A functional B cell antigen receptor is thought to regulate antibody gene rearrangement either by stopping further rearrangement (exclusion) or by promoting additional rearrangement (editing). We have developed a new model to study the regulation of antibody gene rearrangement. In this model, we used gene targeting to replace the JK region with a functional VIc-JK light chain gene. Two different strains of mice were created; one, VK4R, has a VK4-JK4 rearrangement followed by a downstream JK5 segment, while the other, VKSR, has a VKS-JK5 light chain. Here, we analyze the influence of these functional light chains on light chain rearrangement. We show that some V~ c4P, and VK8P, B cells only have the VKR light chain rearrangement, whereas others undergo additional rearrangements. Additional rearrangement can occur not only at the other K allele or isotype ()~), but also at the targeted locus in both VK4R and VK8R. Rearrangement to the downstream JK5 segment is observed in VK4R, as is deletion of the targeted locus in both VK4R and VKSR. The VKR models illustrate that a productively rearranged light chain can either terminate further rearrangement or allow further rearrangement. We attribute the latter to editing of autoantibodies and to corrections of dysfunctional receptors. lelic and isotypic exclusion lead to the expression of only one kind of antigen receptor per B cell. Exclusion is ensured by mechanisms that shut off antibody gene rearrangement (H/L-STOP), an idea based on the finding that at least 50% of plasmacytoma lines and approximately two thirds of murine splenic B cells have only one productively rearranged kappa locus, K+, whereas the other kappa locus in these cells is unrearranged, K~(1). This K+/~ genotype is not expected if rearrangements were to continue indefinitely. Exclusion is thought to be governed by the products of productively rearranged heavy (H) and light (L) chain genes. This hypothesis was tested in transgenic mice; it was demonstrated that a functional, transgene-encoded KL chain and H chain (contributed by endogenous rearrangement) prevented additional antibody gene rearrangements (2). The products of a productive H and L chain rearrangement may not always shut down further rearrangement. Ongoing~ c rearrangement has been inferred from the nature of circular excision products. These episomes, generated by deletional K recombination (3), sometimes contain VK-JK rearrangements, including rearrangements with productive junctions (4). Evidence consistent with ongoing rearrangement has also been obtained in autoantibody transgenic animals (5-7). It has been proposed that ongoing rearrangements allow autoreactive B cells to edit their receptors, thereby escaping tolerance induction (5-7).