK-65,662 to DNA: 1H-n.m.r. studies of drug-inducedchanges in DNA conformation in complexes with d(ACGT)2 and d(GACGTC)2

1994 ◽  
Vol 304 (3) ◽  
pp. 967-979 ◽  
Author(s):  
M S Searle
Keyword(s):  
Hydrogen Bonding ◽  
Nuclear Overhauser Effect ◽  
Drug Binding ◽  
Dna Conformation ◽  
Dna Duplexes ◽  
Base Pairs ◽  
Purine Base ◽  
Nuclear Overhauser ◽  
Nuclear Overhauser Effects

Quinomycin antibiotic UK-65,662 binds selectively to the 5′-CpG-binding sites of the DNA duplexes d(ACGT)2 and d(GACGTC)2; the complexes have been studied in detail by 1H-n.m.r. spectroscopy and molecular-modelling techniques employing nuclear Overhauser effect-restrained energy minimization and molecular dynamics. Whereas the terminal A.T base pairs of the tetamer duplex d(ACGT)2 adopt a stable Hoogsteen alignment (characterized by a syn glycosidic conformation of the purine base), when internalized within the hexamer duplex d(GACGTC)2, the A.T base pairs revert to anti glycosidic torsion angles characteristic of the Watson-Crick hydrogen-bonding scheme. The energetics of base-pair stacking at the terminal 5′-GpA steps of the hexamer complex, with base pairs in the Watson-Crick alignment, are concluded to be important determinants of the adopted conformation, whereas an energetic preference for stacking interactions between terminal Hoogsteen A.T base pairs and the drug quinoline chromophores is evident in the tetramer complex. The internal G.C base pairs in both complexes are highly stabilized, as indicated by the very slow exchange rates of the guanine imino protons; in contrast, the flanking A.T base pairs are no more stable than in the ligand-free DNA duplexes. A large number of intermolecular nuclear Overhauser effects are indicative of many van der Waals contacts and hydrogen-bonding between the antibiotic and the minor groove of the central G.C base pairs in both complexes, indicating that interactions with the G.C base pairs in each duplex are very similar providing the essential features for recognition and tight binding. Despite the difference in the conformation of the A.T base pairs, stacking with the quinoline rings occurs primarily with the adenine bases in both complexes. Relative intensities of intranucleotide versus internucleotide nuclear Overhauser effects indicate that both duplexes are substantially unwound by drug binding (particularly at the CpG step) and this is confirmed by the structure calculations. Both duplexes have ladder-like structures that must lead to significant local distortions of the DNA conformation in vivo.

Molecular Recognition of Watson-Crick-Like Purine-Purine Base Pairs

ChemBioChem ◽  
2011 ◽  
Vol 12 (14) ◽  
pp. 2155-2158 ◽  
Author(s):  
Ragan Buckley ◽  
C. Denise Enekwa ◽  
Loren Dean Williams ◽  
Nicholas V. Hud
Keyword(s):  
Molecular Recognition ◽  
Base Pairs ◽  
Purine Base

Detection of the Glanzmann's Thrombasthenia Mutations in Arab and Iraqi-Jewish Patients by Polymerase Chain Reaction and Restriction Analysis of Blood or Urine Samples

1991 ◽  
Vol 66 (04) ◽  
pp. 500-504 ◽  
Author(s):  
H Peretz ◽  
U Seligsohn ◽  
E Zwang ◽  
B S Coller ◽  
P J Newman
Keyword(s):  
Polymerase Chain Reaction ◽  
Base Pair ◽  
Restriction Analysis ◽  
Urine Samples ◽  
Chain Reaction ◽  
Base Pairs ◽  
Glanzmann’S Thrombasthenia ◽  
Glanzmann's Thrombasthenia ◽  
Base Pair Deletion ◽  
Polymerase Chain

SummarySevere Glanzmann's thrombasthenia is relatively frequent in Iraqi-Jews and Arabs residing in Israel. We have recently described the mutations responsible for the disease in Iraqi-Jews – an 11 base pair deletion in exon 12 of the glycoprotein IIIa gene, and in Arabs – a 13 base pair deletion at the AG acceptor splice site of exon 4 on the glycoprotein IIb gene. In this communication we show that the Iraqi-Jewish mutation can be identified directly by polymerase chain reaction and gel electrophoresis. With specially designed oligonucleotide primers encompassing the mutation site, an 80 base pair segment amplified in healthy controls was clearly distinguished from the 69 base pair segment produced in patients. Patients from 11 unrelated Iraqi-Jewish families had the same mutation. The Arab mutation was identified by first amplifying a DNA segment consisting of 312 base pairs in controls and of 299 base pairs in patients, and then digestion by a restriction enzyme Stu-1, which recognizes a site that is absent in the mutant gene. In controls the 312 bp segment was digested into 235 and 77 bp fragments, while in patients there was no change in the size of the amplified 299 bp segment. The mutation was found in patients from 3 out of 5 unrelated Arab families. Both Iraqi-Jewish and Arab mutations were detectable in DNA extracted from blood and urine samples. The described simple methods of identifying the mutations should be useful for detection of the numerous potential carriers among the affected kindreds and for prenatal diagnosis using DNA extracted from chorionic villi samples.

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