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[Creating a system of conjugated chromosome transfer and genetic mapping of Vibrio cholerae serogroup O139 chromosomes].

A conjugational gene transfer system consisting of donor and recipient strains has been developed for genetic analysis of Vibrio cholerae 0139 serogroup, a new cholera agent. Donor strains constructed using the Tn5-Mob carrying the origin of transfer (ori T) of plasmid RP4 and helper plasmid pRP4-4 were able to perform a directed transfer of chromosomal markers. Recipient strains carried mutations in auxotrophic genes as well as in virulence genes. Based on this gene transfer system, a genetic map of V. cholerae chromosome has been created showing the order of 17 gene markers. Relationship between the genetic structure of V. cholerae 0139 and 01 is discussed.

Chromosome Mapping↗

PubMed2002

[Genetic map of 10 STR loci on chromosome 9].

To understand the genetic polymorphism of 10 STR loci on chromosome 9 and reveal the difference on the linkage maps of different populations, the author used a set of nine tetranucleotide- and one tritranucleotide-repeat STR markers on chromosome 9 chosen from Genome Data Bank. EDTA-blood was collected from unrelated family in Baiyin City, Gansu province. DNA was extracted by Chelex-100 method and amplified by the polymerase chain reaction (PCR). The PCR products were analyzed using PAGE electrophoresis. We calculated the allele frequencies and heterozygosity and PIC of every ten STR loci. Using the data of Chinese Han pedigree, we constructed a genetic map of chromosome 9 making up with 10 STR loci. Then we compared our map with the map in GDB. Our results indicate that there are some differences on the genetic map between Chinese and GDB. That means, it is essential to do some population genetic evaluations before using the data of GDB into Chinese population.

China↗

PubMed1988

Cloning and generation of a genetic map of bacteriophage N4 DNA.

Analysis of coliphage N4 development has been hindered by the lack of a genetic map. Conventional methods of complementation and recombination have been inadequate because N4 shows very high levels of recombination, which are independent of the host recombination system. We have cloned restriction fragments of the 72-kb genome of N4 and have used these clones to rescue a collection of suppressor-sensitive and temperature-sensitive mutants. After mutations were localized to a small region by marker rescue, complementation groups were defined. In this way several functions essential for transcription and replication have been mapped. Finally, a nonessential 6-kb region of the N4 genome has been identified by characterizing phage deletions isolated after heat and citrate treatment of virions.

Chromosome Deletion↗

PubMed1989

Fine-structure genetic map of the maltose transport operon of Salmonella typhimurium.

We have constructed a fine-structure genetic map of the maltose transport operon in Salmonella typhimurium. We have isolated mal mutants by using indicator plates, penicillin selection, or a proton suicide technique. Mutants were obtained as spontaneous events or were induced by chemical mutagenesis and transposon insertion. Tn10 and Mu d(lac Ap)1 insertion mutations were used to create deletions. Mutations were also obtained in a gene that is equivalent to lamB in Escherichia coli, which codes for the lambda bacteriophage receptor. The gene products in the mutants were characterized by sodium dodecyl sulfate-polyacrylamide-gel electrophoresis and immunoblotting. Our data indicate that the location of this operon on the Salmonella chromosome as well as the gene order and its orientation are the same as those in E. coli. This map will be useful in studying the mechanism of periplasmic transport in S. typhimurium.

ATP-Binding Cassette Transporters↗

PubMed2003

Development of a physical and genetic map of the virulent Wolbachia strain wMelPop.

We report here the construction of a physical and genetic map of the virulent Wolbachia strain, wMelPop. This map was determined by ordering 28 chromosome fragments that resulted from digestion with the restriction endonucleases FseI, ApaI, SmaI, and AscI and were resolved by pulsed-field gel electrophoresis. Southern hybridization was done with 53 Wolbachia-specific genes as probes in order to determine the relative positions of these restriction fragments and use them to serve as markers. Comparison of the resulting map with the whole genome sequence of the closely related benign Wolbachia strain, wMel, shows that the two genomes are largely conserved in gene organization with the exception of a single inversion in the chromosome.

Blotting, Southern↗

PubMed2003

Mapping of gene-specific markers on the genetic map of chickpea (Cicer arietinum L.).

With the exception of the fact that it is made up of eight different chromosomes, the physical organization of the 738-Mb genome of the important legume crop chickpea (Cicer arietinum L.) is unknown. In an attempt to increase our knowledge of the basic structure of this genome, we determined the map positions of a series of genes involved in plant defence responses (DR) by genetic linkage analysis. Exploiting the sequence data available in GenBank, we selected genes known to be induced in chickpea and other plants by pathogen attack. Gene-specific primers were designed based on conserved regions, and used to detect the corresponding gene sequences in a segregating population derived from an interspecific cross between Cicer arietinum and C. reticulatum. Forty-seven gene-specific markers were integrated into an existing map based on STMS, AFLP, DAF and other anonymous markers. The potential of this approach is discussed.

Chromosome Mapping↗

PubMed1975

Genetic mapping of a mutation that causes ribonucleases III deficiency in Escherichia coli.

the mutation that causes ribonuclease III (RNase III) deficiency in strain AB301-105 of Kindler et al. (1973) has been mapped by use of F' merodiploids, Hfr matings, and P1 transduction. This mutation, rnc-105, lies close to nadB, near 49 min on the genetic map of Escherichia coli. The rnc-105 mutation has been transferred from its original genetic background by transduction and conjugation, and these new strains have the same defects in ribonucleic acid processing reported previously for AB301-105. Strains that carry rnc-105 grow more slowly than parental rnc+ strains, but the difference in growth rate seems to depend on the genetic background of each strain. Bacteriophage T7 grows about equally well in RNase III+ and III- female strains of E. coli, even though the specific cuts that RNase III makes in T7 ribonucleic acid are not made in the RNase III- strains. A low-phosphate defined medium in which most E. coli strains seem to grow well was developed. This medium is equally useful for labeling ribonucleic acids with 32PO4 and as a selective medium for genetic manipulations. It was used to determine the growth requirements of strain AB301-105, which are biotin and succinate in addition to the methionine and histidine requirements of the parental strain. The biotin mutation lies near the position expected from known mutations of E. coli, but the succinate mutation apparently does not. The possibility that the succinate requirement could be due to the RNase III deficiency is discussed. A uraP mutation was isolated for use in transferring rnc-105 between strains by conjugation. It lies near 47 min, somewhat removed from the commonly accepted position for uraP.

Biotin↗

PubMed1996

Genetic mapping of the spinocerebellar ataxia type 2 gene on human chromosome 12.

The dominant spinocerebellar ataxias are a genetically heterogeneous group of diseases leading to premature death of neurons in the cerebellum and other parts of the nervous system. The mutation causing SCA1 is on human chromosome (CHR) 6p and SCA3 is on CHR 14q. To refine the location of the SCA2 gene on CHR 12q, we performed genetic linkage analysis between the SCA2 locus and nine Ioci (D12S58, D12S78, D12S317, D12S330, D12S353, D12S84, D12S105, D12S79, and PLA2) in three SCA2 families. The highest pairwise lod scores were obtained between SCA2 and D12S84/D12S105 and D12S79. We determined the best order and genetic distances among these loci in ten multigenerational families by multipoint linkage analysis and established the following order: D12S101-D12S58/IGF1- D12S78-D12S317-D12S330/D12S353-D12S84/D 12S105-D12S79-PLA2. Using this genetic map, multipoint linkage analysis placed SCA2 between D12S84/D12S105 and D12S79.

Chromosome Mapping↗

PubMed1970

Genetic mapping and dominance of the amber suppressor, Su1 (supD), in Escherichia coli K-12.

In this report Su1 (supD), which is known to suppress "amber" mutations by means of a specific transfer ribonucleic acid, has been mapped relative to his and uvrC and has been found to be located at about 37.5 min on the Taylor and Trotter genetic map of the Escherichia coli K-12 chromosome. In addition, Su1(+) has been shown to be dominant over Su1(-), which supports the idea that Su1 is the structural gene for the suppressing transfer ribonucleic acid.

Alkaline Phosphatase↗

PubMed1987

[Genetic mapping of transposon Tn5-induced mutation blocking threonine dehydrogenase in Escherichia coli K-12].

The paper deals with a mutant of Escherichia coli K-12 obtained by transposon Tn5 mutagenesis. Insertion of this transposon inactivated the gene for L-threonine dehydrogenase catalysing the first step of L-threonine degradation. The insertion of Tn5 was mapped by using conjugation as well as transduction by T4GT7 and P1. It is located at 81 min of the E. coli genetic map between mtl and pyrE genes.

Alcohol Oxidoreductases↗

PubMed2004

A nearest-neighboring-end algorithm for genetic mapping.

MOTIVATION: High-throughput methods are beginning to make possible the genotyping of thousands of loci in thousands of individuals, which could be useful for tightly associating phenotypes to candidate loci. Current mapping algorithms cannot handle so many data without building hierarchies of framework maps. RESULTS: A version of Kruskal's minimum spanning tree algorithm can solve any genetic mapping problem that can be stated as marker deletion from a set of linkage groups. These include backcross, recombinant inbred, haploid and double-cross recombinational populations, in addition to conventional deletion and radiation hybrid populations. The algorithm progressively joins linkage groups at increasing recombination fractions between terminal markers, and attempts to recognize and correct erroneous joins at peaks in recombination fraction. The algorithm is O (mn3) for m individuals and n markers, but the mean run time scales close to mn2. It is amenable to parallel processing and has recovered true map order in simulations of large backcross, recombinant inbred and deletion populations with up to 37,005 markers. Simulations were used to investigate map accuracy in response to population size, allelic dominance, segregation distortion, missing data and random typing errors. It produced accurate maps when marker distribution was sufficiently uniform, although segregation distortion could induce translocated marker orders. The algorithm was also used to map 1003 loci in the F7 ITMI population of bread wheat, Triticum aestivum L. emend Thell., where it shortened an existing standard map by 16%, but it failed to associate blocks of markers properly across gaps within linkage groups. This was because it depends upon the rankings of recombination fractions at individual markers, and is susceptible to sampling error, typing error and joint selection involving the terminal markers of nearly finished linkage groups. Therefore, the current form of the algorithm is useful mainly to improve local marker ordering in linkage groups obtained in other ways. AVAILABILITY: The source code and supplemental data are http://www.iubio.bio.indiana.edu/soft/molbio/qtl/flipper/ CONTACT: ccrane@purdue.edu.

Algorithms↗

PubMed1998

Genetic mapping of a locus (mass1) causing audiogenic seizures in mice.

Frings audiogenic seizure-susceptible mice are a model for sensory-evoked reflex seizures. Their seizure phenotype is characterized by wild running, loss of righting reflex, tonic flexion, and tonic extension in response to high-intensity sound stimulation. The Frings mice represent an inbred colony that has not been genetically characterized. This investigation studied the mode of inheritance for audiogenic seizures by crossing the Frings mouse with the seizure-resistant C57BL/6J mouse. Among the backcross progeny generated by crossing (Frings x C57BL/6J)F1 mice with the Frings strain, 391 of the 836 N2 progeny were audiogenic seizure susceptible, a finding consistent with monogenic inheritance. Genetic mapping and linkage analysis of hybrid mice using MIT microsatellite marker sequences localized the seizure gene, named mass1 for monogenic audiogenic seizure susceptible, to an approximately 3.6 cM interval in the middle of mouse chromosome 13. Linkage of mass1 to chromosome 13 is an important step in identifying the gene associated with a monogenic seizure disorder in mice, which may ultimately lead to a better understanding of the pathophysiology of human seizure disorders.

Acoustic Stimulation↗

PubMed1990

Genetic mapping of two new DNA markers in Xq26-q28 relative to the fragile-X syndrome locus.

We have characterized and genetically mapped two new DNA markers (DXS311 and DXS312) with respect to 10 existing loci in Xq26----Xq28 in a set of 15 families in which the fragile-X [fra(X)] syndrome was segregating. Two-point and multipoint linkage analyses were performed taking into account the incomplete penetrance of the fra(X) mutation. The most likely order on the basis of these data is centromere-DXS79-DXS10-DXS311-DXS86-(F9-DXS99 )-(DXS98-DXS312)-fra(X)-DXS52- DXS15-F8C-telomere. DXS98 and one of the new loci, DXS312, were found to be the proximal markers closest to the fra(X) locus. The order F9-(DXS98-DXS312)-fra(X) was found to be 5.9 x 10(4) times more likely than the order (DXS98-DXS312)-F9-fra(X).

Chromosome Mapping↗

PubMed2006

Improving estimates of genetic maps: a maximum likelihood approach.

As a result of previous large, multipoint linkage studies there is a substantial amount of existing marker data. Due to the increased sample size, genetic maps estimated from these data could be more accurate than publicly available maps. However, current methods for map estimation are restricted to data sets containing pedigrees with a small number of individuals, or cannot make full use of marker data that are observed at several loci on members of large, extended pedigrees. In this article, a maximum likelihood (ML) method for map estimation that can make full use of the marker data in a large, multipoint linkage study is described. The method is applied to replicate sets of simulated marker data involving seven linked loci, and pedigree structures based on the real multipoint linkage study of Abkevich et al. (2003, American Journal of Human Genetics 73, 1271-1281). The variance of the ML estimate is accurately estimated, and tests of both simple and composite null hypotheses are performed. An efficient procedure for combining map estimates over data sets is also suggested.

Algorithms↗

PubMed1992

Genetic mapping of four dinucleotide repeat loci, DXS453, DXS458, DXS454, and DXS424, on the X chromosome using multiplex polymerase chain reaction.

Dinucleotide CA repeat sequences in the human genome have been shown to be highly polymorphic due to variation in the length of the repeat-containing segment. Therefore, these markers can serve as anchor loci in the construction of a high-resolution genetic map of the human genome. In this study, we improved the efficiency of typing dinucleotide repeats using multiplex polymerase chain reaction (PCR). Dinucleotide repeat sequences of four previously identified markers (DXS453, DXS458, DXS454, and DXS424) on the long arm of the X chromosome were simultaneously amplified in a single PCR reaction. This multiplex PCR was applied to genotype individuals from the 40 CEPH reference families, and the genotypic data were used to determine the map position of the four loci with respect to eight reference markers in the Xq region by linkage analysis.

Base Sequence↗

PubMed1990

Genetic mapping of regulatory mutations of Bacillus subtilis riboflavin operon.

Seven mutations leading to riboflavin overproduction in Bacillus subtilis were found to be linked to the marker dnaF133 (145 degrees on the B. subtilis genetic map) by transformation. Cotransfer indexes (42.5%-61.7%) suggest that the ribC mutations are alleles of the same locus. Results of transduction and transformation crosses suggest the following order of markers:pyrD26-ts-6-dnaF133-ribC-recA1.

Alleles↗

PubMed1981

Genetic mapping of a linked cluster of ribosomal ribonucleic acid genes in Bacillus subtilis.

A ribosomal ribonucleic acid gene set consisting of genes for 16S, 23S, 5S, and 4S ribonucleic acid species has been genetically mapped to a position between the markers recG13 and abrB74 on the Bacillus subtilis chromosome and designated rrnA. A ribosomal mutation, ksgA, was found to be linked to rrnA. This places rrnA in a region of the chromosome where ribosome-related genes occur but that is not directly adjacent to the major cluster of ribosome-related markers.

Bacillus subtilis↗

PubMed1994

Genetic map of the region around grizzled (gr) and mocha (mh) on mouse chromosome 10, homologous to human 19p13.3.

Grizzled (gr) is a recessive mouse mutation resulting in a gray coat color and reduced perinatal viability. Mocha (mh) is one of several recessive mouse mutants characterized by platelet storage pool disorder, pigment abnormalities, reduced fertility, kidney function deficiencies, and, in some mutants, inner ear and natural killer cell deficiencies. Murine platelet storage pool deficient mutants may be models for Chediak-Higashi and Hermansky-Pudlak syndromes in humans. The genes for gr and mh are very closely linked to each other (0 +/- 1.2 cM). However, their relative position with respect to molecular markers was previously unknown. Thus, genetic mapping of the gr locus will also yield information about the mh location. To map these two genes genetically, we have performed an intersubspecific backcross of grizzled mice with Mus musculus castaneus. In 539 progeny tested, we found no recombination between the gr gene, the gene for anti-Muellerian hormone (Amh), and the microsatellite markers D10Mit7, D10Mit21, and D10Mit23. One recombination event for each of the flanking markers Basigin (Bsg) and D10Mit22 was identified. These closely linked markers should provide entry points for positional cloning of the gr and mh genes. The region linked to grizzled is homologous to a gene-rich region on human Chromosome 19p13.3.

Animals↗