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At least 1,243 records · Page 69Linked to original sources
PubMed1998

Genetic mapping of Hessian fly avirulence gene vH6 using bulked segregant analysis.

The Hessian fly, Mayetiola destructor (Say), an important insect pest of wheat, Triticum aestivum L., has a gene-for-gene relationship with wheat: single genes in the insect condition avirulence to specific resistance genes in wheat. We report the discovery of the first molecular genetic marker that is tightly linked to a Hessian fly avirulence gene. This dominant DNA polymorphism (OPG15-1) was identified using bulked segregant analysis and arbitrary primers in polymerase chain reactions. Bulked segregant analysis was modified to accommodate the anomalous chromosome cycle of the Hessian fly. It was used to identify DNA polymorphisms linked to the gene (vH6) that confers avirulence to the resistance gene H6 in wheat. OPG15-1 was cloned and sequenced, and a pair of site-specific primers were designed that converted it into a codominant single-stranded conformational polymorphism. Both OPG15-1 and vH6 were shown to be X-linked, and the genetic distance between the two loci was 2.5 +/- 2.5 cM. In situ hybridization to polytene chromosomes of larval salivary glands indicated that OPG15-1 resides near the centromere of Hessian fly chromosome X1.

Animals↗
PubMed2002

Genetic mapping of the Lr20-Pm1 resistance locus reveals suppressed recombination on chromosome arm 7AL in hexaploid wheat.

The Lr20-Sr15-Pm1 resistance locus in hexaploid wheat confers resistance to three different fungal wheat pathogens (leaf rust, stem rust, and powdery mildew). It was previously localized in the distal region of chromosome arm 7AL. As a first step towards the isolation of this complex locus, we performed molecular mapping of the Lr20 and Pm1 genes in three F2 populations. In two populations, a cluster of 8 and 12 markers, respectively, cosegregated with the resistance genes. In a third population based on a cross between a susceptible lr20 mutant and a resistant cultivar, all clustered markers were monomorphic. However, in this population the recombination frequency proximal to the Lr20 gene was up to 60 times higher, indicating that the complete genetic linkage of the clustered markers is not due to a close physical linkage of the probes but is caused by suppressed recombination. This was supported by the analysis of Triticum monococcum BAC clones where no physical linkage between cosegregating probes was observed. Suppressed recombination at the Lr20-Pm1 locus is likely the result of an alien introgression of chromatin from an unidentified wild relative species or is due to chromosomal rearrangements.

Chromosome Mapping↗
PubMed1989

Simultaneous genetic mapping of multiple human minisatellite sequences using DNA fingerprinting.

We have used several DNA probes which simultaneously recognize multiple loci to follow the segregation of a large number of minisatellite loci through two large reference pedigrees. The segregation data were analyzed for linkage to previously characterized marker loci using RFLP mapping data for these pedigrees from a previous study and from the Centre d'Etude du Polymorphisme Humain data bank. In this way we have mapped 31 separate minisatellite alleles of a total of 146 studied. The results of these analyses suggest that the distribution of minisatellites in the human genome is skewed toward telomeres and is highly clustered in character. A group of at least five separate minisatellites was found at 7 qter, and smaller clusters are present in several other regions. We detected a smaller than expected number of linkages, perhaps because of the clustering of minisatellite loci. The 7qter minisatellite cluster is in a region of excess male meiotic recombination, and in this respect is similar to minisatellite clusters at 16pter and in the X-Y pseudoautosomal region.

Alleles↗
PubMed2002

High-resolution genetic map of Nb, a gene that confers hypersensitive resistance to potato virus X in Solanum tuberosum.

Nb is a single dominant gene in potato that confers hypersensitive resistance to potato virus X (PVX) isolates from strain groups 1 and 2. Genetic and molecular analyses showed that Nb is located on the upper arm of chromosome V and forms part of a cluster of resistance genes encoding specificities to many different pathogens. We describe the genetical localisation of molecular markers tightly linked to the Nb locus and the development PCR-based markers suitable for isolation of the Nb resistance gene by positional cloning. A bulked segregant approach was applied to identify polymorphic AFLP markers tightly linked to the Nb locus. These markers were mapped in a population of segregating S1 progeny (1,300 plants) from a self-pollinated potato cultivar, Pentland Ivory. From this analysis, Nb was placed in an interval of 0.76 cM, flanked by the AFLP markers GM339 and GM637. Recombinant PVX strains carrying different combinations of avirulence genes were used in biological assays to show that Nb was also present in potato cv. Cara but was masked by the extreme PVX resistance conferred by the Rx gene. PCR-based screening of a Cara genomic BAC library with markers closest to the Nb locus identified a new marker tightly linked to Nb.

Journal Article↗
PubMed1997

Linkage studies in erythrokeratodermias: fine mapping, genetic heterogeneity and analysis of candidate genes.

Erythrokeratodermias are a clinically heterogeneous group of rare autosomal dominant disorders of cornification with overlapping features including hyperkeratosis and erythema. We ascertained five extended pedigrees with different phenotypes for a linkage study. Three families presented with localized erythrokeratodermia variabilis, and one with erythrokeratodermia and ataxia. Another family had Greither disease associated with variable hyperkeratotic plaques. Despite their phenotypic differences, both erythrokeratodermia variabilis and erythrokeratodermia with ataxia map to a common region in 1p34-p35. Multipoint linkage and haplotype analyses place erythrokeratodermia variabilis between the marker D1S496 and D1S186 with a maximum LOD score of 12.88. Our linkage results provide compelling evidence for genetic homogeneity among families of mixed European and French-Canadian origin. In contrast, results excluded Greither's disease from the established erythrokeratodermia variabilis gene region indicating genetic heterogeneity of erythrokeratodermias. Based on recombinations, two genes assigned to 1p34-p35 were excluded: cartilage matrix protein and avian myelocytosis viral oncogene. Connexin-37 (GJA4), a member of the connexin gene family, maps within the erythrokeratodermia variabilis region and is an attractive candidate gene. Direct sequencing of the coding region of GJA4 in four patients revealed several variations, including a novel polymorphism within the 5' cytoplasmic domain, but no pathogenic mutations were found, thus excluding Connexin-37 as a candidate. There is evidence, however, that other epidermally expressed connexins cluster in this region, and one may yet be determined to play a role in the pathogenesis of erythrokeratodermia variabilis.

Chromosome Mapping↗
PubMed1998

Genetic mapping of a second myotonic dystrophy locus.

We report the mapping of a second myotonic dystrophy locus, myotonic dystrophy type 2 (DM2). Myotonic dystrophy (DM) is a multi-system disease and the most common form of muscular dystrophy in adults. In 1992, DM was shown to be caused by an expanded CTG repeat in the 3' untranslated region of the dystrophia myotonica-protein kinase gene (DMPK) on chromosome 19 (refs 2-6). Although several theories have been put forth to explain how the CTG expansion causes the broad spectrum of clinical features associated with DM, it is not understood how this mutation, which does not alter the protein-coding region of a gene, causes an affect at the cellular level. We have identified a five-generation family (MN1) with a genetically distinct form of myotonic dystrophy. Affected members exhibit remarkable clinical similarity to DM (myotonia, proximal and distal limb weakness, frontal balding, cataracts and cardiac arrhythmias) but do not have the chromosome-19 D CTG expansion. We have mapped the disease locus (DM2) of the MN1 family to a 10-cM region of chromosome 3q. Understanding the common molecular features of two different forms of the disease should shed light on the mechanisms responsible for the broad constellation of seemingly unrelated clinical features present in both diseases.

Adult↗
PubMed1988

Physical and genetic mapping of the Salmonella dublin virulence plasmid pSDL2. Relationship to plasmids from other Salmonella strains.

Plasmids of approximately 80 kb in size are found in nearly all clinical isolates of Salmonella dublin and are believed to be essential for virulence. We have shown previously that the 80-kb plasmid pSDL2 is required for the S. dublin Lane strain to establish a lethal systemic infection in BALB/c mice after oral or intraperitoneal inoculation. We now present a physical and genetic characterization of pSDL2. We have established a complete restriction endonuclease cleavage map of pSDL2 for five enzymes: Xba I, Bam HI, Xho I, Sal I, and Hind III. The region specifying autonomous replication has been localized to a 10.5-kb region of the Sal I A fragment by subcloning on the vector pBR322. Using transposon insertion mutagenesis with Tn5-oriT, a region encoding the virulence phenotype has been mapped within a 6.4-kb portion of the Sal I B fragment. Deletions generated by partial Eco RI restriction digestion demonstrate that at least 50 kb of the plasmid DNA are not required for replication or virulence functions, confirming the map location of these phenotypes. Plasmids of different sizes and restriction patterns were found in mouse virulent strains of S. dublin Vi+, S. enteritidis, and S. choleraesuis. By Southern hybridization, these putative virulence plasmids share a common 4-kb Eco RI fragment with the virulence region of pSDL2, and the plasmids from S. dublin Vi+ and S. enteritidis were shown to express mouse virulence comparable to pSDL2.

Cloning, Molecular↗
PubMed1978

The genetic mapping of a defective LPS response gene in C3H/HeJ mice.

The expression of a defective LPS response gene Lps and the major urinary protein (Mup-1) are concordantly inherited in backcross (C3H/HeJ x C57BL/6J)F1 x C3H/HeJ mice, indicating genetic linkage of these loci. Mup-1 is known to be linked to the brown coat color locus on chromosome 4 in mice; thus Lps can now be assigned to chromosome 4. A value of 0.06 +/- 0.02 has been estimated for the recombination frequency between Mup-1 and Lps. We have used the polysyndactyly (Ps) mutation further to localize Lps on chromosome 4. Lps is located between the Mup-1 and Ps loci.

Animals↗
PubMed1997

Lac repressor genetic map in real space.

Here, we present a graphic display of the phenotypes of more than 4000 single amino acid substitution mutations on the three-dimensional structure of the lac repressor tetramer bound to DNA. The genetic data and the X-ray diffraction studies contribute to define an allosteric mechanism and yield a visual demonstration of the importance of core or buried residues in protein structure.

Allosteric Site↗
PubMed2002

[Genetic mapping of the intergenomic translocated "taigu" genic sterility gene (Ms2)].

The "Taigu" genic sterility gene Ms2 located on the short arm of the 4D chromosome of common wheat (AABBDD) originally incorporated into hexoploid triticale (AABBRR) and durum wheat (AABB) through intergenomic translocation in distant hybridization was introduced back into the genomes of common wheat. The dominant male sterility was expressed normally in the new "Taigu" genic sterile wheat carrying the intergenomically translocated Ms2, and the female fertility mechanism in its male sterile plants was normal as well. Observation of the chromosome configuration at meiosis of pollen mother cells (PMC) of the young ears of the sterile plants showed that they were euploid plants (2n = 42). No configurations different from those of the "Taigu" genic sterility gene located at the original locus were noticed of the Ms2 intergenomically translocated back into the common wheat. In systematic test crosses with marker genes the intergenomically translocated gene Ms2 was found to be linked with the dominant dwarf marker in common wheat Rht3 and, consequently, remapped and located on the short arm of the 4B chromosome of common wheat with a distance of 9.7 cM from Rht3. The new locus was designated as Ms2 (4BS). Discussions are given of the fate of Ms2 during translocation in the hexoploid triticale, the exchange of the names for 4A and 4B chromosomes in common wheat and the possible exploitation of the new locus Ms2 (4BS), and the following speculations are made: (a) In genic genes of allopolyploid organisms the donor chromosomes tend to be intergenomically translocated to their physiologically and evolutionarily close chromosomes with the same order number and the same arm; (b) it is confirmed that the 7th International Conference of Wheat Genetics was right to exchange the names between chromosomes 4A and 4B of common wheat in 1988; and (c) as a new genetic marker and a breeding tool for all the chromosome B-carrying species in the tribe of Triticeae, Ms2(4BS) may have wide application in building and expanding the gene pool of germplasm resources of various species of wheat.

Chromosome Mapping↗
PubMed1997

Genetic mapping of a mouse ocular malformation locus, Tcm, to chromosome 4.

The Tcm mutation in the mouse is an autosomal dominant ocular malformation manifesting as microphthalmia, iris dysplasia, cataract, and coloboma. As a first step to cloning the Tcm gene, we report the localization of the Tcm mutation with respect to known microsatellite markers. Backcross progeny carrying the Tcm mutation were produced by mating Tcm/+ heterozygous mice to normal C57BL/6 partners. Genomic DNA from each mouse was subjected to PCR analysis to identify simple sequence length polymorphisms. Our results locate Tcm to Chr 4 and suggest candidate genes responsible for the Tcm phenotype. Finally, ocular histopathology was done in 3-week-old animals to define the extent of the malformation.

Abnormalities, Multiple↗
PubMed1979

Genetic mapping of the coding regions for three heat-shock proteins in Drosophila melanogaster.

We describe variants of three heat-shock proteins of Drosophila melanogaster and their use to map the chromosome regions that contain the coding sequences for these proteins. All three map to a region on chromosome 3L that includes only one heat-shock puff, designated as 67B. The results imply that the genes coding for at least three heat-shock proteins are included within the 67B region.

Animals↗
PubMed2003

Genetic mapping and analysis of quantitative trait loci affecting fiber and lignin content in maize.

Plant cell walls of forage provide a major source of energy for ruminant animals. Digestion of cell walls is limited by the presence of lignin, therefore the improving the digestibility of forages by reducing lignin content is a major goal in forage crop breeding programs. A recombinant inbred line maize population was used to map quantitative trait loci (QTL) for neutral detergent fiber (NDF), acid detergent fiber (ADF), and acid detergent lignin (ADL) of leaf-sheath and stalk tissues. All traits were positively genetically correlated. The larger genetic correlations were between NDF and ADF in sheaths (r = 0.84), NDF and ADF (r = 0.96), ADF and ADL (r = 0.83), and NDF and ADL (r = 0.76) in stalks. Twelve QTL were detected for NDF and 11 QTL for ADF in leaf-sheaths. Eight QTL detected for both traits were defined by the same or linked marker loci. Eight QTL were associated with leaf-sheath ADL. Eleven QTL were detected for NDF and ADF, and 12 QTL for ADL in stalks. Nine of eleven QTL detected for both NDF and ADF in stalks coincided in their genomic position. A high proportion of QTL detected for these traits had the same parental effects and genomic locations, suggesting that it is only necessary to select on one fiber component (NDF or ADF) to improve digestibility. Favorable correlated responses of unselected fiber components are expected due to coincident genomic locations of QTL and the high genetic correlation between fiber components. Several QTL detected in this study coincided in their positions with putative cellulose synthase genes from maize.

Cell Wall↗
PubMed1991

Genetic mapping of the chloroquine-resistance locus on Plasmodium falciparum chromosome 7.

The resurgence of malaria in recent decades has been accompanied by the worldwide spread of resistance to chloroquine, a drug once uncontested as the first-line antimalarial agent because of its efficacy and low toxicity. Chloroquine-resistant strains of Plasmodium falciparum counter the drug by expelling it rapidly via an unknown mechanism. In the absence of explicit biochemical knowledge of this efflux mechanism, reverse genetics provides a powerful approach to the molecular basis of chloroquine resistance. Here we report genetic linkage analysis in which 85 restriction fragment length polymorphism markers were used to examine inheritance of the 14 P. falciparum chromosomes in a laboratory cross between a chloroquine-resistant and a chloroquine-sensitive parasite. Inheritance data from 16 independent recombinant progeny show that the rapid efflux, chloroquine-resistant phenotype is governed by a single locus within an approximately 400-kilobase region of chromosome 7. Identification and characterization of genes within this region should lead to an understanding of the chloroquine-resistance mechanism.

Animals↗
PubMed1982

Correlation of the Genetic Map and the Endonuclease Site Map of Bacillus subtilis Bacteriophage SP02.

By marker rescue of bacteriophage SP02 sus mutants with purified bacteriophage SP02 DNA fragments, 11 of the 17 known bacteriophage SP02 sus loci were assigned to discrete DNA fragments. The left-most genetic locus, susA, was found to reside near one bacteriophage SP02 terminus (EcoRI-C1 fragment), whereas the right-most genetic locus, susP, was found to reside near the other bacteriophage SP02 terminus (EcoRI-C2 fragment). The physical locations of the intervening genetic loci were found to be consistent with the previously determined genetic order. Evidence was also obtained which suggested that at least one end of a transforming DNA fragment is degraded during DNA uptake by the competent bacterium.

Journal Article↗