TheB144-H-2D binterval and the location of a mouse homologue of the human D6S81E locus

Wroblewski, Joanne M.; Kaminsky, Steven G.; Milisauskas, Vita K.; Pittman, Anne M.; Chaplin, David; Spies, Thomas A.; Nakamura, Ichiro

doi:10.1007/bf02114974

Cited by 16 publications

(9 citation statements)

References 25 publications

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“…. This extends the previous observation (Spies et al 1989;Wroblewski et al 1990) that the genes designated B144, Tnfa, Tnfb, and BAT1 (G6S81E) are co-linear in the mouse and human MHC.…”

Section: Resultssupporting

confidence: 66%

P1 and cosmid clones define the organization of 280 kb of the mouse H-2 complex containing the Cps-1 and Hsp70 loci

et al. 1994

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A 280 kilobase (kb) contig was isolated from mouse genomic P1 and cosmid libraries, using as probes human cDNA and genomic DNA fragments that map in the interval between the second component of complement and tumor necrosis factor genes of the HLA complex. The clone contig demonstrates synteny of eleven mouse genes that are homologous to genes initially mapped within the human major histocompatibility complex. These include the mouse homologs of BAT2 (HLA-B-associated transcript 2) through BAT9 and also three HSP70-related genes. Five P1 clones form a contig of 240 kb that spans from BAT9 through BAT3. Twelve cosmid clones are arranged in three contigs that confirm most of the structure of the P1 contig and link the mouse BAT3 homolog to the BAT2 homolog approximately 15 kb farther telomeric. Polymorphic DNA markers within the cloned region were used to map the cleft palate susceptibility-1 (Cps-1) locus to the interval between Hsp70.1 and BAT6 (valyl-tRNA synthetase). This refines the location of the Cps-1 locus to a 45 kb region contained in the H2-124 P1 insert.

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“…. This extends the previous observation (Spies et al 1989;Wroblewski et al 1990) that the genes designated B144, Tnfa, Tnfb, and BAT1 (G6S81E) are co-linear in the mouse and human MHC.…”

Section: Resultssupporting

confidence: 66%

P1 and cosmid clones define the organization of 280 kb of the mouse H-2 complex containing the Cps-1 and Hsp70 loci

et al. 1994

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“…All in all, it is quite intriguing that an equal-sized deletion involving this very same region and genes (MICA͞B) has happened at distinct points in time in several different primate species. This very phenomenon might also be the reason why rodents are devoid of MIC genes, because the putative location of functional mouse MICA and MICB genes, the segment linking H2-D (equivalent to HLA-B or Patr-B) and BAT1, is substantially shortened compared with the human MHC: 40 instead of 173 kb (11,29,30). The molecular basis of the existence of such an apparently ''deletion-prone'' segment between MICA and MICB remains to be established, but this could be due to the existence of a HERV-L sequence, which contains a 2.5-kb AT-rich insertion in its 5Ј LTR, which might therefore serve as a recombination hot spot (23,31).…”

Section: Resultsmentioning

confidence: 99%

Comparative sequencing of human and chimpanzee MHC class I regions unveils insertions/deletions as the major path to genomic divergence

Anzai

Shiina²,

Kimura³

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

120

108

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Despite their high degree of genomic similarity, reminiscent of their relatively recent separation from each other (Ϸ6 million years ago), the molecular basis of traits unique to humans vs. their closest relative, the chimpanzee, is largely unknown. This report describes a large-scale single-contig comparison between human and chimpanzee genomes via the sequence analysis of almost one-half of the immunologically critical MHC. This 1,750,601-bp stretch of DNA, which encompasses the entire class I along with the telomeric part of the MHC class III regions, corresponds to an orthologous 1,870,955 bp of the human HLA region. Sequence analysis confirms the existence of a high degree of sequence similarity between the two species. However, and importantly, this 98.6% sequence identity drops to only 86.7% taking into account the multiple insertions͞deletions (indels) dispersed throughout the region. This is functionally exemplified by a large deletion of 95 kb between the virtual locations of human MICA and MICB genes, which results in a single hybrid chimpanzee MIC gene, in a segment of the MHC genetically linked to species-specific handling of several viral infections (HIV͞SIV, hepatitis B and C) as well as susceptibility to various autoimmune diseases. Finally, if generalized, these data suggest that evolution may have used the mechanistically more drastic indels instead of the more subtle singlenucleotide substitutions for shaping the recently emerged primate species.

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“…Similarly, the distance between BAT-1 gene and the H-2L gene i~ the 1-1-2 d haplotype is also 170 kb (Steinmetz et al 1986). On the other hand, the distance between the BAT-1 gene and the class I gene in the H-2 b haplotype is only 10 kb (Wroblewski et al 1990). This suggests that the H-2 d haplotype may possess the ancestral H-2D region chromosome similar to the human HLA-B region while H-2 b haplotypes must have arisen after deletion of a large part of the chromosomal region between BAT-1 and the H-2L gene which must be approximately 160 kb.…”

Section: Resultsmentioning

confidence: 99%

Expression of HLA-B27 in transgenic mice is controlled by gene(s) mapping between H-2D and H-2L loci

1992

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The level of HLA-B27 transgene expression on the cell surface is dependent on the host H-2 haplotype. Mice homozygous for the H-2b, H-2f, H-2s, H-2p, H-2r, and H-2k haplotypes express B27 at high levels. An intermediate level of B27 expression is observed in H-2v mice whereas low levels of B27 are expressed in H-2q and H-2d mice. The decreased expression of B27 maps to the D region of the major histocompatibility complex. Recombinant strain B10.RKDB (DdLb) mapped the low expression gene centromeric to H-2L. In order to determine the low expression within the H-2D region, the B27 transgene was introduced into B10.D2-H-2dm1 and BALB/c-H-2dm2 mice. Expression of B27 in both of these strains was high indicating that neither H-2Dd nor H-2Ld is responsible for the low expression. This maps the effect between the H-2D and H-2L loci. In addition, introduction of human beta 2-microglobulin (beta 2m) into B10.D2-B27 transgenic mice caused a marked enhancement of B27 expression on the cell surface suggesting that the defect in B27 expression in certain haplotypes is due to an inability of B27 to associate with endogenous mouse beta 2m. We propose that gene(s) mapping between D and L (either D2, D3, D4, or some as yet unidentified gene) may be involved in class I assembly by helping association of beta 2m with class I. This putative molecule, designated "Assembly Enhancer (AE)" might have a negative influence in the association between human class I and mouse beta 2m.

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TheB144-H-2D binterval and the location of a mouse homologue of the human D6S81E locus

Cited by 16 publications

References 25 publications

P1 and cosmid clones define the organization of 280 kb of the mouse H-2 complex containing the Cps-1 and Hsp70 loci

P1 and cosmid clones define the organization of 280 kb of the mouse H-2 complex containing the Cps-1 and Hsp70 loci

Comparative sequencing of human and chimpanzee MHC class I regions unveils insertions/deletions as the major path to genomic divergence

Expression of HLA-B27 in transgenic mice is controlled by gene(s) mapping between H-2D and H-2L loci

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