Sequence, expression, and mapping of a rat Mhc class I b gene

Walter, Lutz; Heine, Lutz; Günther, E

doi:10.1007/bf00189232

Cited by 17 publications

(9 citation statements)

References 20 publications

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“…Genes in the grc region, which so far has no equivalent in other species, are rcc (resistance to chemical carcinogenesis), fi (fertility), and dw-3 (dwarf, body size). Some of the rat class Ib genes are expressed (Walter et al 1994). It is obvious from examining different mouse strains that there may be considerable variation in the number of class I genes.…”

Section: Rodentsmentioning

confidence: 99%

?Both man & bird & beast?: comparative organization of MHC genes

1995

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Section: Rodentsmentioning

confidence: 99%

?Both man & bird & beast?: comparative organization of MHC genes

1995

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“…Thirteen clones drove expression of a molecule that behaved serologically like the RT1-A l molecule, whilst the other five led to at best very faint staining with the MRC OX-18 antibody, and no staining with other RT1-A l -reactive mAbs, including F16.4.4. Sequencing of these five clones revealed that one corresponded to the RT1-C l antigen [30], while the other four were highly homologous (>98%) to one another and to a sequence we had previously reported and designated RT1-E g [31]. These clones, and many others identified from other sources representing a total of six MHC haplotypes as well as from additional screening of PCR-generated cDNA clones from LEW neurospheres and from LEW placenta, are listed in Table 1.…”

Section: Resultsmentioning

confidence: 99%

“…In the latter case, it has been clearly shown that the MAPRTLLL or MAPRTLLLL peptides resulting were unable to bind significantly to H2-Qa1 [63], and translation of those class I molecules would therefore not result in the inhibition of NK cells via their CD94/NKG2A receptors. Whilst all rat class Ia sequences where this sequence is known to start with the first methionine, this first ATG is not present in many rat class Ib molecules including RT1-C l [30] and RT1-E u [25], and the second methionine is therefore used. Since both RT1-C l and RT1-E u have been shown to be potential activators of allorecognition by NK cells [62,64], there is therefore a correlation whereby the molecules that can inhibit NK cell activity also have a functional codon for the first methionine, and the ones that can be recognised by NK activatory receptors do not.…”

Section: Discussionmentioning

confidence: 99%

Characterisation of RT1-E2, a multigenic family of highly conserved rat non-classical MHC class I molecules initially identified in cells from immunoprivileged sites

et al. 2003

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BackgroundSo-called "immunoprivileged sites" are tissues or organs where slow allograft rejection correlates with low levels of expression of MHC class I molecules. Whilst classical class I molecules are recognised by cytotoxic T lymphocytes (CTL), some MHC class I molecules are called "non-classical" because they exhibit low polymorphism and are not widely expressed. These last years, several studies have shown that these can play different, more specialised roles than their classical counterparts. In the course of efforts to characterise MHC class I expression in rat cells obtained from immunoprivileged sites such as the central nervous system or the placenta, a new family of non-classical MHC class I molecules, which we have named RT1-E2, has been uncovered.ResultsMembers of the RT1-E2 family are all highly homologous to one another, and the number of RT1-E2 loci varies from one to four per MHC haplotype among the six rat strains studied so far, with some loci predicted to give rise to soluble molecules. The RT1n MHC haplotype (found in BN rats) carries a single RT1-E2 locus, which lies in the RT1-C/E region of the MHC and displays the typical exon-intron organisation and promoter features seen in other rat MHC class I genes. We present evidence that: i) RT1-E2 molecules can be detected at the surface of transfected mouse L cells and simian COS-7 cells, albeit at low levels; ii) their transport to the cell surface is dependent on a functional TAP transporter. In L cells, their transport is also hindered by protease inhibitors, brefeldin A and monensin.ConclusionsThese findings suggest that RT1-E2 molecules probably associate with ligands of peptidic nature. The high homology between the RT1-E2 molecules isolated from divergent rat MHC haplotypes is particularly striking at the level of their extra-cellular portions. Compared to other class I molecules, this suggests that RT1-E2 molecules may associate with well defined sets of ligands. Several characteristics point to a certain similarity to the mouse H2-Qa2 and human HLA-G molecules.

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“…Animals The rat class I genes RT1.A, K, F form a cluster similar to the mouse H2K genes; RT1.E/C is similar to H2D, L; RTI.O is similar to Q; and RT1.N is similar to T . Seven class I genes map to the RT1.E/C-grc region: BM1 (Parker et al 1990); N1, N2, N3 (Kirisits et al 1992(Kirisits et al , 1994b; O (Rushton et al 1994); ll/3R (Rothermel et al 1993); and LW2 (Walter et al_ 1994). Oor RT1.N-type genes have yet been identified in the human.…”

Section: Introductionmentioning

confidence: 99%

Nucleotide sequence and structural analysis of the rat RT1.E u and RT1.Aw3 l genes, and of genes related to RT1.O and RT1.C

1995

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A cDNA library was constructed using mRNA isolated from the R21 strain of rats which have the major histocompatibility complex (MHC) haplotype RT1.AlBlDlEu and the growth and reproduction complex (grc) genotype grc+. The cDNA clones that hybridized with the class I probes pAG64c and pARI.5 and were 1.3-1.7 kilobases were selected. Full-length clones were identified by sequencing partially the 5' and 3' ends of each clone, by the presence of a start codon at the 5' end, and by a polyadenylation sequence at the 3' end. The full-length cDNA clones were examined for in vitro transcription by transfection into human CIR cells using electroporation, and expression was detected by flow cytometry using monoclonal antibodies specific to the heavy chains and polyclonal antibody to beta 2-microglobulin. The RT1.Eu gene was transcribed and expressed optimally, and its nucleotide and deduced amino acid sequences differed significantly from the RT1.Aa, RT1.A(l), RT.Au, LW2, and 11/3R genes but only slightly from the RT1.K gene. The high level of sequence similarity between RT1.Eu and RT1.K suggests that the two genes may have originated from a common ancestral gene. In addition, three new genes (RT1.Aw3l, RT1.C-type, and RT1.O-type) were identified. The RT1.Aw3l gene is almost identical to RT1.A(l) with the exception of an in frame deletion of 21 nucleotides in exon 2 leading to a 7 amino acid deletion in the alpha 1 domain of the deduced amino acid sequence and 11 nucleotide substitutions and insertions in the rest of the sequence. It transcribed optimally, but no significant expression was detected. The RT1.C-type gene 119 is very similar (97%) to the LW2 gene in the 3' untranslated region, which suggests that it is in the RT1.C region. It transcribed optimally, but no significant expression was detected. The RT1.O-type gene 149 has all the features of a class Ib gene, but a premature stop codon in the alpha 1 domain causes incomplete translation. Its in vitro transcription was very low, and no expression was detected. These studies, combined with previous work, indicate that in the MHC of the R21 strain three class Ia genes (Eu, A(l), Aw3l) and three class Ib genes (C-type, O-type, N) are transcribed but only two class Ia genes (Eu, A(l)) are expressed.

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Sequence, expression, and mapping of a rat Mhc class I b gene

Cited by 17 publications

References 20 publications

?Both man & bird & beast?: comparative organization of MHC genes

?Both man & bird & beast?: comparative organization of MHC genes

Characterisation of RT1-E2, a multigenic family of highly conserved rat non-classical MHC class I molecules initially identified in cells from immunoprivileged sites

Nucleotide sequence and structural analysis of the rat RT1.E u and RT1.Aw3 l genes, and of genes related to RT1.O and RT1.C

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