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There are many indications that the mutations at A·T (deoxyadenosine·deoxythymidine) pairs during somatic hypermutation (SHM) are introduced by mutagenic patch repair of activation-induced
deaminase (AID)-generated U·G (deoxyuridine· deoxyguanosine) lesions. Franklin and Blanden rightly state that a popular model is that these mutations are caused by DNA-polymerase-catalysed
incorporation of improperly paired bases during the patch-repair process (that is, polymerase error), whereas we have recently postulated that DNA-polymerase-catalysed incorporation of U
residues, instead of T residues, opposite A residues might provide an alternative mechanism (that is, dUTP (deoxyuridine triphosphate) incorporation)1.
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