An increase in the number of recombinant molecules and other effects of the simultaneous allotype suppression of trans-chromosomal a VH and n Cmu Ig gene products.

The concomitant effects of trans-chromosomal allotype suppression of both an a VH and an n Cmu locus allotype in multiheterozygous rabbits were investigated. For example of the expression of the a2 VH and n81 Cmu allotypes were suppressed in a multiheterozygous rabbit having the a1 chi-y-n81de12,15f73g74/a2 chi 32y33n80de12.14f69g77 genotype. This trans-chromosomal allotype suppression led to the concomitant suppression of other CH allotypes in the same parental haplotype as the suppressed-n81 allotype (i.e. the e15, f73 and g74 allotype) and the partial suppression of the a1 VH allotype (from the normal level of 70% of the total Ig to 10%), and also led to compensation by other VH allotypes from the same parental haplotype as the suppressed-a2 allotype (i.e. the x32 and y33 allotypes). The x32 and y33 allotypes were expressed on Ig molecules with the CH allotypes coded by the same haplotype (i.e. the cis molecules). In a further analysis of the IgG molecules having the partially-suppressed-a1 allotype, one-half (5%) of these molecules were trans-chromosomal recombinant molecules (i.e. a1e14 IgG) and the other half (5%) were cis-chromosomal molecules (i.e. a1e15 IgG). The trans-chromosomal a1e14 IgG molecules probably were derived from the expansion of a limited number of lymphoid clones that normally produce only 1.5% trans-chromosomal recombinant molecules. The cis-chromosomal a1e15 IgG molecules were probably derived either from lymphoid clones that survived the suppression by the anti-n81 Ab, or from lymphoid clones that bore a different subclass of IgM (i.e. n-negative IgM).