Abstract
The molecular basis for the absence of the C H1 domain in naturally occurring heavy-chain antibodies of the camelids was assessed by determining the entire Camelus dromedarius γ2a heavy-chain constant gene. The organization of the camel γ2a constant heavy-chain gene obtained from a liver genomic library appears to be typical of all other mammalian γ genes sequenced to date. It contains the switch, C H1, hinge, C H2, C H3, M1 and M2 exons. In contrast to the case in mouse and human heavy chain diseases, the camel γ2a gene shows no major structural defect, and its equivalent C H1 exon is intact. However, sequence analysis has revealed that the splicing site, immediately after the C H1 exon, is defective due to point mutations, especially the G +1 to A +1 transversion seems to be detrimental. It is concluded that the loss of the splice consensus signal is responsible for the removal of the entire C H1 domain in camel γ2a heavy-chain immunoglobulins. Additionally, a closer analysis of the hinge exon suggests the possible involvement of transposons in the genetic variation of mammalian C γ hinges.
Published Version
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