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Ausgewählte Arbeiten, die Coulondre et al. 1978 / [1] \ PMID 355893; zitieren:

Orig

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DNA methylation: organ specific variations in the methyhtion pattern within and around ovalbumin and other chicken genes

J.L. Mandel and P. Chambon 1979

PMID 523314 PMC 342372 (freier Volltext)

"...If confirmed by further work, such a high variability in restriction sites for "CpG" nucleases would support the hypothesis (55) that the strikingly low "CpG" content in DNA from vertebrates might be due to a higher mutation rate for this dinucleotide [methyl cytosine being deaminated to thymine (4, 56)]. Methyl cytosines have been shown recently to be sites of mutational hot spots in E.coli (57). ..."

4. Holliday, R., and Pugh, J.E. (1975) Science 187, 226-232. \ Holliday & Pugh 1975 / PMID 1111098;[5]

55. Salser, W. (1977) Cold Spring Harbor Symp. Quant. Biol. 42, 985-1002. \ Salser 1977 / keine ID;[6]

56. Scarano, E. (1971) Adv. Cytopharmacol. 1, 13-24. \ Scarano 1971 / PMID 5163242;[7]

57. Coulondre, C., Miller, J.H., Farabaugh, P.J., and Gilbert, W. (1978) Nature 274, 775-780. \

Sequence analysis of cloned cDNA encoding part of an immunoglobulin heavy chain

John Rogers, Patrick Clarke and Winston Salser 1979

PMID 113776 PMC 327935 (freier Volltext)

"... There is a severe underabundance of the dinucleotide CG, comparable to that in total eukaryotic DNAs (44,45) and hemoglobin a genes (33,43,46). Demonstration that CG is not deficient in some other coding sequences, such as hemoglobin a genes (32,45), has ruled out earlier models in which it was proposed that ribosomes are unable to translate CGrich sequences effectively. Subsequently, it has been suggested that CG in eukaryotes is a hotspot for mutation (13). The mechanism may be methylation of the C followed by deamination to yield T (32,45). Coulondre et al. (47) have shown that methylated Cs in E. coli are indeed hotspots for mutation, and suggested the same deamination mechanism. ..."

13 Salser, W. (1977) Cold Spring Harbor Symp. Quant. Biol. 42, 987-1004 \ Salser 1977 / keine ID;

32 Heindell, H.C., Liu, A., Paddock, G.V., Studnicka, G.M. and Salser, W. (1978) Cell 15, 43-54 \[8] Heindell et al. 1978 PMID 699050

33 Efstratiadis, A., Kafatos, F.C. and Maniatis, T. (1977) Cell 10, 571-585 \[9] Efstratiadis et al. 1977 PMID 558827

43 Kafatos, F.C., Efstratiadis, A., Forget, B.G. and Weissman, S.M. (1977) Proc. Nat. Acad. Sci. USA 74, 5618-5622 \[10] Kafatos et al. 1977 / PMID 271989, PMC431834;

44 Russell, G.J., Walker, P.M.B., Elton, R.A. and Subak-Sharpe, J.H. (1976) J. Mol. Biol. 108, 1-23 \[11] / Russell et al. 1976 / PMID 1003479

45 Salser, W., Liu, A., Cummings, I., Strommer, J., Padayatty, J. and Clarke, P. (1978) in: Cellular and Molecular Regulation of Hemoglobin Switching, Stamatoyannopoulos, G. and Nienhuis, A., eds., Grune and Stratton, in press \ Salser et al. 1979, keine PMID; [12].

46 Konkel, D.A., Tilghman, S.M. and Leder, P. (1978) Cell 15, 1125-1132 \[13] / Konkel et al. 1978 / PMID 569555

47 Coulondre, C., Miller, J.H., Farabaugh, P.J. and Gilbert, W. (1978) Nature 274, 775-780 \[1] Coulondre et al. 1978 / PMID 355893;

Nucleic Acids Research, Vol. 20, No. 19 5119-5125

A comparison of the fidelity of copying 5-methylcytosine and cytosine at a defined DNA template site

Jiang-Cheng Shen, Steven Creighton, Peter A. Jones and Myron F. Goodman 1992

PMID 1383939 PMC 334293 (freier Volltext)

" ... An analysis of the mutational spectum of the lacI gene in E. coli revealed that high mutation rates occurred at mC DNA template loci (1,20). Subsequently, anomalously high mutation rates have been correlated with mC sites in procaryotic and eucaryotic organisms (21-24). The widely accepted model to account for these observations was originally proposed to explain the lacI mutational data (20). J. Miller and colleagues (20) proposed that mC-->T mutagenic hot spots could be accounted for by deamination of mC to form T. ..."

1. Coulondre, C., Miller, J. H., Farabaugh, P. J. and Gilbert, W. (1978) Nature, 274, 775-780. \[1] Coulondre et al. 1978 / PMID 355893;

20. Duncan, B. K. and Miller, J. H. (1980) Nature, 287, 560-561. \[14] Duncan et al. 1980 / PMID 6999365

21. Ehrlich, M., Zhang, X.-Y. and Inamdar, N. M. (1990) Mut. Res., 238, 277-286. \[15] Ehrlich et al. 1990/ PMID 2188124

22. Yatagai, F. and Glickman, B. W. (1990) Mut. Res., 243, 21-28. \[16] Yatagai et al. 1990 / PMID 2300081

23. Rideout, W. M. (HI), Coetzee, G. A., Olumi, A. F. and Jones, P. A. (1990) Science, 249, 1288-1290. \[17] Rideout et al. 1990 / PMID 1697983

24. Jones, P. A., Rideout, W. M. (III), Shen, J. -C., Spruck, C. H. and Tsai, Y. C. (1992) BioEssays, 14, 33-36. \[18] Jones et al. 1992 / PMID 1697983


EN

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Selected Articles citing Coulondre et al. 1978 / [1] \ PMID 355893:

"...If confirmed by further work, such a high variability in restriction sites for "CpG" nucleases would support the hypothesis (55: Salser 1977, keine ID;[6]) that the strikingly low "CpG" content in DNA from vertebrates might be due to a higher mutation rate for this dinucleotide [methyl cytosine being deaminated to thymine (4: Holliday & Pugh 1975, PMID 1111098;[5] | 56: Scarano 1971, PMID 5163242;[7]).

Methyl cytosines have been shown recently to be sites of mutational hot spots in E. coli (57: Coulondre et al. 1978, PMID 355893;[1]). ..."

"... There is a severe underabundance of the dinucleotide CG, comparable to that in total eukaryotic DNAs (44: Russell et al. 1976, PMID 1003479;[11] | 45: Salser et al. 1979, keine PMID;[12]) and hemoglobin a genes (33: Efstratiadis et al. 1977, PMID 558827;[9] | 43: Kafatos et al. 1977, PMID 271989;[10] | 46: Konkel et al. 1978, PMID 569555;[13]).

Demonstration that CG is not deficient in some other coding sequences, such as hemoglobin a genes (32: Heindell et al. 1978, PMID 699050;[8] | 45: Konkel et al. 1978, PMID 569555;[13]), has ruled out earlier models in which it was proposed that ribosomes are unable to translate CGrich sequences effectively.

Subsequently, it has been suggested that CG in eukaryotes is a hotspot for mutation (13: Salser 1977, keine ID;).

The mechanism may be methylation of the C followed by deamination to yield T (32: Heindell et al. 1978, PMID 699050;[8] , 45: Salser et al. 1979, keine PMID; [12]).

Coulondre et al. (47: Coulondre et al. 1978, PMID 355893;[1]) have shown that methylated Cs in E. coli are indeed hotspots for mutation, and suggested the same deamination mechanism. ..."

" ... An analysis of the mutational spectum of the lacI gene in E. coli revealed that high mutation rates occurred at mC DNA template loci (1: Coulondre et al. 1978, PMID 355893;[1] | 20: Duncan et al. 1980, PMID 6999365;[14]).

Subsequently, anomalously high mutation rates have been correlated with mC sites in procaryotic and eucaryotic organisms (21: Ehrlich et al. 1990/ PMID 2188124;[15] | 22: Yatagai et al. 1990, PMID 2300081;[16] | 23: Rideout et al. 1990, PMID 1697983;[17] | 24: Jones et al. 1992, PMID 1697983;[18]).

The widely accepted model to account for these observations was originally proposed to explain the lacI mutational data (20: Duncan et al. 1980, PMID 6999365;[14]).

J. Miller and colleagues (20: Duncan et al. 1980, PMID 6999365;[14]) proposed that mC-->T mutagenic hot spots could be accounted for by deamination of mC to form T. ..."

DE

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Ausgewählte Artikel, die Coulondre et al. 1978 / [1] \ PMID 355893 zitieren:

• --Mandel & Chambon 1979 / [2] \ PMID 523314, PMC 342372 (freier Volltext);

"... Durch weitere Arbeiten bestätigt, würde eine derart hohe Variabilität der Restriktionsstellen für "CpG "-Nucleasen die Hypothese stützen (55: Salser 1977, keine ID; [6]), dass der auffallend niedrige "CpG "-Gehalt in der DNA aus Wirbeltiere auf eine höhere Mutationsrate für dieses Dinukleotid zurückzuführen sein könnte {Methylcytosin, das zu Thymin desaminiert wird (4: Holliday & Pugh 1975, PMID 1111098;[5] | 56: Scarano 1971, PMID 5163242;[7]}.

In letzter Zeit wurde gezeigt, dass Methylcytosine Orte für mutationelle Hot Spots in E. coli sind (57: Coulondre et al. 1978, PMID 355893;[1]). ... "

• -- Rogers et al. 1979 / [3] \ PMID 113776, PMC 327935 (freier Volltext);

"... Das Dinukleotid CG weist einen schwerwiegenden Mangel auf, der mit dem geringen Gehalt in der gesamten eukaryotischen DNAs vergleichbar ist (44: Russell et al. 1976, PMID 1003479;[11] | 45: Salser et al. 1979, keine PMID;[12]) und dem geringen Gehalt in Hämoglobin-{alpha}-Genen vergleichbar ist (33: Efstratiadis et al. 1977, PMID 558827;[9] | 43: Kafatos et al. 1977, PMID 271989;[10] | 46: Konkel et al. 1978, PMID 569555;[13]).

Die Demonstration, dass CG in einigen anderen kodierenden Sequenzen, wie Hämoglobin-{alpha}-Genen, nicht defizient ist (32: Heindell et al. 1978, PMID 699050;[8] | 45: Konkel et al. 1978, PMID 569555;[13]), hat frühere Modelle bedingt, in denen vorgeschlagen wurde, dass die CG-reiche Sequenzen von Ribosomen nicht effektiv translatiert werden können.

In der Folge wurde vorgeschlagen, dass CG in Eukaryoten ein Hotspot für Mutationen ist (13: Salser 1977, keine ID;).

Der Mechanismus kann die Methylierung des C sein, gefolgt von der Desaminierung, um T zu ergeben (32: Heindell et al. 1978, PMID 699050;[8] , 45: Salser et al. 1979, keine PMID; [12]).

Coulondre et al. (47: Coulondre et al. 1978, PMID 355893;[1]) haben gezeigt, dass methylierte Cs in E. coli in der Tat Hotspots für Mutationen sind und den gleichen Desaminierungsmechanismus nahelegen. ... "


• -- Shen et al. 1992 / [4] \ PMID 1383939, PMC 334293 (freier Volltext);

"... Eine Analyse des Mutationsspektums des lacI-Gens in E. coli ergab, dass an mC-DNA-Template-Loci hohe Mutationsraten vorlagen(1: Coulondre et al. 1978, PMID 355893;[1] | 20: Duncan et al. 1980, PMID 6999365;[14]).

Anomal hohe Mutationsraten wurden anschließend mit mC-Stellen in prokaryontischen und eukaryontischen Organismen korreliert (21: Ehrlich et al. 1990/ PMID 2188124;[15] | 22: Yatagai et al. 1990, PMID 2300081;[16] | 23: Rideout et al. 1990, PMID 1697983;[17] | 24: Jones et al. 1992, PMID 1697983;[18]).

Das weithin akzeptierte Modell zur Berücksichtigung dieser Beobachtungen wurde ursprünglich zur Erklärung der lacI-Mutationsdaten vorgeschlagen (20: Duncan et al. 1980, PMID 6999365;[14]).

J. Miller und Kollegen (20: Duncan et al. 1980, PMID 6999365;[14]) schlugen vor, dass die mutagenen mC-->T-Hot-Spots durch die Desaminierung von mC zur Bildung von T. erklärt werden könnten. "

Coulondre et al. (47: Coulondre et al. 1978, PMID 355893; [1]) haben gezeigt, dass methylierte Cs in E. coli in der Tat Hotspots für Mutationen sind und den gleichen Desaminierungsmechanismus nahelegen. ... "

  • -- Shen et al. 1992 ---- lacI mutational data (20: Duncan et al. 1980, PMID 6999365;[14]).

J. Miller and colleagues (20: Duncan et al. 1980, PMID 6999365;[14]) proposed that mC-->T mutagenic hot spots could be accounted for by deamination of mC to form T. ..."

Einzelnachweise

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  1. ↑ a b c d e f g h i j k C. Coulondre, J. H. Miller, P. J. Farabaugh, W. Gilbert: Molecular basis of base substitution hotspots in Escherichia coli. In: Nature. Band 274, Nummer 5673, August 1978, S. 775–780, PMID 355893.
  2. ↑ a b J. L. Mandel, P. Chambon: DNA methylation: organ specific variations in the methylation pattern within and around ovalbumin and other chicken genes. In: Nucleic Acids Research. Band 7, Nr. 8, 1979, ISSN 0305-1048, S. 2081–2103, PMID 523314.
  3. ↑ a b c J. Rogers, P. Clarke, W. Salser: Sequence analysis of cloned cDNA encoding part of an immunoglobulin heavy chain. In: Nucleic Acids Research. Band 6, Nr. 10, 1979, ISSN 0305-1048, S. 3305–3321, PMID 113776.
  4. ↑ a b c J. C. Shen, S. Creighton, P. A. Jones, M. F. Goodman: A comparison of the fidelity of copying 5-methylcytosine and cytosine at a defined DNA template site. In: Nucleic Acids Research. Band 20, Nr. 19, 1992, ISSN 0305-1048, S. 5119–5125, PMID 1383939.
  5. ↑ a b c R. Holliday, J. E. Pugh: DNA modification mechanisms and gene activity during development. In: Science. Band 187, Nummer 4173, Januar 1975, S. 226–232, PMID 1111098.
  6. ↑ a b c W. Salser.: Globin mRNA sequences: analysis of base pairing and evolutionary implications. Hrsg.: Cold Spring Harbor Symp. Quant. Biol. Band 42. Cold Spring Harbor 1977, S. 985–1002.
  7. ↑ a b c E. Scarano: The control of gene function in cell differentiation and in embryogenesis. In: Advances in cytopharmacology. Band 1, Mai 1971, S. 13–24, PMID 5163242.
  8. ↑ a b c d e H. C. Heindell, A. Liu, G. V. Paddock, G. M. Studnicka, W. A. Salser: The primary sequence of rabbit alpha-globin mRNA. In: Cell. Band 15, Nr. 1, 1978, ISSN 0092-8674, S. 43–54, PMID 699050.
  9. ↑ a b c A. Efstratiadis, F. C. Kafatos, T. Maniatis: The primary structure of rabbit beta-globin mRNA as determined from cloned DNA. In: Cell. Band 10, Nr. 4, 1977, ISSN 0092-8674, S. 571–585, PMID 558827.
  10. ↑ a b c F. C. Kafatos, A. Efstratiadis, B. G. Forget, S. M. Weissman: Molecular evolution of human and rabbit beta-globin mRNAs. In: Proceedings of the National Academy of Sciences of the United States of America. Band 74, Nr. 12, 1977, ISSN 0027-8424, S. 5618–5622, PMID 271989.
  11. ↑ a b c G. J. Russell, P. M. Walker, R. A. Elton, J. H. Subak-Sharpe: Doublet frequency analysis of fractionated vertebrate nuclear DNA. In: Journal of Molecular Biology. Band 108, Nr. 1, 1976, ISSN 0022-2836, S. 1–23, PMID 1003479.
  12. ↑ a b c d e Salser et al. (1979); bei Rogers et al. (1979, PMID 113776) wird als Referenz Nr. 45 folgendes angegeben: „Salser, W., Liu, A., Cummings, I., Strommer, J., Padayatty, J. and Clarke, P. (1978) in: Cellular and Molecular Regulation of Hemoglobin Switching, Stamatoyannopoulos, G. and Nienhuis, A., eds., Grune and Stratton, in press“.
  13. ↑ a b c d e D. A. Konkel, S. M. Tilghman, P. Leder: The sequence of the chromosomal mouse beta-globin major gene: homologies in capping, splicing and poly(A) sites. In: Cell. Band 15, Nr. 4, 1978, ISSN 0092-8674, S. 1125–1132, PMID 569555.
  14. ↑ a b c d e f g h i B. K. Duncan, J. H. Miller: Mutagenic deamination of cytosine residues in DNA. In: Nature. Band 287, Nr. 5782, 1980, ISSN 0028-0836, S. 560–561, PMID 6999365.
  15. ↑ a b c M. Ehrlich, X. Y. Zhang, N. M. Inamdar: Spontaneous deamination of cytosine and 5-methylcytosine residues in DNA and replacement of 5-methylcytosine residues with cytosine residues. In: Mutation Research. Band 238, Nr. 3, 1990, ISSN 0027-5107, S. 277–286, PMID 2188124.
  16. ↑ a b c F. Yatagai, B. W. Glickman: Specificity of spontaneous mutation in the lacI gene cloned into bacteriophage M13. In: Mutation Research. Band 243, Nr. 1, 1990, ISSN 0027-5107, S. 21–28, PMID 2300081.
  17. ↑ a b c W. M. Rideout, G. A. Coetzee, A. F. Olumi, P. A. Jones: 5-Methylcytosine as an endogenous mutagen in the human LDL receptor and p53 genes. In: Science (New York, N.Y.). Band 249, Nr. 4974, 1990, ISSN 0036-8075, S. 1288–1290, PMID 1697983.
  18. ↑ a b c W. M. Rideout, G. A. Coetzee, A. F. Olumi, P. A. Jones: 5-Methylcytosine as an endogenous mutagen in the human LDL receptor and p53 genes. In: Science (New York, N.Y.). Band 249, Nr. 4974, 1990, ISSN 0036-8075, S. 1288–1290, PMID 1697983.
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