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Results for “Genetic mapping”

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At least 865 records · Page 48Linked to original sources
PubMed1988

Genetic mapping of anhidrotic ectodermal dysplasia: DXS159, a closely linked proximal marker.

Three families with anhidrotic ectodermal dysplasia (AED) have been studied by linkage analysis with seven polymorphic DNA markers from the Xp11-q21 region. Previously reported linkage to DXYS1 (Xq13-q21) has been confirmed (z (theta) = 4.08 at theta = 0.05) and we have also established linkage to another polymorphic locus, DXS159, located in Xq11-q12 (z (theta) = 4.28 at theta = 0.05). Physical mapping places DSX159 proximal to the Xq12 breakpoint of an X autosome translocation found in a female with clinical signs of ectodermal dysplasia. Of all markers that have been used in linkage analysis of AED, DXS159 would appear the closest on the proximal side of the disease locus.

Chromosome Mapping↗
PubMed2003

Genetic mapping of the novel Turnip mosaic virus resistance gene TuRB03 in Brassica napus.

A new source of resistance to the pathotype 4 isolate of Turnip mosaic virus (TuMV) CDN 1 has been identified in Brassica napus (oilseed rape). Analysis of segregation of resistance to TuMV isolate CDN 1 in a backcross generation following a cross between a resistant and a susceptible B. napus line showed that the resistance was dominant and monogenic. Molecular markers linked to this dominant resistance were identified using amplified fragment length polymorphism (AFLP) and microsatellite bulk segregant analysis. Bulks consisted of individuals from a BC(1) population with the resistant or the susceptible phenotype following challenge with CDN 1. One AFLP and six microsatellite markers were associated with the resistance locus, named TuRB03, and these mapped to the same region on chromosome N6 as a previously mapped TuMV resistance gene TuRB01. Further testing of TuRB03 with other TuMV isolates showed that it was not effective against all pathotype 4 isolates. It was effective against some, but not all pathotype 3 isolates tested. It provided further resolution of TuMV pathotypes by sub-dividing pathotypes 3 and 4. TuRB03 also provides a new source of resistance for combining with other resistances in our attempts to generate durable resistance to this virus.

Brassica napus↗
PubMed1990

Genetic mapping of the gene for Ca2+/calmodulin-dependent protein kinase IV (Camk-4) to mouse chromosome 18.

Southern blot analysis of Chinese hamster x mouse somatic cell hybrids was used to map the gene for a serine/threonine protein kinase expressed in brain and testis. This locus, termed Camk-4, encodes Ca2+/calmodulin-dependent protein kinase IV. Progeny of an interspecific backcross were analyzed to position Camk-4 in the centromeric region of chromosome 18 near two mutations known to affect neurological function and fertility. This raises the possibility that a defect in Camk-4 may be responsible for one of these mutant phenotypes.

Animals↗
PubMed2000

Genetic mapping of a locus associated with bovine chronic interstitial nephritis to chromosome 1.

Chronic interstitial nephritis with diffuse zonal fibrosis (CINF) occurs in Japanese Black cattle (Wagyu) as an autosomal recessive disorder leading to death prior to puberty, first six months or a year of life. We performed a genome-wide scan using microsatellite markers in a Wagyu pedigree segregating for CINF and mapped the CINF locus to bovine chromosome 1. CINF was closest to microsatellites BM9019 and INRA49 (Z score = 12.0; P < 3.4 x 10(-10)).

Animals↗
PubMed1980

Genetic mapping of xenotropic murine leukemia virus-inducing loci in five mouse strains.

A single mendelian gene was identified for induction of the endogenous xenotropic murine leukemia virus in five mouse strains (C57BL/10, C57L, C57BR, AKR, and BALB/c). This locus, designated Bxv-1, mapped to the same site on chromosome 1 in all strains: Id-1-Pep-3-[Bxv-1-Lp]. Thus, inducibility loci for xenotropic virus are more limited in number and chromosomal distribution than ecotropic inducibility loci. Virus expression in mice with Bxv-1 was induced by treatment of fibroblasts with 5-iododeoxyuridine or by exposure of spleen cells to a B cell mitogen, bacterial lipopolysaccharide. An analysis of the hamster X mouse somatic cell hybrids indicated that chromosome 1, alone, was sufficient for virus induction.

Alleles↗
PubMed2000

Multipoint estimation of genetic maps for human trisomies with one parent or other partial data.

Centromeric-mapping methods have been used to investigate the association between altered recombination and meiotic nondisjunction in humans. For trisomies, current methods are based on the genotypes from a trisomic offspring and both parents. Because it is sometimes difficult to obtain samples from both parents and because the ability to use sources of DNA previously not available (e.g., stored paraffin-embedded pathological samples) has increased, we have been interested in creating similar maps for trisomic populations in which one of the parents of the trisomic individual is unavailable for genotyping. In this paper, we derive multipoint likelihoods for both missing-parent data and conventional two-parent data. We find that likelihoods for two-parent data and for data generated without a sample from the correctly disjoining parent can be maximized in exactly the same way but also that missing-parent data has a high frequency of partial data of the same sort produced by intercross matings. Previously published centromeric-mapping methods use incorrect likelihoods for intercross matings and thus can perform poorly on missing-parent data. We wrote a FORTRAN program to maximize our multipoint likelihoods and used it in simulation studies to demonstrate the biases in the previous methods.

Algorithms↗
PubMed1979

Genetic mapping of the chromosomal replication origin of Salmonella typhimurium.

Two hundred strains of Escherichia coli harboring Filv+ plasmids which carry a segment of the Salmonella typhimurium chromosome were isolated independently. Among them, two strains were found to harbor F' plasmids that are able to replicate in Hfr cells of E. coli; i.e., they carry a site designated poh (permissive on Hfr) of the S. typhimurium chromosome. The poh site is presumably identical with the replication origin (oriC) of the bacterial chromosome. These two plasmids carry the dnaA-uncA-rbs-ilv-cya-metE region of the chromosome of S. typhimurium. Other F' plasmids which only carried the ilv-cya-metE region were unable to be maintained in Hfr cells. The poh site (= oriC) of S. typhimurium thus is located in the uhp-ilv region of the chromosome. The two plasmids carrying the poh site of S. typhimurium can suppress the temperature-sensitive character of an E. coli mutant that carries the temperature-sensitive dnaA46 allele, when the plasmids exist in the mutant cells. This suggests that the dnaA chromosome in place of the dnaA gene product of E. coli itself. The ability of the plasmids carrying the poh site of S. typhimurium to replicate in Hfr cells of E. coli suggests that the replication system of E. coli can recognize the Salmonella replication origin.

Chromosome Mapping↗
PubMed1982

Genetic mapping of mutations in a highly radiation-resistant mutant of Salmonella typhimurium LT2.

The genes involved in the high radiation resistance of mutant R68 of Salmonella typhimurium LT2 were mapped by conjugation. It was observed that the high radiation resistance involved genes localized in two regions of the chromosome, which have been designated as garA and garB for high gamma resistance. The garA gene mapped near gal and uvrB at about 18 map units, and the garB gene mapped near purC at about 49 map units. The resistance of R68 was reduced to the wild-type level by the acquisition of the two wild-type alleles, garA+ and garB+. Recombinants carrying the garA or garB gene repaired single-strand breaks in their DNA faster than did the wild-type strain. However, only those with the garA mutation showed a marked increase in UV irradiation resistance above the wild-type level, whereas those with garB mutation exhibited an increased rate of spontaneous degradation of DNA beyond the level observed in recA cells.

Chromosome Mapping↗