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At least 451 records · Page 25Linked to original sources
PubMed1993

The genetic map around the tail kinks (tk) locus on mouse chromosome 9.

Tail kinks (tk) is a classical mouse skeletal mutation, located on Chromosome (Chr) 9. As the first step for the positional cloning of the tk gene, we have established a genetic map of a region surrounding the tk locus by generating a backcross segregating for tk. From this backcross, 1004 progeny were analyzed for the coat-color phenotype of the proximally located dilute (d) gene and for the distally flanking microsatellite marker, D9Mit12. Fifty-six recombinants between d and tk and 75 recombinants between tk and D9Mit12 were identified, completing a panel of 130 recombinants including one double recombinant. This panel allowed us to map five microsatellite loci as well as d and Mod-1 with respect to tk. We show that one of the microsatellite markers mapped, D9Mit9, does not recombine at all with tk in our backcross. This indicates that the D9Mit9 locus will serve as a good starting point for a chromosomal walk to the tk gene.

Animals↗
PubMed1992

A genetic map of the mouse suitable for typing intraspecific crosses.

We report the construction of a genetic linkage map of the mouse, consisting entirely of genetic markers that can be rapidly typed by polymerase chain reaction and that show a high degree of polymorphism among inbred laboratory strains. Specifically, the map contains 317 simple sequence length polymorphisms at an average spacing of 4.3 cM and is detectably linked to approximately 99% of the mouse genome. In typical crosses between inbred laboratory strains, about 50% of the markers are polymorphic, making it straightforward to follow inheritance in almost any cross.

Animals↗
PubMed1997

Genetic mapping of 262 loci derived from expressed sequences in a murine interspecific cross using single-strand conformational polymorphism analysis.

We have demonstrated previously that noncoding sequences of genes are a robust source of polymorphisms between mouse species when tested using single-strand conformation polymorphism (SSCP) analysis, and that these polymorphisms are useful for genetic mapping. In this report we demonstrate that presumptive 3'-untranslated region sequence obtained from expressed sequence tags (ESTs) can be analyzed in a similar fashion, and we have used this approach to map 262 loci using an interspecific backcross. These results demonstrate SSCP analysis of genes or ESTs is a simple and efficient means for the genetic localization of transcribed sequences, and is furthermore an approach that is applicable to any system for which there is sufficient sequence polymorphism.

Animals↗
PubMed1996

Incorporation of 35 novel gene transcripts into the physical and genetic map of human chromosome 13.

A panel of somatic cell hybrids carrying a defined set of rearrangements involving chromosome 13 has been used to assign 35 novel gene transcripts regionally. The positions of the chromosome 13 breakpoints in each somatic cell hybrid have previously been defined relative to the Généthon genetic linkage map. As a result, the position of each gene transcript has been determined relative to both the physical and the genetic linkage maps. Analysis of the distribution of these gene transcripts indicates a slight overrepresentation toward locations on the distal long arm of chromosome 13, with no localizations noted in the 13q22-q31 region. Seven of these novel gene transcripts and the gene encoding small ribonucleoprotein U6 have been mapped to YACs known to contain Généthon microsatellite markers, thereby providing further sublocalization relative to the genetic map. The positioning the these gene transcripts within the genetic and physical maps provide candidate genes for disease loci that are being mapped to the same intervals on the chromosome.

Animals↗
PubMed1999

Superimposed histologic and genetic mapping of chromosome 9 in progression of human urinary bladder neoplasia: implications for a genetic model of multistep urothelial carcinogenesis and early detection of urinary bladder cancer.

The evolution of alterations on chromosome 9, including the putative tumor suppressor genes mapped to the 9p21-22 region (the MTS genes), was studied in relation to the progression of human urinary bladder neoplasia by using whole organ superimposed histologic and genetic mapping in cystectomy specimens and was verified in urinary bladder tumors of various pathogenetic subsets with longterm follow-up. The applicability of chromosome 9 allelic losses as non-invasive markers of urothelial neoplasia was tested on voided urine and/or bladder washings of patients with urinary bladder cancer. Although sequential multiple hits in the MTS locus were documented in the development of intraurothelial precursor lesions, the MTS genes do not seem to represent a major target for p21-23 deletions in bladder cancer. Two additional tumor suppressor genes involved in bladder neoplasia located distally and proximally to the MTS locus within p22-23 and p11-13 regions respectively were identified. Several distinct putative tumor suppressor gene loci within the q12-13, q21-22, and q34 regions were identified on the q arm. In particular, the pericentromeric q12-13 area may contain the critical tumor suppressor gene or genes for the development of early urothelial neoplasia. Allelic losses of chromosome 9 were associated with expansion of the abnormal urothelial clone which frequently involved large areas of urinary bladder mucosa. These losses could be found in a high proportion of urothelial tumors and in voided urine or bladder washing samples of nearly all patients with urinary bladder carcinoma.

Chromosome Aberrations↗
PubMed1996

Genetic maps of polymorphic DNA loci on rat chromosome 1.

Genetic linkage maps of loci defined by polymorphic DNA markers on rat chromosome 1 were constructed by genotyping F2 progeny of F344/N x LEW/N, BN/SsN x LEW/N, and DA/Bkl x F344/Hsd inbred rat strains. In total, 43 markers were mapped, of which 3 were restriction fragment length polymorphisms and the others were simple sequence length polymorphisms. Nineteen of these markers were associated with genes. Six markers for five genes, gamma-aminobutyric acid receptor beta3 (Gabrb3), syntaxin 2 (Stx2), adrenergic receptor beta1 (Adrb1), carcinoembryonic antigen gene family member 1 (Cgm1), and lipogenic protein S14 (Lpgp), and 20 anonymous loci were not previously reported. Thirteen gene loci (Myl2, Aldoa, Tnt, Igf2, Prkcg, Cgm4, Calm3, Cgm3, Psbp1, Sa, Hbb, Ins1, and Tcp1) were previously mapped. Comparative mapping analysis indicated that a large portion of rat chromosome 1 is homologous to mouse chromosome 7, although the homologs of two rat genes are located on mouse chromosomes 17 and 19. Homologs of the rat chromosome 1 genes that we mapped are located on human chromosomes 6, 10, 11, 12, 15, 16, and 19.

Animals↗
PubMed1990

A detailed genetic map of the long arm of chromosome 11.

We describe 14 new restriction fragment length polymorphisms, corresponding to 13 loci on the long arm of chromosome 11. A detailed genetic map of chromosome 11q has been constructed from these and other loci (a total of 31 loci) typed in 59 reference families. The 23 most informative markers were selected to establish a map with a strongly supported order; regional localizations are provided for eight other markers. The loci span 88 cM in males and 148 cM in females and form a dense continuum on 11q. These ordered polymorphic markers will be of help in studying the genes responsible for several diseases that have been localized to this region, including genes responsible for multiple endocrine neoplasia type I (MEN1), ataxia telangiectasia (AT), tuberous sclerosis (TSC), and some forms of asthma and rhinitis.

Chromosome Mapping↗
PubMed1999

Statistical aspects of genetic mapping in autopolyploids.

Many plant species of agriculture importance are polyploid, having more than two copies of each chromosome per cell. In this paper, we describe statistical methods for genetic map construction in autopolyploid species with particular reference to the use of molecular markers. The first step is to determine the dosage of each DNA fragment (electrophoretic band) from its segregation ratio. Fragments present in a single dose can be used to construct framework maps for individual chromosomes. Fragments present in multiple doses can often be used to link the single chromosome maps into homologous groups and provide additional ordering information. Marker phenotype probabilities were calculated for pairs of markers arranged in different configurations among the homologous chromosomes. These probabilities were used to compute a maximum likelihood estimator of the recombination fraction between pairs of markers. A likelihood ratio test for linkage of multidose markers was derived. The information provided by each configuration and power and sample size considerations are also discussed. A set of 294 RFLP markers scored on 90 plants of the species Saccharum spontaneum L. was used to illustrate the construction of an autopolyploid map. Previous studies conducted on the same data revealed that this species of sugar cane is an autooctaploid with 64 chromosomes arranged into eight homologous groups. The methodology described permitted consolidation of 54 linkage groups into ten homologous groups.

Chromosomes↗
PubMed1978

Genetic mapping of a putative temperature-sensitive transcription mutation in Escherichia coli K12.

A putative temperature-sensitive transcription mutant described earlier (Jabbar and Jayaraman, 1976) has been genetically mapped. The locus maps at 38 min to the left of aroD. The mutation is recessive to the wild type and it affects a gene probably other than the genes coding for the alpha and beta subunits of phenylalanine tRNA synthetase and protein synthesis initiation factor IF-3 which also map in the same region.

Chromosome Mapping↗
PubMed2001

Genetic mapping of quantitative trait loci governing longevity of Caenorhabditis elegans in recombinant-inbred progeny of a Bergerac-BO x RC301 interstrain cross.

Recombinant-inbred populations, generated from a cross between Caenorhabditis elegans strains Bergerac-BO and RC301, were used to identify quantitative trait loci (QTL) affecting nematode longevity. Genotypes of young controls and longevity-selected worms (the last-surviving 1% from a synchronously aged population) were assessed at dimorphic transposon-specific markers by multiplex polymerase chain reaction. The power of genetic mapping was enhanced, in a novel experimental design, through map expansion by accrual of recombinations over several generations, internally controlled longevity selection from a genetically heterogeneous, homozygous population, and selective genotyping of extremely long-lived worms. Analysis of individual markers indicated seven life-span QTL, situated near markers on chromosomes I (tcbn2), III (stP127), IV (stP13), V (stP6, stP23, and stP128), and X (stP41). These loci were corroborated, and mapped with increased precision, by nonparametric interval mapping-which supported all loci implicated by single-marker analysis. In addition, a life-span QTL on chromosome II (stP100-stP196), was significant only by interval mapping. Congenic lines were constructed for the longevity QTL on chromosomes III and X, by backcrossing the Bergerac-BO QTL allele into an RC301 background with selection for flanking markers. Survival data for these lines demonstrated consistent and significant effects of each QTL on life span.

Alleles↗
PubMed2003

Concomitant reiterative BAC walking and fine genetic mapping enable physical map development for the broad-spectrum late blight resistance region, RB.

The wild potato species Solanum bulbocastanum is a source of genes for potent late blight resistance. We previously mapped resistance to a single region of the S. bulbocastanum chromosome 8 and named the region RB (for "Resistance from S. Bulbocastanum"). We now report physical mapping and contig construction for the RB region via a novel reiterative method of BAC walking and concomitant fine genetic mapping. BAC walking was initiated using RFLP markers previously shown to be associated with late blight resistance. Subcontig extension was accomplished using new probes developed from BAC ends. Significantly, BAC end and partial BAC sequences were also used to develop PCR-based markers to enhance map resolution in the RB region. As they were developed from BAC clones of known position relative to RB, our PCR-based markers are known a priori to be physically closer to the resistance region. These markers allowed the efficient screening of large numbers of segregating progeny at the cotyledon stage, and permitted us to assign the resistance phenotype to a region of approximately 55 kb. Our markers also directed BAC walking efforts away from regions distantly related to RB in favor of the 55-kb region. Because the S. bulbocastanum genotype used in BAC library construction is heterozygous for RB (RB/rb), codominant PCR-based markers, originally developed for fine-scale mapping, were also used to determine homolog origins for individual BAC clones. Ultimately, BAC contigs were constructed for the RB region from both resistant (RB) and susceptible (rb) homologs.

Chromosome Walking↗
PubMed1970

A genetic map of non-Mandelian genes in Chlamydomonas.

A group of eight non-Mendelian genes have been shown by recombination analysis to be linked into a linear structure or chromosome. Similar genetic maps of gene order and relative distances between genes have been constructed by two methods, one based on additivity of recombination frequencies, the other on frequency of reciprocal recombination with a postulated attachment point. The data indicate that the progeny are diploid for this linkage group, and that the strands are distributed in a precisely oriented manner at mitosis. Evidence is discussed in support of the view that this linkage group is located in chloroplast DNA.

Chloroplasts↗
PubMed1993

Chromosomal structure of Rhodobacter capsulatus strain SB1003: cosmid encyclopedia and high-resolution physical and genetic map.

A combination of cosmid genome walking and pulsed-field gel electrophoresis was used to construct a high-resolution physical and genetic map of the 3.8-megabase (Mb) genome of Rhodobacter capsulatus SB1003. The mapping was done by hybridization of pulsed-field gel blots and by grouping and further mapping of the cosmids and bacteriophages from genomic libraries. Cosmid clones formed two uninterrupted and ordered groups, one corresponding to the chromosome of R. capsulatus, the other to its 134-kb plasmid. Cos site end-labeling and partial EcoRV digestion of cosmids were used to construct a high-resolution EcoRV map of the genome. Overlapping of the cosmids was confirmed by the resemblance of the cosmid restriction maps and by direct end-to-end hybridization with SP6- and T7-specific transcripts. Twenty-three previously cloned genes and eight groups of repeated sequences, revealed in this work, were located in the ordered gene library and mapped with an accuracy of 1-10 kb. Blots of a minimal set of 192 cosmids, covering the chromosome and the plasmid with the known map position of each cosmid, give to R. capsulatus the same advantages that the Kohara phage panel gives to E. coli.

Chromosome Mapping↗
PubMed2001

Analysis of the Relationship between Globally Regulated Genes and Their Chromosomal Genetic Map Loci during Adipogenesis.

About a third of the expressed genes had expression level dramatically changed during adipocyte differentiation. By locating their chromosomal genetic map positions, the positional correlation of these differentiation-regulated genes with their expression regulation was analyzed. The results indicated that there was no chromosomal positional effect in regulating these genes'expression during adipocyte differentiation.

Journal Article↗
PubMed1991

Genetic mapping by single sperm typing.

The polymerase chain reaction makes it possible to analyse DNA sequences in a single cell and has led to a new approach for constructing genetic maps. We describe a procedure called 'sperm typing' which can accurately classify individual meiotic products as recombinant of non-recombinant. This permits the linkage relationships among DNA polymorphisms to be determined without pedigree analysis.

Chromosome Mapping↗
PubMed2001

Genetic mapping and DNA sequence-based analysis of deleted regions on chromosome 16 involved in progression of bladder cancer from occult preneoplastic conditions to invasive disease.

Histologic and genetic mapping with 30 hypervariable markers mapped to chromosome 16 were performed on 234 DNA samples of five cystectomy specimens from patients with invasive bladder cancer. Allelic losses of individual markers were related to microscopically identified precursor conditions in the entire bladder mucosa and invasive cancer. Their significance for the development and progression of neoplasia from in situ preneoplastic conditions to invasive disease was analysed by the nearest neighbor algorithm and binomial maximum likelihood analysis. Using this approach we identified five distinct regions of allelic losses defined by their flanking markers and predicted size as follows. p13.3(D16S418-D16S406, 1.2 cM), p13.1(D16S748-D16S287, 12.9 cM), q12 1(D16S409-D16S514, 24.0 cM), q22.1 (D16S496-D16S515, 5.4 cM), and q24 (D16S507-D16S511, 5.9 cM and D16S402-D16S413, 17.4 cM). The regions mapping to p13.1 and q24 were involved in early intraurothelial phases of bladder neoplasia such as mild to moderate dysplasia. On the other hand the deleted region mapping to p13.3 was involved in progression of severe dysplasia/carcinoma in situ to invasive bladder cancer. Testing of markers that exhibited statistically significant LOH in relation to progression of neoplasia from precursor conditions to invasive cancer on 28 tumors and voided urine samples from 25 patients with bladder cancer revealed that q12.1 showed LOH in 46.4% of tumor and 32.0% of voided urine samples. The LOH of a single marker D16S541 could be detected in approximately 28% of tumors and 20% of voided urine samples of patients with bladder cancer. These data imply that the deleted region centered around marker D16S541 spanning approximately 10 cM and flanked by D16S409 and D16S415 contains a novel putative tumor suppressor gene or genes playing an important role in the development of human bladder cancer. To facilitate more precise positional mapping and identification of pathogenetically relevant genes, we analysed of human genome contig and sequence databases spanning the deleted regions. Multiple known candidate genes and several smaller gene-rich areas mapping to the target regions of chromosome 16 were identified.

Aged↗
PubMed1982

Chiasma derived genetic maps and recombination fractions: chromosome 13 with reference to the proposed 13q14 retinoblastoma locus.

Provided that there is no chromatid interference, no movement of chiasmata, and no discrepancies between meiotic and mitotic chromosome lengths, then genetic maps and recombination fractions may be directly derived from our meiotic chiasma distribution data. This is illustrated by male chiasma derived genetic lengths and recombination fractions along chromosome 13. The recombination fraction between 13p fluorescent markers and the proposed retinoblastoma locus at 13q14 is estimated at 0.27 to 0.37 and preliminary female chiasma studies suggest a recombination fraction of 0.5 between these two sites. Therefore, it seems unlikely that 13p fluorescent markers may be of any practical help in identifying retinoblastoma gene carriers. This is also borne out by the discordant segregation which has been found in six out of seven retinoblastoma families, which gives a calculated recombination fraction of 0.39 (SE 0.15), not significantly different from 0.5.

Chromosome Banding↗