Rat Encodes the Paralogous Gene Equivalent of the Human Histo-blood Group ABO Gene

Iwamoto, Sadahiko; Kumada, Maki; Kamesaki, Toyomi; Okuda, Hiroshi; Kajii, Eiji; Inagaki, Takeshi; Saikawa, Daisuke; Takeuchi, Kouichi; Ohkawara, Sigeo; Takahashi, Riichi; Ueda, Shigetomo; Inoue, Seiichiro; Tahara, Kazunori; Hakamata, Yoji; Kobayashi, Eiji

doi:10.1074/jbc.m206439200

Cited by 21 publications

(8 citation statements)

References 30 publications

(25 reference statements)

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“…Thus the frequencies of the different A and B phenotypes (A+B+, A+B− and A−B−) in the various populations that we studied cannot be explained by the polymorphism of a single ABO gene as in humans and our preliminary genetic analysis indicates that there are at least 6 Abo genes in rabbits located in tandem in the genome. A similar situation has already been described in rats which have been reported to have a variable number of Abo genes (up to 5), with some genes encoding A enzymes and others encoding B enzymes [36], [37]. Therefore, despite a generally conserved expression of ABH antigens across mammalian species, the genetic mechanisms leading to diversity of expression and intraspecies polymorphism are quite variable.…”

Section: Discussionsupporting

confidence: 63%

Histo-Blood Group Antigens Act as Attachment Factors of Rabbit Hemorrhagic Disease Virus Infection in a Virus Strain-Dependent Manner

Gall-Reculé²,

et al. 2011

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Rabbit Hemorrhagic disease virus (RHDV), a calicivirus of the Lagovirus genus, and responsible for rabbit hemorrhagic disease (RHD), kills rabbits between 48 to 72 hours post infection with mortality rates as high as 50–90%. Caliciviruses, including noroviruses and RHDV, have been shown to bind histo-blood group antigens (HBGA) and human non-secretor individuals lacking ABH antigens in epithelia have been found to be resistant to norovirus infection. RHDV virus-like particles have previously been shown to bind the H type 2 and A antigens. In this study we present a comprehensive assessment of the strain-specific binding patterns of different RHDV isolates to HBGAs. We characterized the HBGA expression in the duodenum of wild and domestic rabbits by mass spectrometry and relative quantification of A, B and H type 2 expression. A detailed binding analysis of a range of RHDV strains, to synthetic sugars and human red blood cells, as well as to rabbit duodenum, a likely gastrointestinal site for viral entrance was performed. Enzymatic cleavage of HBGA epitopes confirmed binding specificity. Binding was observed to blood group B, A and H type 2 epitopes in a strain-dependent manner with slight differences in specificity for A, B or H epitopes allowing RHDV strains to preferentially recognize different subgroups of animals. Strains related to the earliest described RHDV outbreak were not able to bind A, whereas all other genotypes have acquired A binding. In an experimental infection study, rabbits lacking the correct HBGA ligands were resistant to lethal RHDV infection at low challenge doses. Similarly, survivors of outbreaks in wild populations showed increased frequency of weak binding phenotypes, indicating selection for host resistance depending on the strain circulating in the population. HBGAs thus act as attachment factors facilitating infection, while their polymorphism of expression could contribute to generate genetic resistance to RHDV at the population level.

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Section: Discussionsupporting

confidence: 63%

Histo-Blood Group Antigens Act as Attachment Factors of Rabbit Hemorrhagic Disease Virus Infection in a Virus Strain-Dependent Manner

Gall-Reculé²,

et al. 2011

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“…Cloning of genomic and complementary DNA sequences from murine ABO gene equivalents has confirmed the earlier suggestion that such sequences are arranged around exonintron units similar but not identical to human counterpart [2]. In addition, the transgenic technology gives promising results, rats being able to encode paralogous gene equivalents of the human histo-blood group ABO genes [10]. It will also be possible to produce knockout (group O) mice at the ABO locus using cloned genomic DNA sequence from the murine AB gene.…”

Section: Animal Experiments With Abo Histo-blood Groups Now Becoming supporting

confidence: 51%

ABO histo-blood group system-incompatible allografting

Nydegger¹,

Mohaçsi²,

Koestner³

et al. 2005

International Immunopharmacology

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“…1 A (AGG) and 2 B (MGA) gene sequences, rather than 1 A and 3 B , were mapped for this strain. In another strain, Wistar, 3 A and 1 B gene sequences were cloned although they have not been mapped33. Different cloning results were obtained from inbred GOT-W strain35 and the BDIX strain36, further complicating the understanding of rat ABO genes.…”

Section: Resultsmentioning

confidence: 99%

“…Even if sequence alignment all failed from the same caveats, the case still stands with rats at least. Because three different A and one B gene sequences were cloned from a single Wistar rat, they cannot be allelic at a single genetic locus3337.…”

Section: Resultsmentioning

confidence: 99%

“…However, because this was observed in several different species, it seems unlikely that all those findings may be artifacts. In case of rats ABO gene duplication seems undeniably proved3337. The number of species having both A and B gene sequences is expected to increase as new genome sequencing projects proceed, providing that duplicated regions are properly solved, which may be somewhat difficult in most NextGen sequencing projects.…”

Section: Discussionmentioning

confidence: 99%

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An integrative evolution theory of histo-blood group ABO and related genes

Yamamoto

Cid

Yamamoto

et al. 2014

Sci Rep

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The ABO system is one of the most important blood group systems in transfusion/transplantation medicine. However, the evolutionary significance of the ABO gene and its polymorphism remained unknown. We took an integrative approach to gain insights into the significance of the evolutionary process of ABO genes, including those related not only phylogenetically but also functionally. We experimentally created a code table correlating amino acid sequence motifs of the ABO gene-encoded glycosyltransferases with GalNAc (A)/galactose (B) specificity, and assigned A/B specificity to individual ABO genes from various species thus going beyond the simple sequence comparison. Together with genome information and phylogenetic analyses, this assignment revealed early appearance of A and B gene sequences in evolution and potentially non-allelic presence of both gene sequences in some animal species. We argue: Evolution may have suppressed the establishment of two independent, functional A and B genes in most vertebrates and promoted A/B conversion through amino acid substitutions and/or recombination; A/B allelism should have existed in common ancestors of primates; and bacterial ABO genes evolved through horizontal and vertical gene transmission into 2 separate groups encoding glycosyltransferases with distinct sugar specificities.T he human histo-blood group ABO system is crucial in safe blood transfusion and cell/tissue/organ transplantation 1,2 . This system consists in A and B oligosaccharide antigens expressed on red blood cells (RBCs) as glycoproteins and glycolipids and antibodies against those antigens in serum. A and B antigens are also expressed by epithelial and endothelial cells, and in secretor type individuals they are also expressed on mucins secreted by exocrine glands. The immuno-dominant structures of A and B antigens are GalNAca1-.3(Fuca1-.2)Gal-and Gala1-.3(Fuca1-.2)Gal-, respectively. A and B alleles of the ABO genetic locus encode A and B transferases, which respectively transfer an N-acetyl-D-galactosamine (GalNAc) or a D-galactose (Gal) to H substances with an a1,3-glycosidic linkage. H substances with the Fuca1-.2Gal-structure are synthesized by fucosylation catalyzed by a1,2-fucosyltransferases (a1,2-FTs) encoded by FUT1/FUT2/SEC1 genes. FUT1-encoded a1,2-FTs and FUT2/SEC1-encoded a1,2-FTs exhibit distinct acceptor substrate specificity, and are differentially expressed amongst tissues. In humans SEC1 is a pseudogene and FUT2 gene presents frequent null alleles so that about 20% of individuals are incapable of expressing either H, A, or B antigens in secretions (nonsecretor type). In the absence of a1,2-FTs no H antigens are produced. Therefore, A/B transferases function only when at least one active a1,2-FT is simultaneously present.In 1990 we correlated the nucleotide sequences of A, B, and O allelic cDNAs and the expression of A and B antigens, and elucidated the molecular genetic basis of human histo-blood group ABO system 3,4 . Four amino acid substitutions (Arg176Gly, Gly235Ser, Leu266Met, an...

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Rat Encodes the Paralogous Gene Equivalent of the Human Histo-blood Group ABO Gene

Cited by 21 publications

References 30 publications

Histo-Blood Group Antigens Act as Attachment Factors of Rabbit Hemorrhagic Disease Virus Infection in a Virus Strain-Dependent Manner

Histo-Blood Group Antigens Act as Attachment Factors of Rabbit Hemorrhagic Disease Virus Infection in a Virus Strain-Dependent Manner

ABO histo-blood group system-incompatible allografting

An integrative evolution theory of histo-blood group ABO and related genes

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