Intra- and interspecies analyses of the carcinoembryonic antigen (CEA) gene family reveal independent evolution in primates and rodents

Abstract

Summary. Various rodent and primate DNAsexhibit a stronger intra-than interspecies cross-hybridization with probes derived from the N-terminal domain exons of human and rat carcinoembryonic antigen (CEA)-like genes. Southern analyses also reveal that the human and rat CEA gene families are of similar complexity. We counted at least 10 different genes per human haploid genome. In the rat, approximately seven to nine different N-terminal domain exons that presumably represent different genes appear to be present. We were able to assign the corresponding genomic restriction endonuclease fragments to already isolated CEA gene family members of both human and rat. Highly similar subgroups, as found within the human CEA gene family, seem to be absent from the rat genome. Hybridization with an intron probe from the human nonspecific cross-reacting antigen (NCA) gene and analysis of DNA sequence data indicate the conservation of noncoding regions among CEA-like genes within primates, implicating that whole gene units may have been duplicated. With the help of a computer program and by calculating the rate of synonymous substitutions, evolutionary trees have been derived. From this, we propose that an independent parallel evolution, leading to different CEA gene families, must have taken place in, at least, the primate and rodent orders.

The human pregnancy-specific glycoprotein genes are tightly linked on the long arm of chromosome 19 and are coordinately expressed

“…This suggests that during evolution, the IgC-like exon pairs within a primordial gene duplicated prior to the whole gene unit, whose own duplication gave rise to new PSG genes more recently. This supplements the evolutionary models which we have reported elsewhere (17,40). (5) and FL-NCA3 (h), respectively, both contain stop codons.…”

Characterization of murine carcinoembryonic antigen gene family members

“…None of these subgroups or individual genes, however, can be assigned to a human counterpart. This is probably owing to a rapid evolution of the CEA-related genes after separation of the primate and rodent orders (Rudert et al 1989). Rodent subgroup 1 contains the murine genes mmCGM1 and mmCGM2 (McCuaig et al 1992;Turbide et al 1991) and the rat gene coding for ectoATPase (Lin and Guidotti 1989), which was recently shown to be identical to C-CAM 105 (Aurivillius et al 1990).…”

“…For the cosmid library the following mixture of [32p]labeled genomic and cDNA probes was used: The 289-bp HindIII/BamHI fragment from XrnCGM2-1 (Rudert et al 1989), the 661-bp PvuII/PstI fragment from XrnCGM3-1, as well as the 748-bp SstI/BamHI fragment from XrnCGM4/5-1 (Kodelja et al 1989) and the EcoRI cDNA inserts of XrnCGMla and XrnCGMlb (Rebstock et al 1990). The cDNA library was screened with the 296 bp XmnI/EcoRI fragment from XrnCGMI-I (Rudert et al 1989). The filters were washed at low stringency in 2 x SSPE, 0.1% SDS at 60~ (1 x SSPE: 180 mM NaCI, 10 mM sodium phosphate pH 7.4, 1 mM EDTA).…”

“…Several immunoglobulin variable-like (IgV) domains are followed by one immunoglobulin constant-like (IgC) domain (Rebstock et al 1990), whereas one IgV and two or three IgC domains are present in human PSGs . These observations, together with detailed "silent site" mutation analyses, imply that the CEA gene families have evolved independently in rodents and primates (Rudert et al 1989). For these reasons, a direct assignment of individual members or subgroups of the rodent CEA gene family to their human counterparts simply by sequence comparisons has not been possible.…”

Transcriptional regulation of the non‐specific cross‐reacting antigen gene, a member of the carcinoembryonic antigen gene family up‐regulated in colorectal carcinomas

“…This that was active only in the NCA non-expressing cell lines tested. Our results with constructs containing as much as 1240 bp upstream of the translational start site indicated no cell-type specinally generated by the replication of a single gene [44]. As has ficity for expression, so it is possible that such specificity is at commonly been observed in the course of evolutionary drift, least partially conferred by this novel regulatory element.…”