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Importance of poly(ADP-ribose) glycohydrolase in the control of poly(ADP-ribose) metabolism.

Poly(ADP-ribosyl)ation is a posttranslational modification that alters the functions of the acceptor proteins and is catalyzed by the poly(ADP-ribose) polymerase (PARP) family of enzymes. Following DNA damage, activated poly(ADP-ribose) polymerase-1 (PARP-1) catalyzes the elongation and branching of poly(ADP-ribose) (pADPr) covalently attached to nuclear target proteins. Although the biological role of poly(ADP-ribosyl)ation has not yet been defined, it has been implicated in many important cellular processes such as DNA repair and replication, modulation of chromatin structure, and apoptosis. The transient nature and modulation of poly(ADP-ribosyl)ation depend on the activity of a unique cytoplasmic enzyme called poly(ADP-ribose) glycohydrolase which hydrolyzes pADPr bound to acceptor proteins in free ADP-ribose residues. While the PARP homologues have been recently reviewed, there are relatively scarce data about PARG in the literature. Here we summarize the latest advances in the PARG field, addressing the question of its putative nucleo-cytoplasmic shuttling that could enable the tight regulation of pADPr metabolism. This would contribute to the elucidation of the biological significance of poly(ADP-ribosyl)ation.

Active Transport, Cell Nucleus↗

Cyclic aristeromycin diphosphate ribose: a potent and poorly hydrolysable Ca(2+)-mobilising mimic of cyclic adenosine diphosphate ribose.

Cyclic aristeromycin diphosphate ribose, a carbocyclic analogue of cyclic adenosine diphosphate ribose, was synthesised using a chemo-enzymatic route involving activation of aristeromycin 5'-phosphate by diphenyl phosphochloridate. The calcium-releasing properties of this novel analogue were investigated in sea urchin egg homogenates. While cyclic aristeromycin diphosphate ribose has a calcium release profile similar to that of cyclic adenosine diphosphate ribose (EC50 values are 80 nM and 30 nM, respectively), it is degraded significantly more slowly (t1/2 values are 170 min and 15 min, respectively) and may, therefore, be a useful tool to investigate the activities of cyclic adenosine diphosphate ribose.

Adenosine↗

Misregulation of poly(ADP-ribose) polymerase-1 activity and cell type-specific loss of poly(ADP-ribose) synthesis in the cerebellum of aged rats.

Protein modification by ADP-ribose polymers is a common regulatory mechanism in eukaryotic cells and is involved in several aspects of brain physiology and physiopathology, including neurotransmission, memory formation, neurotoxicity, ageing and age-associated diseases. Here we show age-related misregulation of poly(ADP-ribose) synthesis in rat cerebellum as revealed by: (i) reduced poly(ADP-ribose) polymerase-1 (PARP-1) activation in response to enzymatic DNA cleavage, (ii) altered protein poly(ADP-ribosyl)ation profiles in isolated nuclei, and (iii) cell type-specific loss of poly(ADP-ribosyl)ation capacity in granule cell layer and Purkinje cells in vivo. In particular, although PARP-1 could be detected in virtually all granule cells, only a fraction of them appeared to be actively engaged in poly(ADP-ribose) synthesis and this fraction was reduced in old rat cerebellum. NAD(+), quantified in tissue homogenates, was essentially the same in the cerebellum of young and old rats suggesting that in vivo factors other than PARP-1 content and/or NAD(+) levels may be responsible for the age-associated lowering of poly(ADP-ribose) synthesis. Moreover, PARP-1 expression was substantially down-regulated in Purkinje cells of senescent rats.

Aging↗

D-ribose stabilizes precursor and mature ribose-binding proteins of Escherichia coli.

Heat- and guanidine hydrochloride-induced unfolding and refolding of precursor as well as mature ribose-binding proteins of Escherichia coli were studied in the presence of D-ribose using intrinsic tyrosine fluorescence and circular dichroism. The precursor and mature proteins have shown virtually identical unfolding-folding behavior. It was observed that D-ribose refolds partially unfolded precursor and mature ribose binding proteins into native structure and decreases the unfolding rate of the these proteins. The conformational stabilities of these proteins were found to increase with increasing D-ribose concentration.

Carrier Proteins↗

Mutagenicity of gamma-irradiated oxygenated and deoxygenated solutions of 2-deoxy-D-ribose and D-ribose in Salmonella typhimurium.

Solutions of 2-deoxy-D-ribose and D-ribose were gamma-irradiated under different experimental conditions and tested for mutagenicity, with and without preincubation, in Salmonella typhimurium. The irradiated sugar solutions were mutagenic in the tester strains TA100 and TA98. Except for malonaldehyde (MDA), which is not mutagenic in the concentrations produced radiolytically, the relative mutagenicities of the individual radiolytic products are unknown. With irradiated solutions of 2-deoxy-D-ribose, a relationship was found between the level of non-MDA aldehydes and the mutagenicity in TA100. Heating the irradiated solutions of 2-deoxy-D-ribose resulted in a temperature-dependent reduction of the mutagenicity. Autoclaved, non-irradiated solutions of 2-deoxy-D-ribose were not mutagenic in the Salmonella test.

Aerobiosis↗

Synthesis of stable and cell-type selective analogues of cyclic ADP-ribose, a Ca(2+)-mobilizing second messenger. Structure--activity relationship of the N1-ribose moiety.

We previously developed cyclic ADP-carbocyclic ribose (cADPcR, 2) as a stable mimic of cyclic ADP-ribose (cADPR, 1), a Ca(2+)-mobilizing second messenger. A series of the N1-ribose modified cADPcR analogues, designed as novel stable mimics of cADPR, which were the 2"-deoxy analogue 3, the 3"-deoxy analogue 4, the 3"-deoxy-2"-O-(methoxymethyl) analogue 5, the 3"-O-methyl analogue 6, the 2",3"-dideoxy analogue 7, and the 2",3"-dideoxydidehydro analogue 8, were successfully synthesized using the key intramolecular condensation reaction with phenylthiophosphate-type substrates. We investigated the conformations of these analogues and of cADPR and found that steric repulsion between both the adenine and N9-ribose moieties and between the adenine and N1-ribose moieties was a determinant of the conformation. The Ca(2+)-mobilizing effects were evaluated systematically using three different biological systems, i.e., sea urchin eggs, NG108-15 neuronal cells, and Jurkat T-lymphocytes. The relative potency of Ca(2+)-mobilization by these cADPR analogues varies depending on the cell-type used: e.g., 3"-deoxy-cADPcR (4) > cADPcR (2) > cADPR (1) in sea urchin eggs; cADPR (1) >> cADPcR (2) approximately 3"-deoxy-cADPcR (4) in T-cells; and cADPcR (2) > cADPR (1) > 3"-deoxy-cADPcR (4) in neuronal cells, respectively. These indicated that the target proteins and/or the mechanism of action of cADPR in sea urchin eggs, T-cells, and neuronal cells are different. Thus, this study represents an entry to cell-type selective cADPR analogues, which can be used as biological tools and/or novel drug leads.

Animals↗

Structural and functional basis for ADP-ribose and poly(ADP-ribose) binding by viral macro domains.

Macro domains constitute a protein module family found associated with specific histones and proteins involved in chromatin metabolism. In addition, a small number of animal RNA viruses, such as corona- and toroviruses, alphaviruses, and hepatitis E virus, encode macro domains for which, however, structural and functional information is extremely limited. Here, we characterized the macro domains from hepatitis E virus, Semliki Forest virus, and severe acute respiratory syndrome coronavirus (SARS-CoV). The crystal structure of the SARS-CoV macro domain was determined at 1.8-Angstroms resolution in complex with ADP-ribose. Information derived from structural, mutational, and sequence analyses suggests a close phylogenetic and, most probably, functional relationship between viral and cellular macro domain homologs. The data revealed that viral macro domains have relatively poor ADP-ribose 1"-phosphohydrolase activities (which were previously proposed to be their biologically relevant function) but bind efficiently free and poly(ADP-ribose) polymerase 1-bound poly(ADP-ribose) in vitro. Collectively, these results suggest to further evaluate the role of viral macro domains in host response to viral infection.

Adenosine Diphosphate Ribose↗

Roles for adenosine ribose hydroxyl groups in cyclic adenosine 5'-diphosphate ribose-mediated Ca2+ release.

Cyclic adenosine diphosphate ribose (cADPR) is a naturally occurring and potent Ca2+-mobilizing agent. Structural analogues are currently required as pharmacological tools for the investigation of this topical molecule, but modifications to date have concentrated primarily upon the purine ring. Two novel dehydroxylated analogues of cADPR have now been prepared from chemically synthesized nicotinamide adenine dinucleotide (NAD+) precursors modified in the ribose moiety linked to adenine. ADP-ribosyl cyclase of Aplysia californica catalyzed the conversion of 2'A-deoxy-NAD+ and 3'A-deoxy-NAD+ into the corresponding 2'A-deoxy-cADPR and 3'A-deoxy-cADPR analogues, respectively. These analogues were used to assess the effect of 2'- and 3'-hydroxyl group deletion in the adenosine ribose moiety of cADPR on the Ca2+-releasing potential of cADPR. These compounds were found to have comparatively markedly different activities as agonists for Ca2+ mobilization in sea urchin egg homogenate. 2'A-Deoxy-cADPR is similar to cADPR, whereas 3'A-deoxy-cADPR is at least 100-fold less potent, indicating that the 3'A-hydroxyl group, but not the 2'A-hydroxyl group, is essential for calcium releasing activity. EC50 values recorded were 32 nM, 58 nM, and 5 microM for cADPR, 2'A-deoxy-cADPR, and 3'A-deoxy-cADPR, respectively. Moreover, 200 nM 2'A-deoxy-cADPR was required to desensitize the cADPR-sensitive Ca2+ channel to a subsequent addition of 100 nM cADPR, but 20 microM 3'A-deoxy-cADPR was required to produce the same desensitizing effect. This is in accordance with the 100-fold lower potency exhibited by the latter analogue. To further investigate the importance of the 3'-hydroxyl group, we have also synthesized 3'A-O-methyl-cADPR, in which the 3'-hydroxyl group of adenosine has been methylated and its ability potentially to donate a hydrogen atom in a hydrogen bond has been removed. Although inactive in releasing Ca2+, 3'A-O-methyl-cADPR inhibited cADPR-induced Ca2+ release in a dose-dependent manner with an approximate IC50 value of 5 microM, whereas 3'-O-methyladenosine had no effect. This further supports the requirement of a 3'-OH group for Ca2+ releasing activity. In addition, however, it suggests that this group may not be crucial for ligand-receptor recognition. Thus, replacement of the hydrogen atom of the hydroxyl with a methyl group effects a change of activity from an agonist to an antagonist of cADPR-induced Ca2+ release. Two other analogues with modifications in the 2' and/or 3' positions, 3'-cADPR phosphate and 2',3'-cyclic-cADPR phosphate, were synthesized and tested for their Ca2+-mobilizing activity in sea urchin egg homogenates. Both analogues were inactive with respect to both agonistic and antagonistic activities on the cADPR-sensitive Ca2+ release mechanism. These are the first steps toward a wider structure-activity relationship for cADPR, and this is the first study to implicate a crucial role for the adenosine ribose hydroxyl groups of cADPR in the biological activity of this cyclic nucleotide. Additionally, this is the first report of a cADPR receptor antagonist that is not modified at the 8-position of the purine ring.

Adenosine Diphosphate Ribose↗

Selective loss of poly(ADP-ribose) and the 85-kDa fragment of poly(ADP-ribose) polymerase in nucleoli during alkylation-induced apoptosis of HeLa cells.

Alkylation treatment of HeLa cells results in the rapid induction of apoptosis as revealed by DNA laddering and cleavage of poly(ADP-ribose) polymerase (PARP) into the 29-and 85-kDa fragments (Kumari S. R., Mendoza-Alvarez, H. & Alvarez-Gonzalez, R. (1998) Cancer Res. 58, 5075-5078). Here, we performed a time-course analysis of (i) poly(ADP-ribose) synthesis and degradation as well as (ii) the subnuclear localization of PARP and its fragments by using confocal laser scanning immunofluorescence microscopy. PARP was activated within 15 min post-treatment, as revealed by nuclear immunostaining with antibody 10H (recognizing poly(ADP-ribose)). This was followed by a late, time-dependent, progressive decline of 10H signals that coincide with the time of PARP cleavage. Strikingly, nucleolar immunostaining with antibodies 10H and C-II-10 (recognizing the 85-kDa PARP fragment) was lost by 15 min post-treatment, whereas F-I-23 signals (recognizing the 29-kDa fragment) persisted. We hypothesize that the 85-kDa PARP fragment is translocated, along with covalently bound poly(ADP-ribose), from nucleoli to the nucleoplasm, whereas the 29-kDa fragment is retained, because it binds to DNA strand breaks. Our data (i) provide a link between the known time-dependent bifunctional role of PARP in apoptosis and the subcellular localization of PARP fragments and also (ii) add to the evidence for early proteolytic changes in nucleoli during apoptosis.

Alkylation↗

Poly(ADP-ribose) synthase is the major endogenous nonhistone acceptor for poly(ADP-ribose) in alkylated rat hepatoma cells.

The endogenous poly(ADP-ribosyl)--nonhistone protein conjugates were isolated from dimethyl-sulfate-treated rat hepatoma AH 7974 cells using aminophenylboronic-acid--agarose chromatography. Seven major components could be discerned on dodecyl sulfate gels (molecular mass 43, 60, 66, 86, 100, 110 and 170 kDa) while control cells indicated only slight staining at above 200 kDa. The most abundant conjugate formed in response to alkylation damage was further purified using preparative gel electrophoresis and identified on the basis of its intrinsic enzymic activity as automodified poly(APD-ribose) synthase. In addition, topoisomerase I activity was found associated with a 60-kDa peptide. ADP-ribosylated endonuclease and actin were not detect-able. The purified conjugate fraction contained maximally 8.8 nmol/mg ADP-ribose and 7.9 nmol/mg oligo(ADP-ribose) with a mean chain length of 2.3 residues. The modifying (ADP-ribosyl)n groups were attached to its acceptors by a hydroxylamine-insensitive bond and had practically no effect on the DNA affinity of either poly(ADP-ribose) synthase or topoisomerase I.

Alkylating Agents↗

Inhibition and ADP-ribose pyrophosphatase-I by nitric-oxide-generating systems: a mechanism linking nitric oxide to processes dependent on free ADP-ribose.

Rat liver ADP-ribose pyrophosphatase-I (ADPRibase-I; EC 3.6.1.13) hydrolyzes ADP-ribose with high specificity and a low Km. Thus it can participate in the control of free ADP-ribose and nonenzymatic ADP-ribosylation of proteins. Here we show that ADPRibase-I was inactivated by acidified nitrite, whereas sodium nitroprusside (SNP) or 3-morpholinosydnonimine (SIN-1) at pH 7.5 produced a dose- and time-dependent Km increase from 0.5 microM to 2 microM. The effects of SNP and SIN-1 depended on the presence and concentration of dithiothreitol, pointing to S-nitrosylation of enzyme thiols. It is suggested that, by inhibiting ADPRibase-I, NO can stimulate nonenzymatic ADP-ribosylation of targets susceptible to micromolar free ADP-ribose. This is discussed in relation to apparently contradictory earlier reports on the role of NO in the ADP-ribosylation of actin.

Adenosine Diphosphate Ribose↗

10-100 eV Ar+ ion induced damage to D-ribose and 2-deoxy-D-ribose molecules in condensed phase.

We report that 10-100 eV Ar+ ion irradiation induces severe damage to the biologically relevant sugar molecules D-ribose and 2-deoxy-D-ribose in the condensed phase on a polycrystalline Pt substrate. Ar+ ions with kinetic energies down to 15 eV induce effective decomposition of both sugar molecules, leading to the desorption of abundant cation and anion fragments, including CH3+, C2H3+, C3H3+, H3O+, CHO+, CH3O+, C2H3O+, H-, O-, and OH-, etc. Use of isotopically labelled molecules (5- 13C D-ribose and 1-D D-ribose) reveals the site specificity for some of the fragment origins, and thus the nature of the chemical bond breaking. It is found that all of the chemical bonds in both molecules are vulnerable to ion impact at energies down to 15 eV, particularly both the endo- and exocyclic C-O bonds. In addition to molecular fragmentation, several chemical reactions are also observed. A small amount of O-/O fragments abstract hydrogen to form OH-. It is found that the formation of the H3O+ ion is related to the hydroxyl groups of the sugar molecules, and is associated with additional hydrogen loss from the parent or adjacent molecules via hydrogen abstraction or proton transfer. The formation of several other cation fragments also requires hydrogen abstraction from its parent or an adjacent molecule. These fragmentations and reactions are likely to occur in a real biomedium during ionizing radiation treatment of tumors and thus bear significant radiobiological relevance.

Argon↗

Box C/D RNA guides for the ribose methylation of archaeal tRNAs. The tRNATrp intron guides the formation of two ribose-methylated nucleosides in the mature tRNATrp.

Following a search of the Pyrococcus genomes for homologs of eukaryotic methylation guide small nucleolar RNAs, we have experimentally identified in Pyrococcus abyssi four novel box C/D small RNAs predicted to direct 2'-O-ribose methylations onto the first position of the anticodon in tRNALeu(CAA), tRNALeu(UAA), elongator tRNAMet and tRNATrp, respectively. Remarkably, one of them corresponds to the intron of its presumptive target, pre-tRNATrp. This intron is predicted to direct in cis two distinct ribose methylations within the unspliced tRNA precursor, not only onto the first position of the anticodon in the 5' exon but also onto position 39 (universal tRNA numbering) in the 3' exon. The two intramolecular RNA duplexes expected to direct methylation, which both span an exon-intron junction in pre-tRNATrp, are phylogenetically conserved in euryarchaeotes. We have experimentally confirmed the predicted guide function of the box C/D intron in halophile Haloferax volcanii by mutagenesis analysis, using an in vitro splicing/RNA modification assay in which the two cognate ribose methylations of pre-tRNATrp are faithfully reproduced. Euryarchaeal pre-tRNATrp should provide a unique system to further investigate the molecular mechanisms of RNA-guided ribose methylation and gain new insights into the origin and evolution of the complex family of archaeal and eukaryotic box C/D small RNAs.

Base Sequence↗

Loss of poly(ADP-ribose) synthetase activity without change in arginine-specific ADP-ribosyltransferase activity by acid-treatment; application of the treatment to simple assay for transferase in the presence of poly(ADP-ribose) synthetase.

We investigated the effects of acid treatment (pH 3.5) on the activities of arginine-specific ADP-ribosyltransferase (mono(ADP-ribosyl)transferase) (EC 2.4.2.31) and poly(ADP-ribose) synthetase (EC 2.4.2.30) purified from chicken liver, and we observed that the former enzyme retained completely its activity while there was no evidence for activity of the latter enzyme. Kinetic parameters, including Km values for NAD and whole histones in the reaction catalyzed by acid-treated ADP-ribosyltransferase, were the same as those in the reaction catalyzed by non-treated enzyme. The stereospecificities of the reaction forming ADP-ribosylarginine by acid-treated and non-treated ADP-ribosyltransferases were indistinguishable. We made use of this acid treatment to determine ADP-ribosyltransferase activity in chicken and chick-embryo liver extracts, with a filter assay. The enzyme activities (means +/- S.D. for three separate experiments) of 1-year-old chicken and 13-day-old chick embryo livers were 372.7 +/- 80.20 and 110.6 +/- 27.22 nmol ADP-ribose/g wet liver per h, respectively. This acid treatment is useful for filter assay with labelled NAD of arginine-specific ADP-ribosyltransferase in the fraction containing poly(ADP-ribose) synthetase.

ADP Ribose Transferases↗

Synthetic study on carbocyclic analogs of cyclic ADP-ribose, a novel second messenger: an efficient synthesis of cyclic IDP-carbocyclic-ribose.

An efficient synthesis of cyclic IDP-carbocyclic-ribose, as a stable mimic for cyclic ADP-ribose, was achieved. 8-Bromo-N1-carbocyclic-ribosylinosine derivative 10, prepared from N1-(2,4-dinitrophenyl)inosine derivative 5 and an optically active carbocyclic amine 6, was converted to 8-bromo-N1-carbocyclic-ribosylinosine bisphosphate derivative 15. Treatment of 15 with I2 in the presence of molecular sieves in pyridine gave the desired cyclic product 16 quantitatively, which was deprotected and reductively debrominated to give the target cyclic IDP-carbocyclic-ribose (3).

Adenosine Diphosphate Ribose↗

Two proteolytic degradation products of calf-thymus poly(ADP-ribose) polymerase are efficient ADP-ribose acceptors. Implications for polymerase architecture and the automodification of the polymerase.

Two polypeptides with molecular masses of 76 and 59 kDa were found to copurify with poly(ADP-ribose) polymerase from calf thymus, and to be as efficient acceptors of ADP-ribose as the polymerase itself. Analysis of their CNBr fragments by sodium dodecylsulfate/polyacrylamide gel electrophoresis revealed that the polypeptides were derived from the 112-kDa polymerase. Isolation of poly(ADP-ribose) polymerase in the absence of protease inhibitors resulted in a loss of more than 90% of the polymerase activity and an increased proportion of the 76-kDa and 59-kDa polypeptides in the final polymerase preparation. When the polymerase and the two polypeptides were separated by gel filtration or polyacrylamide gel electrophoresis in 5% acetic acid, no polymerase activity was found associated with the two fragments. Analysis of the CNBr fragments of the three polypeptides after incubation of the enzyme preparation with [32P]NAD showed that most of the fragments were radioactive, indicating multiple ADP-ribosylation sites. Several ADP-ribosylated fragments were found to be common to all three polypeptides, or to two of them.

Adenosine Diphosphate Ribose↗

Intramolecular ADP-ribose transfer reactions and calcium signalling. Potential role of 2'-phospho-cyclic ADP-ribose in oxidative stress.

Intramolecular ADP-ribose transfer reactions result in the formation of cyclic ADP-ribose (cADPR) and 2'-phospho-cyclic ADP-ribose (P-cADPR) from NAD and NADP, respectively. The potent Ca2+ releasing activity of these cyclic nucleotides has led to the postulation that they function as second messengers of Ca2+ signalling. The synthesis and hydrolysis of cADPR and P-cADPR are catalyzed by NAD(P) glycohydrolases, but the metabolic signals that regulate their metabolism are poorly understood. To investigate the physiological roles of cADPR and P-cADPR, it is essential to have methods that allow the routine measurement of these nucleotides in cellular systems. As described here, a sensitive and selective radioimmunoassay (RIA) for cADPR has been adapted to search for the natural occurrence of P-cADPR in mammalian tissues. Perchloric acid extracts prepared from bovine tissues and purified by anion exchange chromatography were found to contain immunoreactive material which was identified as P-cADPR. P-cADPR may play an important role in oxidative stress as a link between NADP(H) metabolism and alteration of intracellular Ca2+ homeostasis.

Adenosine Diphosphate Ribose↗