Sequence-Ready BAC Contig, Physical, and Transcriptional Map of a 2-Mb Region Overlapping the Mouse Chromosome 6 Host-Resistance Locus Cmv1

Depatie, Chantal; Lee, Seung Hwan; Stafford, Amanda; Avner, Philip; Belouchi, Abdelmajid; Gros, Philippe; Vidal, Silvia M.

doi:10.1006/geno.2000.6186

Cited by 40 publications

(41 citation statements)

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“…This requires high-resolution genetic and physical mapping of the Soa region. The chromosomal region proximal to Prp has been physically mapped (Brown et al 1999;Depatie et al 2000), but it does not include the whole Soa interval.To begin positional cloning of Soa, we conducted this study aimed to determine a Soa nonrecombinant interval. Replicate Soa-congenic strains were used to define an overlapping part of the donor fragments as a Soa critical region.…”

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confidence: 99%

High-resolution genetic mapping of the sucrose octaacetate taste aversion (Soa) locus on mouse Chromosome 6

Bachmanov

et al. 2001

Mammalian Genome

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An acetylated sugar, sucrose octaacetate (SOA), tastes bitter to humans and has an aversive taste to at least some mice and other animals. In mice, taste aversion to SOA depends on allelic variation of a single locus, Soa. Three Soa alleles determine 'taster' (Soa a ), 'nontaster' (Soa b ), and 'demitaster' (Soa c ) phenotypes of taste sensitivity to SOA. Although Soa has been mapped to distal Chromosome (Chr) 6, the limits of the Soa region have not been defined. In this study, mice from congenic strains SW.B6-Soa b , B6.SW-Soa a , and C3.SW-Soa a/c and from an outbred CFW strain were genotyped with polymorphic markers on Chr 6. In the congenic strains, the limits of introgressed donor fragments were determined. In the outbred mice, linkage disequilibrium and haplotype analyses were conducted. Positions of the markers were further resolved by using radiation hybrid mapping. The results show that the Soa locus is contained in a ~1-cM (3.3-4.9 Mb) region including the Prp locus.Presumably, sensitivity to bitter compounds arose as a means of detecting toxic agents. Consequently, many structurally diverse compounds taste bitter to humans and other animals. An ability to detect bitter is now thought to be based on specific recognition by a family of putative bitter taste receptors (Adler et al. 2000;Matsunami et al. 2000) and perhaps other mechanisms (Lindemann 1996).One important model system for investigating the bitter taste mechanism involves the acetylated sugar, sucrose octaacetate (SOA), which tastes bitter to humans and has an aversive taste to at least some mice and other animals. In mice, taste aversion to SOA depends on allelic variation of a single locus, Soa, with three known alleles. The Soa a allele determines a 'taster' phenotype of strong SOA avoidance, the Soa b allele determines a 'nontaster' phenotype of indifference to SOA, and the Soa c allele determines a 'demitaster' phenotype of intermediate SOA sensitivity (demitasters are indifferent to 0.1 mM SOA, but avoid 1 mM SOA). An order of a phenotypic dominance of these alleles is taster > nontaster > demitaster (Harder et al. 1992 1995;Harder et al. 1996). Within an outbred CFW strain, there is a phenotypical variation in SOA avoidance, which is due to segregation of taster and demitaster Soa alleles (Gannon and Whitney 1989;Harder et al. 1992).The Soa locus has been mapped to distal Chr 6 (Azen 1991;Capeless et al. 1992;Lush et al. 1995). This region contains several candidate genes thought to be involved in bitter taste perception. A recent study has shown that one of these genes, Prp, is a less likely candidate for Soa (Harder et al. 2000). Several genes encoding G protein-coupled receptors expressed in taste tissue were also found in the Soa region (Adler et al. 2000;Matsunami et al. 2000).However, there is still no evidence that one or some of these receptors bind SOA as a ligand. A mechanism for transduction of SOA bitter taste could be identified by using positional cloning of the Soa locus. This requires high-resolution genetic an...

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confidence: 99%

High-resolution genetic mapping of the sucrose octaacetate taste aversion (Soa) locus on mouse Chromosome 6

Bachmanov

et al. 2001

Mammalian Genome

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“…Segregation analysis of polymorphic markers, including microsatellite markers, gene sequences and anonymous probes, with respect to Cmv1 lead to the localization of Cmv1 to a 0.35-cM interval in two independent genetic maps. [110][111][112] The map generated by our group revealed gene order and intergene distances (in cM) in the vicinity of Cmv1 as: (Figure 2a). A high-resolution physical map of the Cmv1 genetic interval based on long-range restriction mapping by PFGE and the assembly of a contig of YAC and BAC clones translated the genetic interval into 1.6 Mb of genomic DNA containing a minimum of 18 transcription units including the 14 Ly49 gene cluster (Figure 2b, c).…”

Section: Cloning Of Cmv1mentioning

confidence: 99%

“…A high-resolution physical map of the Cmv1 genetic interval based on long-range restriction mapping by PFGE and the assembly of a contig of YAC and BAC clones translated the genetic interval into 1.6 Mb of genomic DNA containing a minimum of 18 transcription units including the 14 Ly49 gene cluster (Figure 2b, c). 112 These results excluded Nk1.1, Cd94 and Nkg2d, while retaining the Ly49 gene cluster as candidates for Cmv1. [110][111][112] Interestingly, a similar mapping approach being performed by a second group initially excluded Ly49 genes as potential candidates by placing Cmv1 distal to Ly49b gene, raising the possibility that one or more NKC genes could be involved in the resistance/susceptibility phenotype.…”

Section: Cloning Of Cmv1mentioning

confidence: 99%

“…112 These results excluded Nk1.1, Cd94 and Nkg2d, while retaining the Ly49 gene cluster as candidates for Cmv1. [110][111][112] Interestingly, a similar mapping approach being performed by a second group initially excluded Ly49 genes as potential candidates by placing Cmv1 distal to Ly49b gene, raising the possibility that one or more NKC genes could be involved in the resistance/susceptibility phenotype. 115 Sequence comparison between Cmv1 r and Cmv1 s strains indicated allelic differences for transcripts analyzed in the Cmv1 interval 116,117 (Figure 2b, Figure 3), precluding assessment of their candidacy based upon mutation analysis.…”

Section: Cloning Of Cmv1mentioning

confidence: 99%

“…All markers have been previously reported. 111,112,115,118,119 determined by the two previously described genetic maps 112,115 made it difficult to rule out a possible contribution of several linked loci to the susceptibility/ resistance phenotype.…”

Section: Cloning Of Cmv1mentioning

confidence: 99%

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Genetic control of innate immune responses against cytomegalovirus: MCMV meets its match

2002

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Cytomegalovirus (CMV) is a widespread pathogen that is All Ly49 receptors characterized to date interact with MHC class I molecules on potential target cells, resulting in the accumulation of signals to the NK to either 'kill' or 'ignore' the cell based upon the repertoire of MHC class I molecules expressed. The identification of Cmv1 as Ly49H, a stimulatory member of the Ly49 family, adds an interesting twist to the Ly49 story. Although the ligand of Ly49H is not yet known, there is already compelling evidence that the ligand is upregulated on virally infected cells, resulting in specific activation of Ly49H-expressing NK cells. This review provides an historical perspective of the MCMV infection model from its inception to the discovery of the gene responsible for the phenotype and provides a basis for further experiments aimed at understanding the role of NK cells, in general, and Ly49H, in particular, in mediating resistance to cytomegalovirus.

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NK cells developing in vitro from fetal mouse progenitors express at least one member of the Ly49 family that is acquired in a time-dependent and stochastic manner independently of CD94 and NKG2

Fraser¹,

Gays²,

Robinson³

et al. 2002

Eur. J. Immunol.

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NK cells developing in vitro from fetal progenitors in the presence of IL-2 are phenotypically and functionally indistinguishable from mature adult NK cells, with the exception that they generally lack surface expression of any of the Ly49 molecules that have previously been examined. Using two recently developed anti-Ly49 mAb, we show here that most of these NK cells in fact express high levels of at least one previously uncharacterized member of the Ly49 family, most likely Ly49E. Detailed kinetic and clonal analysis revealed that these Ly49 molecules were acquired in a progressive and stochastic manner independently of CD94 and NKG2. CD94 and NKG2 were both expressed early in NK cell development, sometimes in the absence of NK1.1, with CD94 invariably being expressed at two different levels. IL-4 differentially inhibited the expression of CD94 and Ly49 receptors, but had little or no effect on the expression of NKRP1 molecules.

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Sequence-Ready BAC Contig, Physical, and Transcriptional Map of a 2-Mb Region Overlapping the Mouse Chromosome 6 Host-Resistance Locus Cmv1

Cited by 40 publications

References 58 publications

High-resolution genetic mapping of the sucrose octaacetate taste aversion (Soa) locus on mouse Chromosome 6

High-resolution genetic mapping of the sucrose octaacetate taste aversion (Soa) locus on mouse Chromosome 6

Genetic control of innate immune responses against cytomegalovirus: MCMV meets its match

NK cells developing in vitro from fetal mouse progenitors express at least one member of the Ly49 family that is acquired in a time-dependent and stochastic manner independently of CD94 and NKG2

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