A Human t-Complex-Related Gene (TCP1) Is Not Closely Linked to the HLA Complex

Abstract

The t-complex of the mouse constitutes a 20 to 30 megabasepairs long genetic region on the centromeric part of chromosome 17 in linkage with the major histocompatibility complex (MHC), the H-2 system (1,2). Due to some bizarre genetic properties, this region has attracted considerable interest, and the possible existence of a human homologue of the t-complex has been controversial (3,4,5). A mouse chromosome 17 can either carry a t haplotype, which often occurs among wild mice, or the “wild type” (+) form. Since t haplotypes are transmitted at a much higher than the expected 50% ratio from male t/+ mice to their offspring, recessive male sterility or embryonic lethality genes which are part of these haplotypes, remain in the population (6). All complete t haplotypes are distinguished from standard chromosome 17 DNA by two nonoverlapping large inversions (7–10), as a consequence of which recombination between t haplotypes and wild type DNA is suppressed. If t haplotypes existed in humans at an analogous chromosomal position, this property could contribute to linkage disequilibrium in the HLA complex. To clarify this question, we have determined the chromosomal localization of the human homologue (TCP1) (11) of the Tcp-1 locus which is part of the proximal t-complex and codes for an abundant testicular germ cell protein in the mouse.