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'''Depurination''' is a [[DNA]] alteration in which the hydrolysis of the beta-N-glycocidic link between a [[purine]] base (Adenine or Guanine) and the [[deoxyribose]]-[[phosphate]] backbone occurs. After a depurination, the sugar phosphate backbone remains and the sugar ring has a [[hydroxyl]] (-OH) group in the place of the Adenine or Guanine. Studies estimate that as many as 10,000 Purines are lost this way each day in a typical human cell, however this represents only 1/30,000 of the human genome.<ref name=instability> Lindahl T. (1993) ''[[Instability and decay of the primary structure of DNA.]]'' Nature 103; 362:709-715; {{}} </ref> One of the main causes of depurination is the presence of endogenous metabolites in cell undergoing chemical reactions. This breaks the bond linking the purine with the pentose sugar. Depurinations are efficiently repaired by portions of the [[Base excision repair]] (BER) pathway, and very few depurinations lead to mutations.
'''Depurination''' is an alteration of [[DNA]] in which the [[purine]] base ([[Adenine]] or [[Guanine]])is removed from the [[deoxyribose]] sugar by hydrolysis of the beta-N-glycosidic link between them. After depurination, the sugar phosphate backbone remains and the sugar ring has a [[hydroxyl]] (-OH) group in the place of the purine. Studies estimate that as many as 10,000 purines are lost this way each day in a typical human cell, however this represents only 1/30,000 of the human genome.<ref name=instability> Lindahl T. (1993) ''[[Instability and decay of the primary structure of DNA.]]'' Nature 103; 362:709-715; {{}} </ref> One of the main causes of depurination is the presence of endogenous metabolites in cell undergoing chemical reactions. Depurinated bases in double-stranded DNA are efficiently repaired by portions of the [[Base Excision Repair]] (BER) pathway. Depurinated bases in single-stranded DNA undergoing [[replication]] can lead to [[mutations]], because in the absence of information from the complementary strand, BER can add an incorrect base at the apurinic site, resulting in either a [[transition]] or [[transversion]] mutation[http://www.mun.ca/biology/scarr/Depurination_transversion.html]. Loss of [[pyrimidine]] bases ([[Cytosine]] and [[Thymine]]) occurs by a similar mechanism, but at a substantially lower rate.


Hydroyltic depurination is one of the principle forms of damage to [[ancient DNA]] in fossil or subfossil material, since the base remains unreparied. This results in both loss of information (the base sequence), and difficulties in ''in vitro'' replication of the damaged molecule by the [[polymerase chain reaction]].
N.B. depurination can occur on pyrimidine bases also, but at a substantially lower rate


==References==
==References==

Revision as of 15:31, 3 August 2009

Depurination is an alteration of DNA in which the purine base (Adenine or Guanine)is removed from the deoxyribose sugar by hydrolysis of the beta-N-glycosidic link between them. After depurination, the sugar phosphate backbone remains and the sugar ring has a hydroxyl (-OH) group in the place of the purine. Studies estimate that as many as 10,000 purines are lost this way each day in a typical human cell, however this represents only 1/30,000 of the human genome.[1] One of the main causes of depurination is the presence of endogenous metabolites in cell undergoing chemical reactions. Depurinated bases in double-stranded DNA are efficiently repaired by portions of the Base Excision Repair (BER) pathway. Depurinated bases in single-stranded DNA undergoing replication can lead to mutations, because in the absence of information from the complementary strand, BER can add an incorrect base at the apurinic site, resulting in either a transition or transversion mutation[1]. Loss of pyrimidine bases (Cytosine and Thymine) occurs by a similar mechanism, but at a substantially lower rate.

Hydroyltic depurination is one of the principle forms of damage to ancient DNA in fossil or subfossil material, since the base remains unreparied. This results in both loss of information (the base sequence), and difficulties in in vitro replication of the damaged molecule by the polymerase chain reaction.

References

  1. ^ Lindahl T. (1993) Instability and decay of the primary structure of DNA. Nature 103; 362:709-715; {{}}

Hartwell, Hood, Goldberg, Reynolds, Silver, Veres. Genetics: From Genes to Genomes. Second Edition. McGraw-Hill Companies Inc. New York, NY: 2004.

Weinberg. The Biology of Cancer. First Edition. Garland Science. 2006

Alberts, Johnson, Lewis, Raff, Roberts, Walter. "Molecular Biology of the Cell". Fourth Edition. Garland Science. New York, NY: 2002.