Mice whose IgH alleles are engineered to encode two distinct antibody
heavy (H) chains generate a normal-sized B cell compartment in which m
ost cells stably express the two heavy chains. This demonstrates that
''toxicity'' of bi-allelic H chain expression and cell-autonomous mech
anisms of silencing in-frame IgH gene rearrangements do not significan
tly contribute to allelic exclusion at the IgH locus. Notwithstanding,
the stability of the various engineered IgH loci during B cell develo
pment in the bone marrow differed substantially from each other.