Structural analysis of the RH-like blood group gene products in nonhuman primates

Salvignol, I.; Calvas, Patrick; Socha, W. W.; Colin, Yves; Kim, Caroline Le Van; Bailly, Pascal; Ruffié, J; Cartron, Jean‐Pierre; Blancher, Antoine

doi:10.1007/bf00172151

Cited by 45 publications

(35 citation statements)

References 51 publications

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“…A recent report by Salvignol et al (1995) indicated that 330-Ser was present in a chimpanzee cDNA, but the 33 l-Ile and the silent substitution appear to be human specific and, therefore, may have arisen since the divergence of humans and apes. Chimpanzees and gorillas do not show any species-specific residues, as no amino acids unique to all members of either species were found.…”

Section: Pcr Amplification Of Exon 7from Genomic Dnamentioning

confidence: 99%

Investigation of the RH locus in gorillas and chimpanzees

Westhoff

Wylie

1996

J Mol Evol

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The human Rh blood-group system is encoded by two homologous genes, RhD and RhCE. The RH genes in gorillas and chimpanzees were investigated to delineate the phylogeny of the human RH genes. Southern blot analysis with an exon 7-specific probe suggested that gorillas have more than two RH genes, as has recently been reported for chimpanzees. Exon 7 was well conserved between humans, gorillas, and chimpanzees, although the exon 7 nucleotide sequences from gorillas were more similar to the human D gene, whereas the nucleotide sequences of this exon in chimpanzees were more similar to the human CE gene. The intron between exon 4 and exon 5 is polymorphic and can be used to distinguish the human D gene from the CE gene. Nucleotide sequencing revealed that the basis for the intron polymorphism is an Alu element in CE which is not present in the D gene. Examination of gorilla and chimpanzee genomic DNA for this intron polymorphism demonstrated that the D intron was present in all the chimpanzees and in all but one gorilla. The CE intron was found in three of six gorillas, but in none of the seven chimpanzees. Sequence data suggested that the Alu element might have previously been present in the chimpanzee RH genes but was eliminated by excision or recombination. Conservation of the RhD gene was also apparent from the complete identity between the 3'-noncoding region of the human D cDNA and a gorilla genomic clone, including an Alu element which is present in both species. The data suggest that at least two RH genes were present in a common ancestor of humans, chimpanzees, and gorillas, and that additional RH gene duplication has taken place in gorillas and chimpanzees. The RhCE gene appears to have diverged more than RhD among primates. In addition, the RhD gene deletion associated with the Rh-negative phenotype in humans seems to have occurred after speciation.

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Section: Pcr Amplification Of Exon 7from Genomic Dnamentioning

confidence: 99%

Investigation of the RH locus in gorillas and chimpanzees

Westhoff

Wylie

1996

J Mol Evol

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“…Thus, the absence of reactivity of LOR-15C9 with these variants strongly suggests that exon 7 encoded sequence of RhD (amino acids 314-358) is critical for the binding of LOR-15C9. This conclusion was supported by the reactivity of LOR-15C9 with red cells of nonhuman primates: (i) the reactivity of the antibody with D gor -positive red cells of gorilla 'Mabeke' is correlated with the presence of three D-specific residues Asp 350 -Gly 353 -Ala 354 in the region encoded by exon 7 of Mabeke's Rh-like cDNA (Salvignol et al, 1995); (ii) the motif Asp 350 -Gly 353 -Ala 354 was absent from all chimpanzee Rh-like polypeptides (Salvignol et al, 1995) and all chimpanzee red cell samples were found LOR-15C9 negative.…”

Section: Discussionmentioning

confidence: 87%

A human monoclonal anti‐D antibody which detects a nonconformation‐dependent epitope on the RhD protein by immunoblot

Apoil

Halverson

et al. 1997

Br J Haematol

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Summary.We describe the first human monoclonal anti-D (LOR-15C9) which reacts with a D-specific motif exposed either on a native form on intact D-positive red cells or on a denatured form of the RhD protein (33 kD), and detected by immunoblotting. LOR-15C9 was able to precipitate RhD but not RhcE proteins produced by in vitro transcriptiontranslation assays. The reactivity of the antibody, using panels of red cells with various partial D phenotypes known to lack some D epitopes and corresponding in RHD gene variants, suggested that LOR-15C9 reactivity depends on the portion of the RhD polypeptide encoded by the exon 7 (amino acids 314-358). These findings correlate well with the reactivity of LOR-15C9 with erythrocytes of some nonhuman primates (D gor -positive gorillas), but not of chimpanzee and Old or New World monkeys.In membrane proteins from partial D VI red cells, LOR-15C9 detected two proteins of molecular weight 33 and 21 kD; the presence of the latter was specific for category D VI and presumably represented the product of an alternatively spliced RHD VI transcript in these cells. This is consistent with the finding that LOR-15C9 can precipitate a shortened D protein mutant resulting from in vitro transcriptiontranslation and lacking amino-acids 163-313 encoded by exons 4-6. In addition, a 21 kD band polypeptide was detected by immunoblot in all red cell samples but D ¹¹ , using a rabbit anti-Rh polypeptide antibody (MPC8) raised against the C-terminal domain of Rh proteins. This 21 kD polypeptide most probably results from the translation of an alternatively spliced RHCE gene transcript.This study demonstrates that LOR-15C9 detects an epitope on the RhD protein that is independent of the membrane environment, and therefore could be a useful tool for the study of RhD polypeptides.

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“…Differences in the number of duplicated genes and pseudogenes have been reported in humans and chimpanzees. For example, chimpanzees have three copies of the RhD blood group gene (Westhoff and Wylie, 1996;Salvignol et al, 1995;Apoil and Blancher, 2000) and an additional triosephosphate isomerase pseudogene (Craig et al, 1991) in comparison to humans. The hominid lineage also underwent a duplication of V k immunoglobulin light-chain genes (Ermert et al, 1995).…”

Section: Gene Duplicationmentioning

confidence: 99%