The occurrence and distribution of thymine and three methylated-adenine bases in ribonucleic acids from several sources

Littlefield, John W.; Dunn, David B.

doi:10.1042/bj0700642

Cited by 210 publications

(38 citation statements)

References 35 publications

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“…AdoMet concentrations varied in direct proportion to (30,31). An alkaline hydrolysate of unfractionated RNA was treated with alkaline phosphatase, and nucleosides were separated by high-performance liquid chromatography in a system that gives good separation between 5-methylcytidine, 5-methyluridine, and other pyrimidine nucleosides and bases.…”

Section: Resultsmentioning

confidence: 99%

S -Adenosylhomocysteine toxicity in normal and adenosine kinase-deficient lymphoblasts of human origin

Kredich

Hershfield

1979

Proc. Natl. Acad. Sci. U.S.A.

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The human lymphoblast line WI-L2 is subject to growth inhibition by a combination of the adenosine deaminase (ADA; adenosine aminohydrolase, EC 3.5.4.4.) inhibitor erythro-9-2-hydroxy-3-nonyl)adenine (EHNA) and adenosine.Although adenosine-induced pyrimidine starvation appears to contribute to this effect, uridine only partially reverses adenosine toxicity in WI-L2 and not at all in strain 107, an adenosine kinase(ATP:adenosine 5'-phosphotransferase, EC 2.7.1.20) deficient derivative of WI-L2. Treatment of both cell lines with EHNA and adenosine leads to striking elevations in intracellular S-adenosyl-L-homocysteine (AdoHcy), a potent inhibitor of Sadenosyl-L-methionine (AdoMet)-dependent methylation reactions. The methylation in vivo of both DNA and RNA is inhibited by concentrations of EHNA and adenosine that elevate intracellular AdoHcy. Addition of 100 jiM L-homocysteine thiolactone to cells treated with EHNA and adenosine enhances adenosine toxicity and further elevates Adolcy to levels approximately 60-fold higher than those obtained in the absence of this amino acid, presumably by combining with adenosine to form AdoHcy in a reaction catalyzed by S-adenosylhomocysteine hydrolase (EC 3.3.1.1). In the adenosine kinase-deficient strain 107, a combination of ADA inhibition and L-homocysteine thiolactone markedly increases intracellular AdoHcy and inhibits growth even in the absence of exogenous adenosine. These results demonstrate a form of toxicity from endogenously produced adenosine and support the view that AdoHcy, by inhibiting methylation, is a mediator of uridine-resistant adenosine toxicity in these human lymphoblast lines. Furthermore, they suggest that AdoHcy may play a role in the pathogenesis of the severe combined immunodeficiency disease found in most children with heritable ADA deficiency.

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Section: Resultsmentioning

confidence: 99%

S -Adenosylhomocysteine toxicity in normal and adenosine kinase-deficient lymphoblasts of human origin

Kredich

Hershfield

1979

Proc. Natl. Acad. Sci. U.S.A.

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“…Nucleoside modifications of rRNA were reported almost 50 years ago (Littlefield and Dunn, 1958a;Littlefield and Dunn, 1958b;Smith et al, 1992) and are found in all organisms. They occur mostly on the pre-rRNA during ribosome synthesis and essentially consist of two types: methylation of the 29-hydroxyl group of sugar residues (29-O-methylation) and conversion of uridine residues to pseudouridine by base rotation.…”

Section: Box 2 Role Of Small Nucleolar (Sno)rnps In Rrna Modificatiomentioning

confidence: 99%

Eukaryotic ribosome biogenesis at a glance

Thomson

Ferreira-Cerca

Hurt

2013

Journal of Cell Science

269

249

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Summary Ribosomes play a pivotal role in the molecular life of every cell. Moreover, synthesis of ribosomes is one of the most energetically demanding of all cellular processes. In eukaryotic cells, ribosome biogenesis requires the coordinated activity of all three RNA polymerases and the orchestrated work of many (>200) transiently associated ribosome assembly factors. The biogenesis of ribosomes is a tightly regulated activity and it is inextricably linked to other fundamental cellular processes, including growth and cell division. Furthermore, recent studies have demonstrated that defects in ribosome biogenesis are associated with several hereditary diseases. In this Cell Science at a Glance article and the accompanying poster, we summarise the current knowledge on eukaryotic ribosome biogenesis, with an emphasis on the yeast model system.

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“…The ultraviolet absorption spectrum of nucleoside N* exhibits the maximum at 265 nm (Fig. 3A, inset) and is similar to that of 5-methyluridine (mW ; Littlefield and Dunn, 1958) rather than that of mnm5 s' U (Shaw et al, 1958). By using the molar absorption coefficient of m5U (Cline et al, 1959), the amount of nucleoside N* was estimated to be much the same as those of m' U and 2-thiocytidine (s'C) each of which occupies a single position in argU tRNA.…”

Section: Modified Nucleotide (Pn*) In Position 34 Of Argu Trnamentioning

confidence: 76%

A modified uridine in the first position of the anticodon of a minor species of arginine tRNA, the argU gene product, from Escherichia coli

Sakamoto

Kawai

Niimi

et al. 1993

European Journal of Biochemistry

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The argU (dnaY) gene product, a minor tRNAArg, from Escherichia coii has the anticodon N*CU with an unidentified modified nucleoside N* in position 34 [Kiesewetter, S., Fisher, W. & Sprinzl, M. (1987) Nucleic Acids Res. 15, 3184]. In the present study, argU tRNA was purified from E. coli A 19 strain and nucleoside N* was characterized by the TLC and HPLC analyses. Nucleoside N* was found to be different from any naturally occurring modified nucleosides. From unfractionated E. coli tRNA species, nucleoside N* was prepared in an amount sufficient for 1H‐NMR experiments. By the analyses of one‐dimensional and two‐dimensional NMR spectra, nucleoside N* was suggested to be 5‐methylaminomethyluridine (mnm5U), which was confirmed by comparison with a chemically synthesized preparation of mnm5U. Thus, the occurrence of mnm5U in mature tRNA was found for the first time. Further, the modification of U(34) to mnm5U in this tRNA was found to contribute to the strict recognition of two degenerate codons terminating in A and G.

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The occurrence and distribution of thymine and three methylated-adenine bases in ribonucleic acids from several sources

Cited by 210 publications

References 35 publications

S -Adenosylhomocysteine toxicity in normal and adenosine kinase-deficient lymphoblasts of human origin

S -Adenosylhomocysteine toxicity in normal and adenosine kinase-deficient lymphoblasts of human origin

Eukaryotic ribosome biogenesis at a glance

A modified uridine in the first position of the anticodon of a minor species of arginine tRNA, the argU gene product, from Escherichia coli

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