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At least 703 records · Page 39Linked to original sources
PubMed1991

Genetic mapping of the gene for androgen-binding protein/sex hormone-binding globulin to mouse chromosome 11.

Southern blot analysis of DNAs from Chinese hamster x mouse and rat x mouse somatic cell hybrids showed that the mouse gene encoding androgen-binding protein/sex hormone-binding globulin (ABP-SHBG) is on Chromosome 11. Progeny from an intersubspecies backcross were analyzed to position this locus, termed Shbg, between Il-3 and Int-4 in the middle of this chromosome. Shbg is thus closely linked to several neurological mutations, one of which, Tr, is also associated with male sterility. The recent finding that ABP-SHBG is found throughout the rat brain raises the possibility that one of these mutations may be due to a defect in Shbg.

Androgen-Binding Protein↗
PubMed1996

Genetic mapping of the mouse stromal cell-derived factor gene (Sdf1) to mouse and rat chromosomes.

Stromal cell-derived factor 1 (SDF1) is a new member of the Cys-X-Cys chemokine family. The chromosomal location of Sdf1, the gene coding mouse SDF1, was determined by fluorescence in situ hybridization (FISH) and molecular linkage analysis. The mouse Sdf1 gene was localized to the R-band-positive F1 band of chromosome 6 by direct R-banding FISH. Interspecific backcross analysis identified the mouse Sdf1 gene locus at 0.8 cM terminal to D6Nit55 and 3.0 cM proximal to D6Mit12. With in situ hybridization using a mouse cDNA clone as a probe, the rat Sdf1 gene was localized to the R-band-positive band 4q42.1, where conserved linkage homology to mouse chromosome 6 has been identified. Although other Cys-X-Cys chemokine genes have been mapped on human chromosome 4, the chromosomal segment where the mouse and rat Sdf1 gene reside have no conserved linkage homology to human chromosome 4. This result suggests that SDF1 is a new chemokine class.

Amino Acid Sequence↗
PubMedDate not supplied

Refined genetic mapping of juvenile X-linked retinoschisis.

Juvenile X-linked retinoschisis (RS) is an eye disease that causes acuity reduction and peripheral visual field loss typically beginning early in life. In further work towards positional cloning of the RS gene, we restudied our previously reported seven large American families and one additional new family, with a total of 63 affected males. RS linkage analysis using microsatellite repeat markers gave the following results: DXS207 (Z = 24.89, theta = 0.01), DXS987 (Z = 24.04, theta 0.01) and DXS999 (Z = 14.70, theta = 0.00). Recombination events in four individuals were studied further with additional markers (AFM291wf5, DXS443, DXS1052, DXS274 and DXS1226), and a flanking interval was obtained (DXS43, DXS207, DXS987)-RS-(AFM291wf5, DXS443). This study moves the RS centromeric boundary to (AFM291wf5, DXS443), about 5.5 cM closer than the previously reported boundary at DXS274 and narrows the RS inclusion interval to about 3.7 cM (using distances from CEPH family data).

Chromosome Mapping↗
PubMed2000

Genetic mapping of blood pressure quantitative trait loci in Milan hypertensive rats.

In a previous study, by using a candidate gene approach, we detected in both Milan hypertensive rats and humans a polymorphism in the alpha-adducin gene (ADD1) that was associated with blood pressure and renal sodium handling. In the present study, a genomewide search with 264 informative markers was undertaken in 251 (Milan hypertensive strain x Milan normotensive strain) F2 rats to further investigate the contribution of the adducin gene family (Add1, Add2, and Add3) and to identify novel quantitative trait loci (QTLs) that affect blood pressure. The influence of 2 different methods of blood pressure measurement, the intracarotid catheter and the tail-cuff method, was also evaluated. We found evidence that QTLs affected systolic blood pressure (SBP) measured at the carotid (direct SBP) on rat chromosome 1 with a logarithm of the odds (LOD) score peak of 3.3 on D1Rat121 and on rat chromosome 14 on Add1 locus (LOD=3.2). A QTL for SBP measured at the tail (indirect SBP) was found on rat chromosome 10 around D10Rat33 (LOD=5.0). All of these QTLs identified chromosomal regions not detected in other rat studies and harbor genes (Na(+)/H(+) exchanger A3; alpha-adducin; alpha(1B)-adrenergic receptor) that may be involved in blood pressure regulation. Therefore, these findings may be relevant to human hypertension, also in consideration of the biochemical and pathophysiological similarities between MHS and a subgroup of patients of primary hypertension, which led to the identification of alpha-adducin as a candidate gene in both species.

Animals↗
PubMed2000

X-linked vacuolar myopathies: two separate loci and refined genetic mapping.

X-linked vacuolar myopathies can be divided into two forms: one that is associated with cardiomyopathy and mental retardation (XVCM-MR) and a second form, termed X-linked myopathy with excessive autophagy (XMEA), that spares cardiac muscle and has no central nervous system involvement. In this article, we demonstrate linkage between XMEA and markers on chromosome Xq28 and assign the XMEA gene locus to the most telomeric 10.5 cM of chromosome X. We also show that XVCM-MR is not allelic to XMEA.

Adolescent↗
PubMed2001

Construction of a genetic map of barley (Hordeum vulgare L.) cross 'Azumamugi' x 'Kanto Nakate Gold' using a simple and efficient amplified fragment-length polymorphism system.

We have devised a simple and efficient amplified fragment-length polymorphism (AFLP) system consisting of small slab gels, a discontinuous buffer system, and silver staining. Using this system, a single worker developed a barley map with 227 polymorphic fragments in 2 months. As a mapping population, 99 recombinant inbred lines of barley cultivars 'Azumamugi' x 'Kanto Nakate Gold' were used. Most of the 227 AFLP fragments showed a Mendelian segregation ratio of 1:1, and all were assigned to the seven barley chromosomes. Thus, these fragments are useful as molecular markers. They were integrated with 40 previously characterized sequence-tagged sites, 3 isozymes, and 2 morphological markers to construct an integrated map. The resulting map covered 925.6 cM with 272 markers (detecting 150 loci) at an average interval of 6.5 cM/locus. This system greatly simplifies map construction.

Chromosome Mapping↗
PubMed2002

Genetic mapping and tagging of wheat genes using RAPD, STS and SSR markers.

We applied SSR markers for mapping genes determining red coleoptile colour in wheat (Rc1, Rc2, Rc3) using F2 populations. All three genes map at about 15 to 20 cM distally from the centromere of chromosomes 7AS, 7BS and 7DS, respectively. The locations of the glume colour (Bg, Rg1) and glume hairiness (Hg) genes relative to the SSR markers of the homoeologous chromosomes group 1 were determined using molecular analysis of near-isogenic lines (NILs). One RAPD marker for the vernalisation response gene Vrn-A1 was identified by screening 95 random primers against two pairs of NILs. New PCR (STS) markers were developed based on RFLP-markers PSR426 (5A, 5B, 5D) and PSR1201 (1A, 5A, 5B). Analysis of nulli-tetrasomic and near-isogenic lines of wheat using the STS markers developed gave an indication that these new STS markers have the same chromosomal and intrachromosomal positions as the correspondent RFLP markers. Therefore, they could be used for mapping and/or tagging the vernalisation response (Vrn-A1, Vrn-B1, Vrn-D1) and homoeologous pairing (Ph1) genes.

Base Sequence↗
PubMed1976

Phosphatidylserine synthetase mutants of Escherichia coli. Genetic mapping and membrane phospholipid composition.

Mutants of Escherichia coli K-12 defective in CDP-diglyceride:L-serine phosphatidyltransferase (phosphatidylserine synthetase) can be isolated by a rapid autoradiographic screening assay described previously (Raetz, C. R. H. (1975) Proc. Natl. Acad. Sci. U. S. A. 72, 2274-2278). Four organisms of this kind have now been characterized. The gene (designated pss) which is altered in these mutants is closely linked to the nadB locus near minute 49 on the E. coli chromosome. Strains carrying the pss-8 mutation do not grow at elevated temperatures and have low levels of an altered synthetase in cell extracts. An analysis of several hundred transductants and temperature-resistant revertants reveals that the pss-8 mutation is responsible both for the enzyme defect and for the phenotype. When a pss-8 mutant is shifted to the nonpermissive temperature, the cells stop dividing and form long filaments. After 3 hours at 44 degrees the level of phosphatidylethanolamine drops from 66 to 32% (percentage of the total lipid phosphorus), while the combined levels of phosphatidylglycerol and cardiolipin rise from 34 to 68%.

CDPdiacylglycerol-Serine O-Phosphatidyltransferase↗
PubMed1991

Detailed genetic mapping of the A-raf proto-oncogene on the mouse X chromosome.

The transcribed murine A-raf proto-oncogene has been localized to the proximal region of the mouse X chromosome, within the context of four other active genes in this region which together constitute a conserved linkage group between mouse and man. This localization has been accomplished using species-specific restriction fragment length variation and DNAs from a previously defined informative subset of progeny representative of a set of 100 progeny from an interspecific backcross between inbred C57BL/6JRos and wild-derived Mus spretus. This new data regionally orders the mouse A-raf locus relative to the 24 X-linked markers previously examined in this backcross. We find that A-raf co-localizes with two other active genes, tissue inhibitor of metalloproteinases (Timp) and synapsin (Syn-1), 4.0 +/- 2.0 cM distal to the Otc gene at the proximal end of the mouse X chromosome, for a partial gene order in this region of: centromere-Cybb-Otc-Timp/A-raf/Syn-1-Xlr-1-Hprt.

Animals↗
PubMed1990

Structure, genetic mapping, and expression of the gene for pyruvate, orthophosphate dikinase from maize.

Pyruvate, orthophosphate dikinase is a key enzyme in photosynthesis in some plants that exploit the C4 photosynthetic pathway for the fixation of CO2. The gene for this enzyme has been cloned and its primary structure has been analyzed. The sequence of the cloned genes spans about 12 kilobase pairs and consists of 19 exons. The site of initiation of transcription is located 211 nucleotides upstream from the first nucleotide of the initiation codon (position -211). Typical TATA and inverted CCAAT elements are present in the anticipated regions, as well as a sequence that is homologous to the binding site of Sp-1 protein (-51 to -42). Three long, direct-repeated sequences are present contiguously in the 5'-flanking region (-286 to -172), and two of the repeated sequences include sequences homologous to the core sequence of SV40 enhancer in the 3'-end portions. Southern blot analysis, coupled with mapping by analysis of restriction fragment length polymorphism, indicates that the gene for the enzyme involved in C4 photosynthesis is encoded by a single-copy gene and is located on chromosome 6. To test the promoter activity of the isolated gene, a chimeric gene composed of the 5'-flanking region of the gene and a structural gene for bacterial beta-glucuronidase was constructed and introduced into tobacco protoplasts by electroporation or used to transform tobacco plants by Agrobacterium-mediated transfer of the gene. In both cases, expression of the beta-glucuronidase gene was observed, indicating that the 5'-flanking region of the gene can act as a promoter in tobacco cells.

Base Sequence↗
PubMed1990

Escherichia coli molecular genetic map (1000 kbp): update I.

The sequenced genes from Escherichia coli that are available in the EMBL library (release 21) have been localized on an updated and corrected version of the restriction map of the chromosome generated by Kohara et al. (1987). One thousand kbp of sequenced DNA are incorporated in this update; this is equivalent to 23% of the total genome. The accuracy of the map is assessed, and it is corrected and updated where appropriate. A significant number of sites were missing from the original map, mainly involving two of the eight enzymes used by Kohara et al. (1987), ie. PvuII and EcoRV. The nucleotide environment of such missing sites was examined and, using an Artificial Intelligence approach, it appears that the site for these enzymes is sensitive to context effects. Several genes of known position on the E. coli chromosome could not be placed on the restriction map; this suggests that additional gaps are likely to exist on the restriction map, in addition to the original seven identified by Kohara et al. We have also obtained information about the probable direction of transcription of chromosomal genes with respect to the map. Most genes are transcribed in the same direction as the replication forks, particularly around oriC at 84 min.

Artificial Intelligence↗
PubMed1988

[Genetic mapping of the ilv7434 mutation providing threonine deaminase resistance to isoleucine inhibition in Escherichia coli].

Location of previously isolated ilv7434 mutation was determined by use of transductional shortening of the F'14 episome. The ilv7434 mutation causes resistance of threonine deaminase (coded for by ilvA gene) to feed-back inhibition by isoleucine. Another phenotype characteristics of the ilv7434 mutant is the ability to feed a lawn of isoleucine auxotrophs in the cross-streak test. The F'14 strain AB1206 carrying ilv7434 mutation was used as a donor for making transductionally shortened episomes in recA recipient. These shortened F'14 episomes containing variable segments of the ilv cluster were then tested for their ability to transfer ilv7434 phenotype by complementation with ilv recA recipients. The data of complementation test suggest that ilv7434 is situated between ilvD and ilvC genes. One of 20 tested shortened episomes carrying, as shown by complementation test, incomplete ilvA gene was found to transfer ilv7434 phenotype by recombination with ilvA527 recA+ recipient. These data allow to conclude that ilv7434 mutation is located within the ilvA gene.

Chromosome Mapping↗