A radiation hybrid map of mouse genes

Hudson, Thomas J.; Church, Deanna M.; Greenaway, Simon; Nguyen, Huy; Cook, April; Steen, Robert; Etten, William J. Van; Castle, Andrew B.; Strivens, Mark; Trickett, Pamela; Heuston, Christine; Davison, Claire; Southwell, Anne; Hardisty, Rachel E.; Varela-Carver, Anabel; Haynes, Andrew R.; Rodriguez-Tomé, Patricia; Doi, Hirofumi; Ko, Minoru S.H.; Pontius, Joan; Schriml, Lynn M.; Wagner, Lukas; Maglott, Donna; Brown, Steve; Lander, Eric S.; Schuler, Greg; Denny, Paul

doi:10.1038/ng1001-201

Cited by 89 publications

(38 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Each cell line within the panel contains the full hamster genome and approximately 25% of the mouse genome. The composition of mouse genomic fragments present within each cell line has been determined to allow for linkage analysis of phenotypic data (18,32,42,52). Pseudotyped virus incorporating FB29 or TR1.3 Env with a beta-galactosidase reporter gene was used to transduce each cell line in the panel.…”

Section: Resultsmentioning

confidence: 99%

Linkage of Reduced Receptor Affinity and Superinfection to Pathogenesis ofTR1.3 Murine Leukemia Virus

Murphy

Chung-Landers

Honczarenko

et al. 2006

J Virol

View full text Add to dashboard Cite

TR1.3 is a Friend murine leukemia virus (MLV) that induces selective syncytium induction (SI) of brain capillary endothelial cells (BCEC),The ecotropic Friend murine leukemia virus (MLV) TR1.3 was previously defined as an acutely cytopathic, syncytiuminducing (SI) variant of the noncytopathic, non-syncytium-inducing (NSI) MLV FB29. When inoculated into neonatal BALB/c mice, TR1.3 infected and caused syncytium formation in brain capillary endothelial cells (34-36). These cytopathic effects paralleled a breakdown of the blood brain barrier and hemorrhagic stroke formation. The molecular basis of both the SI phenotype and in vivo neurologic disease was previously mapped to a tryptophan (W)-to-glycine (G) substitution at amino acid position Env 102 (37). Introduction of the W102G substitution into the NSI FB29 molecular clone yielded an SI pathogenic phenotype that was identical to that seen with TR1.3. The mechanism(s) whereby mutations at Env 102 mediate SI and disease is unknown.The MLV Env consists of surface and transmembrane subdomains. Amino acids 1 to 236 of SU encompass the putative receptor binding domain (RBD) (10). Analysis of the RBD crystal structure indicates that amino acid 102 lies at the base of the predicted receptor binding pocket (13). Interaction between RBD and the ecotropic receptor murine cationic amino acid transporter 1 (mCAT-1) is essential for MLV membrane fusion and entry and for syncytium formation (1,22,53). Previous studies assessed the impact of multiple amino acid changes in Env on expression, binding, and viral entry in MLV with related genetic backgrounds (11,33). These studies showed that nonconservative substitutions of glycine or threonine for tryptophan at Env 102 altered receptor binding and transduction efficiency. However, unlike with TR1.3 and W102G, Env substitutions on these backgrounds did not result in the SI phenotype (11,33).Following MLV infection, Env downmodulates the level of available receptor on the cell surface (16,31). This process, known as superinfection interference, prevents a virally infected cell from undergoing additional rounds of infection by the same or related viruses that utilize the same cellular receptor (44,50,55). In rare circumstances, failure of MLV Env to establish superinfection interference is linked to either low Env expression levels and/or diminished mCAT-1 binding (3,4,49).Important pathological consequences can result from retroviral superinfection. Superinfection can lead to the accumulation of unintegrated linear DNA in the cytoplasm (51); by virtue of the similarity between unintegrated viral DNA and damaged DNA, this may trigger apoptosis induction in superinfected cells (9, 51). Failure to block superinfection has been linked to the in vivo cytotoxicity of mink cell focus-forming virus M13 and the neuropathogenic MLV Moloney ts1 (51, 56).Murine leukemia viruses are facile tools for investigating the mechanisms of retroviral pathogenesis (26). Several correlates of increased fusion activity have been attributed to Env including ...

show abstract

Section: Resultsmentioning

confidence: 99%

Linkage of Reduced Receptor Affinity and Superinfection to Pathogenesis ofTR1.3 Murine Leukemia Virus

Murphy

Chung-Landers

Honczarenko

et al. 2006

J Virol

View full text Add to dashboard Cite

show abstract

“…Widely used techniques include (1) cytogenetic analysis of chromosome duplications, deletions, and rearrangements (Khush and Rick 1968;Berger 2004); (2) genetic analysis of radiation hybrids whereby genes are assigned to particular chromosomal fragments on the basis of presence vs. absence tests (Hudson et al 2001;Kynast et al 2004); and (3) fluorescence in situ hybridization (FISH) involving hybridization of labeled DNA fragments to intact chromosomes to show the positions of complementary sequences De Jong et al 1999;Jackson et al 2000). While these techniques have been used to localize many genes on chromosomes, they are limited by special requirements, and they are not high throughput.…”

Section: W Hile Linkage Maps Accurately Describe Genementioning

confidence: 99%

Predicting and Testing Physical Locations of Genetically Mapped Loci on Tomato Pachytene Chromosome1

Chang¹,

Anderson

Sherman

et al. 2007

Genetics

View full text Add to dashboard Cite

Predicting the chromosomal location of mapped markers has been difficult because linkage maps do not reveal differences in crossover frequencies along the physical structure of chromosomes. Here we combine a physical crossover map based on the distribution of recombination nodules (RNs) on Solanum lycopersicum (tomato) synaptonemal complex 1 with a molecular genetic linkage map from the interspecific hybrid S. lycopersicum 3 S. pennellii to predict the physical locations of 17 mapped loci on tomato pachytene chromosome 1. Except for one marker located in heterochromatin, the predicted locations agree well with the observed locations determined by fluorescence in situ hybridization. One advantage of this approach is that once the RN distribution has been determined, the chromosomal location of any mapped locus (current or future) can be predicted with a high level of confidence.

show abstract

“…Some of the mismapped MIT SSLP markers have been used as RHMAPPER framework markers in the Whitehead T31 RH map (Hudson et al 2001), thus causing several linked markers to appear to be poorly linked to surrounding data. A case in point is D10Mit278, which in fact maps to Chr 15 in the RH data.…”

Section: Discussionmentioning

confidence: 99%

“…The Whitehead Institute Genome Center RH map (Hudson et al 2001) includes 734 of the markers in our framework map. In the Release 10 version of the Whitehead map there are 45 genomic regions that contain two to four misordered markers by comparison to our curated framework marker TJL BSB/BSS recombination data.…”

Section: Comparing the Different T31 Rh Mapsmentioning

confidence: 99%

See 1 more Smart Citation

The Comprehensive Mouse Radiation Hybrid Map Densely Cross-Referenced to the Recombination Map: A Tool to Support the Sequence Assemblies

Rowe

Barter²,

Kelmenson³

et al. 2002

Genome Res.

View full text Add to dashboard Cite

We have developed a unique comprehensive mouse radiation hybrid (RH) map of nearly 23,000 markers integrating data from three international genome centers and over 400 independent laboratories. We have cross-referenced this map to the 0.5-cM resolution recombination-based Jackson Laboratory (TJL) backcross panel map, building a complete set of RH framework chromosome maps based on a high density of known-ordered anchor markers. We have systematically typed markers to improve coverage and resolve discrepancies, and have reanalyzed data sets as needed. The cross-linking of the RH and recombination maps has resulted in a highly accurate genome-wide map with consistent marker order. We have compared these linked framework maps to the Ensembl mouse genome sequence assembly, and show that they are a useful medium resolution tool for both validating sequence assembly and elucidating chromosome biology.

show abstract

A radiation hybrid map of mouse genes

Cited by 89 publications

References 17 publications

Linkage of Reduced Receptor Affinity and Superinfection to Pathogenesis ofTR1.3 Murine Leukemia Virus

Linkage of Reduced Receptor Affinity and Superinfection to Pathogenesis ofTR1.3 Murine Leukemia Virus

Predicting and Testing Physical Locations of Genetically Mapped Loci on Tomato Pachytene Chromosome1

The Comprehensive Mouse Radiation Hybrid Map Densely Cross-Referenced to the Recombination Map: A Tool to Support the Sequence Assemblies

Contact Info

Product

Resources

About