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At least 577 records · Page 32Linked to original sources
PubMed2006

Assignment of 117 genes from HSA5 to the porcine IMpRH map and generation of a dense human-pig comparative map.

Twenty-two and eight significant quantitative trait loci for economically important traits have been located on porcine chromosomes (SSC) 2q and SSC16 respectively, both of which have been shown to correspond to human chromosome 5 (HSA5) by chromosome painting. To provide a comprehensive comparative map for efficient selection of candidate genes, we assigned 117 genes from HSA5 using a porcine radiation hybrid (IMpRH) panel. Sixty-six genes were assigned to SSC2 and 48 to SSC16. One gene was suggested to link to SSC2 markers and another to SSC6. One gene did not link to any gene, expressed sequence tag or marker in the map, including those in the present investigation. This study demonstrated the following: (1) SSC2q21-q28 corresponds to the region ranging from 74.0 to 148.2 Mb on HSA5q13-q32 and the region from 176.0 to 179.3 Mb on HSA5q35; (2) SSC16 corresponds to the region from 1.4 to 68.7 Mb on HSA5p-q13 and to the region from 150.4 to 169.1 Mb on HSA5q32-q35 and (3) the conserved synteny between HSA5 and SSC2q21-q28 is interrupted by at least two sites and the synteny between HSA5 and SSC16 is also interrupted by at least two sites.

Animals↗
PubMed1999

Epicardial mapping and radiofrequency catheter ablation of ischemic ventricular tachycardia using a three-dimensional nonfluoroscopic mapping system.

Endocardial radiofrequency catheter ablation of ischemic left ventricular tachycardia has been of variable success due to multiple factors. Two such factors include the location of the reentrant circuit in the deep myocardium or on the epicardial surface and the inherent limitations of fluoroscopy as a guide for target localization. We report a patient in whom successful epicardial mapping and radiofrequency catheter ablation of an ischemic left ventricular tachycardia was performed using pericardial access and the CARTO electroanatomic mapping system.

Aged↗
PubMed1999

Fine genetic mapping of diffuse non-epidermolytic palmoplantar keratoderma to chromosome 12q11-q13: exclusion of the mapped type II keratins.

Diffuse non-epidermolytic palmoplantar keratoderma (NEPPK) belongs to the heterogeneous group of skin diseases characterized by thickening of the stratum corneum of the palms and soles (1). This autosomal dominant PPK is characterized by a diffuse pattern of palmar and plantar hyperkeratosis giving the affected areas a thickened yellowish appearance with a marked erythematous edge. Linkage of diffuse NEPPK to chromosome 12q11-q13 has been demonstrated in two independent reports (2, 3). In this study, we describe detailed haplotyping with microsatellite markers mapping to this chromosomal region in three diffuse NEPPK pedigrees from the south of England. Fine mapping of a previously identified recombination event and the identification of a common disease haplotype segregating in the three pedigrees places the diffuse NEPPK locus proximal to the type II keratin gene cluster.

Chromosome Mapping↗
PubMed1982

Genetic mapping in mammals: chromosome map of domestic cat.

A genetic map of 31 biochemical loci located on 17 feline syntenic (linkage) groups has been derived by somatic cell genetic analysis of cat-rodent hybrids. Most of these syntenic groups have been assigned to one of the 19 feline chromosomes. Comparative linkage analysis of the feline biochemical loci and homologous human loci revealed considerable conservation of linkage associations between the primates and the Felidae (order Carnivora). Many of these same linkage groups have not been conserved in the murine genome. The genetic and evolutionary implications of comparative mapping analysis among mammalian species are discussed.

Animals↗
PubMed1994

Physical map of the genome of Acholeplasma oculi ISM1499 and construction of a Tn4001 derivative for macrorestriction chromosomal mapping.

A physical chromosomal map of Acholeplasma oculi ISM1499 was constructed by using field inversion gel electrophoresis. To assist in the ordering of the chromosomal fragments, a modified transposon, Tn4001.1064, was constructed. It was also used to rescue mycoplasmal chromosomal sequences adjacent to transposon insertion sites in a one-step cloning procedure. The total size of the A. oculi ISM1499 genome was estimated to be 1,633 kb. The restriction enzyme sites for ApaI, BssHII, EagI, and SmaI were positioned on the map along with several transposon insertion sites.

Acholeplasma↗
PubMed1980

Derivation of a restriction map of bacteriophage T3 DNA and comparison with the map of bacteriophage T7 DNA.

The DNA of bacteriophage T3 was characterized by cleavage with seven restriction endonucleases. AvaI, XbaI, BglII, and HindIII each cut T3 DNA at 1 site, KpnI cleaved it at 2 sites, MboI cleaved it at 9 sites, and HpaI cleaved it at 17 sites. The sizes of the fragments produced by digestion with these enzymes were determined by using restriction fragments of T7 DNA as molecular weight standards. As a result of this analysis, the size of T3 DNA was estimated to be 38.74 kilobases. The fragments were ordered with respect to each other and to the genetic map to produce a restriction map of T3 DNA. The location and occurrence of the restriction sites in T3 DNA are compared with those in the DNA of the closely related bacteriophage T7.

Base Sequence↗
PubMed1980

Correlation between genetic map and map of cleavage sites for sequence-specific endonucleases SalI, KpnI, BglI, and BamHI in bacteriophage T4 cytosine-containing DNA.

Cleavage sites for SalI, KpnI, BglI, and BamHI in cytosine-containing DNA from T4 alc10(alc) nd28(denA) D2a2(denB) amE51x5(56) amN55x5(42) have been mapped relative to each other, and the positions of deletions sa delta 9 (D1-stp), r1589(rII), del(39-56)12, and tk2(rI-tk) relative to these cleavage sites have been determined. Based on these analyses, a physical map of the T4 genome containing 166 kilobase pairs has been constructed.

Chromosome Mapping↗
PubMed1984

Direct demonstration that the abundant 6-kilobase herpes simplex virus type 1 mRNA mapping between 0.23 and 0.27 map units encodes the major capsid protein VP5.

The two partially colinear 6-kilobase (kb) and 1.5-kb mRNAs mapping between 0.23 and 0.27 map units on the herpes simplex virus type 1 genome were precisely located. The 5' end of the 6-kb mRNA was located 28 bases downstream of the sequence ATATATT and was 10 bases to the left of the BamHI site at 0.268. This position is ca. 90 bases to the left of our earlier reported sequence (R. J. Frink, K. G. Draper, and E. K. Wagner, Proc. Natl. Acad. Sci. U.S.A. 78:6139-6143, 1981). We used a polyclonal antibody made against purified herpes simplex virus type 1 VP5 to demonstrate that the 155,000-dalton translation product of the 6-kb mRNA is this capsid protein. The antibody did not react with the 35,000-dalton translation product of the 1.5-kb mRNA. We also confirmed our identification of VP5 as the translation product of the 6-kb mRNA by comparison of tryptic peptides of the in vitro-translated protein and authentic VP5.

Antibodies, Viral↗
PubMed2005

Selective activation of mitogen-activated protein (MAP) kinase kinase 3 and p38alpha MAP kinase is essential for cyclic AMP-dependent UCP1 expression in adipocytes.

The sympathetic nervous system regulates the activity and expression of uncoupling protein 1 (UCP1) through the three beta-adrenergic receptor subtypes and their ability to raise intracellular cyclic AMP (cAMP) levels. Unexpectedly, we recently discovered that the cAMP-dependent regulation of multiple genes in brown adipocytes, including Ucp1, occurred through the p38 mitogen-activated protein kinases (MAPK) (W. Cao, K. W. Daniel, J. Robidoux, P. Puigserver, A. V. Medvedev, X. Bai, L. M. Floering, B. M. Spiegelman, and S. Collins, Mol. Cell. Biol. 24:3057-3067, 2004). However, no well-defined pathway linking cAMP accumulation or cAMP-dependent protein kinase (PKA) to p38 MAPK has been described. Therefore, in the present study using both in vivo and in vitro models, we have initiated a retrograde approach to define the required components, beginning with the p38 MAPK isoforms themselves and the MAP kinase kinase(s) that regulates them. Our strategy included ectopic expression of wild-type and mutant kinases as well as targeted inhibition of gene expression using small interfering RNA. The results indicate that the beta-adrenergic receptors and PKA lead to a highly selective activation of the p38alpha isoform of MAPK, which in turn promotes Ucp1 gene transcription. In addition, this specific activation of p38alpha relies solely on the presence of MAP kinase kinase 3, despite the expression in brown fat of MKK3, -4, and -6. Finally, of the three scaffold proteins of the JIP family expressed in brown adipocytes, only JIP2 co-immunoprecipitates p38alpha MAPK and MKK3. Therefore, in the brown adipocyte the recently described scaffold protein JIP2 assembles the required factors MKK3 and p38alpha MAPK linking PKA to the control of thermogenic gene expression.

Adaptor Proteins, Signal Transducing↗
PubMed1998

Linkage map of Escherichia coli K-12, edition 10: the physical map.

A physical map, EcoMap10, of the now completely sequenced Escherichia coli chromosome is presented. Calculated genomic positions for the eight restriction enzymes BamHI, HindIII, EcoRI, EcoRV, BglI, KpnI, PstI, and PvuII are depicted. Both sequenced and unsequenced Kohara/Isono miniset clones are aligned to this calculated restriction map. DNA sequence searches identify the precise locations of insertion sequence elements and repetitive extragenic palindrome clusters. EcoGene10, a revised set of genes and functionally uncharacterized open reading frames (ORFs), is also depicted on EcoMap10. The complete set of unnamed ORFs in EcoGene10 are assigned provisional names beginning with the letter "y" by using a systematic nomenclature.

Chromosome Mapping↗
PubMed2000

Cloning and mapping of murine superoxide dismutase copper chaperone (Ccsd) and mapping of the human ortholog.

Copper does not exist in a free state within cells but is found consistently bound to metalloproteins. Specific metallochaperones escort copper to numerous targets within the cell, providing protection from the toxic effects of intracellular free copper. Many metallochaperones have been characterized in yeast, mouse, and human. To further characterize mouse metallochaperones, we cloned murine Ccsd from an adult mouse cDNA brain library, including both the coding region and the 5' and 3' UTRs. We obtained a 1,174-bp cDNA with an 825-bp open reading frame, translating a 274 amino acid protein that is 86.9% identical to human CCS. Using a mouse x hamster radiation hybrid panel, we mapped Ccsd to a proximal position on mouse chromosome 19. We mapped human CCS to 11q13 (homologous with mouse chromosome 19), utilizing a human x hamster radiation hybrid panel. The human and mouse metallochaperones are ubiquitously expressed in the major tissues of the body but seem to have different transcription products.

Amino Acid Sequence↗
PubMedDate not supplied

Mapping genes through the use of linkage disequilibrium generated by genetic drift: 'drift mapping' in small populations with no demographic expansion.

Linkage disequilibrium has been a powerful tool in identifying rare disease alleles in human populations. To date, most research has been directed to isolated populations which have undergone a bottleneck followed by rapid exponential expansion. While this strategy works well for rare diseases in which all disease alleles in the population today are clonal copies of some common ancestral allele, for common disease genes with substantial allelic heterogeneity, this approach is not predicted to work. In this paper, we describe the dynamics of linkage disequilibrium in populations which have not undergone a demographic expansion. In these populations, it is shown that genetic drift creates disequilibrium over time, while in expanded populations, the disequilibrium decays with time. We propose that common disease alleles might be more efficiently identified by drift mapping - linkage disequilibrium mapping in small, old populations of constant size where the disequilibrium is the result of genetic drift, not founder effect. Theoretical models, empirical data, and simulated population models are presented as evidence for the utility of this approach.

Chromosome Mapping↗
PubMed2003

Mapping of 195 genes in cattle and updated comparative map with man, mouse, rat and pig.

Our on-going goal is to improve and update the comparative genome organization between cattle and man but also among the most detailed mammalian species genomes i.e. cattle, mouse, rat and pig. In this work, we localized 195 genes in cattle and checked all human/bovine non-concordant localizations found in the literature. Next, we compiled all the genes mapped in cattle, goat, sheep and pig (2,166) for which the human ortholog with its chromosomal position is known, added corresponding data in mouse and rat, and ordered the genes relatively to the human genome sequence. We estimate that our compilation provides bovine mapping information for about 89% of the human autosomes. Thus, a near complete, overall and detailed picture of the number, distribution and extent of bovine conserved syntenies (regardless of gene order) on human R-banded autosomes is proposed as well as a comparison with mouse, rat and pig genomes.

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↗
PubMed1997

Map integration at human chromosome 10: molecular and cytogenetic analysis of a chromosome-specific somatic cell hybrid panel and genomic clones, based on a well-supported genetic map.

Well-characterized, chromosome-specific somatic cell hybrid panels are powerful tools for the analysis of the human genome. We have characterized a panel of human x hamster somatic cell hybrids retaining fragments of human chromosome 10 by fluorescence in situ hybridization and associated them to genetic markers. Most of the hybrids were generated by the radiation-reduction method, starting from a chromosome 10-specific monochromosomal hybrid, whereas some were collected from hybrids retaining chromosome 10-specific fragments as a result of spontaneous in vitro rearrangements. PCR was used to score the retention of 57 microsatellite markers evenly distributed along a well-supported framework genetic map containing 149 loci uniquely placed at 69 anchor points (odds exceeding 1,000:1), with an average spacing of 2.8 cM. As an additional resource for genomic studies involving human chromosome 10, we report the cytogenetic localization of a series of YAC and PAC clones recognized by at least one genetic marker. Somatic cell hybrids provide a powerful source of partial chromosome paints useful for detailed clinical cytogenetic and primate chromosome evolution investigations. Furthermore, correlation of the above physical, genetic, and cytogenetic data contribute to an emerging consensus map of human chromosome 10.

Animals↗
PubMed2005

Linkage disequilibrium maps and association mapping.

The causal chain between a gene and its effect on disease susceptibility cannot be understood until the effect has been localized in the DNA sequence. Recently, polymorphisms incorporated in the HapMap Project have made linkage disequilibrium (LD) the most powerful tool for localization. The genetics of LD, the maps and databases that it provides, and their use for association mapping, as well as alternative methods for gene localization, are briefly described.

Databases, Genetic↗
PubMed2004

Use of a dense single nucleotide polymorphism map for in silico mapping in the mouse.

Rapid expansion of available data, both phenotypic and genotypic, for multiple strains of mice has enabled the development of new methods to interrogate the mouse genome for functional genetic perturbations. In silico mapping provides an expedient way to associate the natural diversity of phenotypic traits with ancestrally inherited polymorphisms for the purpose of dissecting genetic traits. In mouse, the current single nucleotide polymorphism (SNP) data have lacked the density across the genome and coverage of enough strains to properly achieve this goal. To remedy this, 470,407 allele calls were produced for 10,990 evenly spaced SNP loci across 48 inbred mouse strains. Use of the SNP set with statistical models that considered unique patterns within blocks of three SNPs as an inferred haplotype could successfully map known single gene traits and a cloned quantitative trait gene. Application of this method to high-density lipoprotein and gallstone phenotypes reproduced previously characterized quantitative trait loci (QTL). The inferred haplotype data also facilitates the refinement of QTL regions such that candidate genes can be more easily identified and characterized as shown for adenylate cyclase 7.

Adenylyl Cyclases↗