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pubmed-article:2345133pubmed:abstractTextExtracellular nonreplicating bacteriophage T4 particles accumulate mutations as functions of temperature, time, pH, and ionic environment via two mechanisms: 5-hydroxymethylcytidine deamination produces G.C----A.T transitions while a guanosine modification produces transversions. Neither frameshift mutations nor mutations at A.T base pairs are appreciably induced. We now show that heat induces G.C----T.A transversions which we suggest may arise via a G*.A mispair, in which G* is a modified guanosine that has experienced a glycosylic bond migration. The rate of this reaction at 37 degrees C is sufficient to present a genetic hazard, particularly to large genomes; thus, the lesion is probably efficiently repaired in cellular genomes.lld:pubmed
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pubmed-article:2345133pubmed:authorpubmed-author:DrakeJ WJWlld:pubmed
pubmed-article:2345133pubmed:authorpubmed-author:KrickerM CMClld:pubmed
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pubmed-article:2345133pubmed:volume172lld:pubmed
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pubmed-article:2345133pubmed:pagination3037-9lld:pubmed
pubmed-article:2345133pubmed:dateRevised2009-11-18lld:pubmed
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pubmed-article:2345133pubmed:year1990lld:pubmed
pubmed-article:2345133pubmed:articleTitleHeat mutagenesis in bacteriophage T4: another walk down the transversion pathway.lld:pubmed
pubmed-article:2345133pubmed:affiliationLaboratory of Molecular Genetics, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709.lld:pubmed
pubmed-article:2345133pubmed:publicationTypeJournal Articlelld:pubmed
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