Class (Switch) Wars

THE DEAMINATOR:© 2004 Cell PressTwo proposed models of activation-induced cytidine deaminase activity. At left AID edits RNA allowing translation of a functional DNA endonuclease that works on both variable (V) and switch (S) region DNA. This results in somatic hypermutation (SHM) through nicks and error prone repair and class switch recombination (CSR) through staggered nicks and nonhomologous DNA end-joining (NHEJ). An alternative model proposes that AID modifies DNA directly and that CSR

Written byAileen Constans

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Two proposed models of activation-induced cytidine deaminase activity. At left AID edits RNA allowing translation of a functional DNA endonuclease that works on both variable (V) and switch (S) region DNA. This results in somatic hypermutation (SHM) through nicks and error prone repair and class switch recombination (CSR) through staggered nicks and nonhomologous DNA end-joining (NHEJ). An alternative model proposes that AID modifies DNA directly and that CSR and SHM occur through uracil-DNA glycosylase (UNG). (From T. Honjo et al., Immunity, 20:659–68, 2004.)

A battle of sorts has been brewing over the contribution to antibody diversity made by a B-cell specific protein called activation-induced cytidine deaminase (AID). This issue's Hot Papers present AID as a DNA mediator and dismantle predictions that AID works on RNA. By clearing some experimental inconsistencies, the new hypothesis has become popular, but not everyone agrees with the newfound DNA-editing role.

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