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At least 1,333 records · Page 74Linked to original sources
PubMed1996

Gene mapping by chromosome microdissection and microisolation in the chicken.

A chromosome microdissection and microisolation technique in combination with filter hybridization was developed for chromosomal localization of cloned chicken genes. The DNA was obtained from microdissected chromosome regions of metaphase spreads. Dissected DNA was amplified by polymerase chain reaction (PCR). The chicken MHC gene located on the nucleolar chromosome and beta-actin gene located on chromosome 2q were chosen as tests for the procedure and then detected by dot blot analysis using amplified chromosomal DNA probed with biotinylated DNA. The study establishes the technique of using chromosome microdissection and microisolation for localization of cloned genes as a complementary or alternative approach to both in situ DNA/chromosome hybridization and fluorescent in situ hybridization.

Actins↗
PubMed2001

Resistance to xenobiotic-induced autoimmunity maps to chromosome 1.

Although evidence indicates that environmental factors play a major role in precipitating systemic autoimmunity in genetically susceptible individuals, little is known about the mechanisms involved. Certain heavy metals, such as mercury, are potent environmental immunostimulants that produce a number of immunopathologic sequelae, including lymphoproliferation, hypergammaglobulinemia, and overt systemic autoimmunity. Predisposition to such metal-induced immunopathology has been shown to be influenced by both MHC and non-MHC genes, as well as susceptibility to spontaneous lupus, in mice and other experimental animals. Among the various mouse strains examined to date, the DBA/2 appears to uniquely lack susceptibility to mercury-induced autoimmunity (HgIA), despite expressing a susceptible H-2 haplotype (H-2d). To define the genetic basis for this trait, two genome-wide scans were conducted using F2 intercrosses of the DBA/2 strain with either the SJL or NZB strains, both of which are highly susceptible to HgIA. A single major quantitative trait locus on chromosome 1, designated Hmr1, was shown to be common to both crosses and encompassed a region containing several lupus susceptibility loci. Hmr1 was linked to glomerular immune complex deposits and not autoantibody production, suggesting that DBA/2 resistance to HgIA may primarily involve the later stages of disease pathogenesis. Identification and characterization of susceptibility/resistance genes and mechanisms relevant to the immunopathogenesis of mercury-induced autoimmunity should provide important insights into the pathogenesis of autoimmunity and may reveal novel targets for intervention.

Animals↗
PubMed1987

Enhancement of the apparent cleavage specificities of restriction endonucleases: applications to megabase mapping of chromosomes.

We have described how DNA methylases may be used to enhance the apparent specificities of restriction endonucleases [9-11, 17, 18] to generate DNA fragments averaging 6000 to 270,000,000 base pairs on random DNA. Taking into account the non-random arrangement of natural DNA, we have predicted the rarity of certain recognition sequences in the genomes of several species.

Base Sequence↗
PubMed1979

De novo partial trisomy of chromosome 18(pter yields q11:). Some observations on the phenotype mapping of chromosome 18 imbalances.

An infant with a partial trisomy 18(pter yields q11:) is described. The patient's phenotype consists of many features of complete trisomy 18. The findings are compared with those from similar cases reported in the literature permitting to conclude that 18q121-q122 segment is the "critical" zone which when trisomic, causes the severe stigmata (inner organ malformations and early death) of the complete trisomy 18.

Child, Preschool↗
PubMed1981

Fv-4: gene controlling resistance to NB-tropic Friend murine leukemia virus. Distribution in wild mice, introduction into genetic background of BALB/c mice, and mapping of chromosomes.

A gene controlling resistance to NB-tropic Friend murine leukemia virus (F-MuLV) was studied in wild mice. Mice of various subspecies were crossed with inbred BALB/c mice, and their F1 hybrids were tested for resistance to F-MuLV. Some mice of Mus musculus molossinus (Japan), M. musculus castaneus (Taiwan and the Philippines), and M. musculus urbanus (Sri Lanka) appeared to have a dominant resistance gene. A partially congenic strain, BALB/c-Fv-4wr (C4W), was established by the introduction of the gene Fv-4wr from a M. musculus molossinus into the genetic background of BALB/c mice. [(C4W X DBA/2) X C57BL/6-Fvs] crosses revealed that Fv-4wr is located on chromosome 12 with the gene order of Fv-4w-Pre-1-lgh-1, apparently at the same site as the Fv-4. The resistance of C4W mice was indistinguishable from the Fv-4-controlled resistance of FRG mice.

Animals↗
PubMed1996

Mapping of chromosomal imbalances in pancreatic carcinoma by comparative genomic hybridization.

To identify recurrent chromosomal imbalances in pancreatic adenocarcinoma, 27 tumors were analyzed by using comparative genomic hybridization. In 23 cases chromosomal imbalances were found. Gains of chromosomal material were much more frequent than losses. The most common overrepresentations were observed on chromosomes 16p (eight cases), 20q (seven cases), 22q (six cases), and 17q (five cases) and under-representations on a subregion of chromosome 9p (eight cases). Distinct high-level amplifications were found on 1p32-p34, 6q24, 7q22, 12p13, and 22q. These data provide evidence for a number of new cytogenetically defined recurrent aberrations which are characteristic of pancreatic carcinoma. The overrepresented or underrepresented chromosomal regions represent candidate regions for potential oncogenes and tumor suppressor genes, respectively, possibly involved in pancreatic tumorigenesis.

Adenocarcinoma↗
PubMed1996

New approaches to the mapping of chromosomal domains.

Although it is generally accepted that the chromosome is divided into elementary subunits, the structural and functional domains, the organisation of these structures at the molecular level is not well understood. In particular, the domain boundaries are not easily identifiable. Several possible candidates such as MARs/SARs, insulators, LCRs, palindromic sequences, or easily melting sequences have been found in the regions having properties one would except for boundaries. None of these elements, however, has been found in all of the constructs functioning as boundaries in tests in vivo. Recent work suggests that the common denominator might be the presence og GC-rich oligonucleotide stretches and the formation of the chromatin hypersensitive sites. A model is discussed in which "unusual" structures, in particular the four-stranded DNA sequence elements containing unpaired bases, play the role of domain boundaries.

Animals↗
PubMed1996

Genes specifying receptors for F18 fimbriated Escherichia coli, causing oedema disease and postweaning diarrhoea in pigs, map to chromosome 6.

The study comprised 236 pigs selected for resistance or susceptibility to oedema disease. The susceptibility to colonization of the small intestine by an Escherichia coli strain causing oedema disease was determined: (1) by monitoring faecal excretion of weaned pigs orally inoculated with E. coli strain O139:K12(B):H1:F18ab serotype; and (2) by an in vitro adhesion assay using an F18ab positive E. coli strain and small intestinal enterocyte preparations. Susceptibility to adhesion by these bacteria was shown to be controlled by a dominant (B) allele of the ECF18R locus and resistance by the alternative recessive allele (b). Pigs were typed for 14 blood group systems, 11 biochemical polymorphisms and the polymorphism at nucleotide 1843 of the RYR1 locus. Linkage was demonstrated between the locus for F18 E. coli receptors and the loci S, RYR1, GPI, EAH, A1BG and PGD (Z > 20). The most likely gene orders are: S-ECF18R-RYR1-GPI-PGD or GPI-RYR1-ECF18R-S-PGD. The recombination frequencies between ECF18R-S and ECF18R-RYR1 were estimated to be theta = 0.5% and 3.1%, respectively.

Adhesins, Bacterial↗
PubMed1998

Multiple lupus susceptibility loci map to chromosome 1 in BXSB mice.

BXSB mice spontaneously develop a lupus-like syndrome that is accelerated by the Yaa gene (Y-linked autoimmune accelerator). We studied the phenotype of disease in (B10 x BXSB)F1 and (BXSB x (B10 x BXSB)F1) backcross mice and genotyped 224 backcross animals to allow a microsatellite-based genome-wide linkage analysis to be conducted. In the backcross population, three intervals on chromosome 1 showed significant linkage to disease, suggesting that multiple loci contribute to the production of autoimmune disease. D1Mit5 at 32.8 cM was linked to development of nephritis (chi(2) = 15.68, p = 7.5 x 10(-5)), as was D1Mit12 at 63.1 cM (chi(2) = 20.17, p = 7.1 x 10(-6)). D1Mit403 at 100 cM was linked to anti-dsDNA Ab production (chi(2) = 17.28, p = 3.2 x 10(-5)). Suggestive linkages to antinuclear Abs and nephritis were identified on chromosome 3, to splenomegaly on chromosome 4, and to anti-ssDNA Ab production on chromosome 10. Chromosome 4 and the telomeric region of chromosome 1 have previously been linked to disease in other mouse models of systemic lupus erythematosus; however, the centromeric regions of chromosome 1 and chromosomes 3 and 10 are unique to BXSB. This implies that, though some loci may be common to a number of mouse models of lupus, different clusters of disease genes confer disease susceptibility in different strains of mice.

Animals↗
PubMed1994

Seven genes on the short arm of human chromosome 3 map to two regions on Macropus eugenii (tammar wallaby) chromosome 2.

Seven genes were mapped by in situ hybridization to metaphase chromosomes of the marsupial species Macropus eugenii, using a series of human-derived cloned probes (six cosmids and one cDNA). The genes were located in two widely separated clusters on the long arm of M. eugenii chromosome 2, in contrast to their location in a single cluster on the distal half of the short arm of human chromosome 3. Multiple rearrangements had to be involved in the evolutionary divergence of these chromosome segments from the unknown arrangement in the common ancestor.

Animals↗
PubMed1995

Construction of a complete genomic library of Saccharomyces cerevisiae and physical mapping of chromosome XI at 3.7 kb resolution.

A consortium of European laboratories has been organized to systematically sequence the genome of Saccharomyces cerevisiae. As part of the BIOTECH program aimed at sequencing chromosomes XI and II, we have constructed a total genomic library of yeast strain FY1679 (a direct S288C derivative) into cosmid vectors pWE15 and pOU61cos. Primary clones from four independent libraries totalling 190 genome equivalents have been stored at -80 degrees C. A subset of 1939 independent clones (six genome equivalents) was hybridized using purified chromosomes XI and X as probes. A total of 147 chromosome XI-specific cosmid clones was used to construct the physical map of that chromosome. Mapping methods included a combination of classical bottom-up strategies (fingerprinting, hybridizations) and a novel top-down strategy using I-SceI chromosome fragmentation. The 147 cosmid clones form a unique contig covering the entire chromosome XI (666 kb) with the sole exceptions of the (C1-3A)n repeats of the telomeres. Colinearity of cosmid inserts with yeast DNA was directly verified. A complete EcoRI map of chromosome XI was deduced from partial overlaps of cosmids and used for the sequencing program. Comparison of this map with the genetic map shows unexpected divergences that have been solved by subsequent genetic analysis, yet underline the necessity of independent physical mapping in genome projects.

Base Sequence↗
PubMed2003

Chromosomal breakpoint mapping by arrayCGH using flow-sorted chromosomes.

Despite the recent completion of the human genome project, the mapping of disease-related chromosomal translocation breakpoints and genes has remained laborious. Here, we describe a novel and rapid procedure to map such translocation breakpoints using flow-sorted chromosomes in combination with array-based comparative genomic hybridization (arrayCGH). To test the feasibility of this approach, we used a t(12;15)(q13;q25)-positive cell line with known breakpoint positions as a model. The derivative 12 chromosomes were flow-sorted, labeled, and hybridized to a genome-wide array containing 3648 well-characterized human genomic clones. The exact locations of the breakpoints on both chromosome 12 and 15 could be determined in a single hybridization experiment. In addition, we have tested the minimal amount of material necessary to perform these experiments and show that it is possible to obtain highly reliable profiles using as little as 10,000 flow-sorted chromosomes.

Chromosome Breakage↗
PubMed2003

A comparative map of bovine chromosome 19 based on a combination of mapping on a bacterial artificial chromosome scaffold map, a whole genome radiation hybrid panel and the human draft sequence.

We have constructed a medium density physical map of bovine chromosome 19 using a combination of mapping loci on both a bovine bacterial artificial chromosome (BAC) scaffold map and a whole genome radiation hybrid (WGRH) panel. The resulting map contains 70 loci spanning the length of bovine chromosome 19. Three contiguous groups of BACs were identified on the basis of multiple loci mapping to individual BAC clones. Bovine chromosome 19 was found in this study to be comprised almost entirely from regions of human chromosome 17, with a small region putatively assigned to human chromosome 10. Fourteen breakpoints between the bovine and human chromosomes were detected, with a possibility of five more based on ordering of the WGRH map.

Animals↗
PubMed1997

The rat 5S rRNA bona fide gene repeat maps to chromosome 19q12-->qter and the pseudogene repeat maps to 12q12.

The bona fide 5S rRNA genes in the rat are found in a 1.8-kb tandem repeat and the pseudogenes occur in a 2.5-kb tandem repeat. Three bona fide 5S rRNA genes and one gene variant with one base substitution in the coding region were isolated from the 1.8-kb repeat. Six pseudogenes were isolated from the 2.5-kb repeat. The total number of genes/gene variants/pseudogenes is 700-1200 copies per haploid genome, and the pseudogene repeat contains about 50% more 5S rDNA related sequences compared with the bona fide gene repeat. Various well-defined 5' - and 3'-flanking sequences of the bona fide gene and of the pseudogene were used for in situ hybridization to metaphase chromosomes. The results showed that the bona fide 5S rRNA gene repeat Rn5s maps to chromosome 19q12 and the pseudogene repeat Rn5sp maps to 12q12.

Animals↗