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Results for “Genetic mapping”

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At least 631 records · Page 35Linked to original sources
PubMed1995

Loss of heterozygosity in chromosomes 1, 5, 7 and 13 in mouse hepatoma detected by systematic genome-wide scanning using RLGS genetic map.

We have developed an RLGS-based scanning system to detect DNA alteration in tumor tissues, using 575 mapped spots/loci in a single gel. This system is very powerful for screening and identifying not only loss of heterozygosity (LOH) but also DNA methylation change. In this study, we applied this system to search for the LOH of hepatoma from an interspecific F1 hybrid between Mus spretus and C57BL/6 with SV40 early T antigen transgene connected to a mouse major urinary protein enhancer/promoter. Comparing the RLGS profiles of each tumor to that of the normal tissue showed significant LOH in chromosomes 1, 5, 7 and 13.

Animals↗
PubMed1994

A high-resolution genetic map of mouse chromosome 5 encompassing the reeler (rl) locus.

Using interspecific crosses between BALB/c and Mus spretus (SEG) mice, the murine reeler (rl) gene was mapped to the proximal region of chromosome 5 between the hepatocyte growth factor gene (Hgf) and the D5Mit66 microsatellite. The following order was defined: (centromere)-Cchl2a/Hgf-D5Mit1-D5Nam1/D5-Nam2 -rl/D5Mit61-D5Mit72-Xmv45-Htr5a- Peplb-D5Nam3-D5Mit66. Estimated distances between reeler and the nearest flanking markers D5Nam1 and D5Mit72 are 1.5 and 1.0 cM, respectively (95% confidence level), suggesting that the region could be physically mapped using a manageable number of YAC clones.

Alleles↗
PubMed1995

Genetic mapping of Cmv1 in the region of mouse chromosome 6 encoding the NK gene complex-associated loci Ly49 and musNKR-P1.

The Cmv1 resistance gene controls splenic replication of murine cytomegalovirus (MCMV) and confers natural killer (NK) cell-mediated resistance to otherwise lethal infection. The Cmv1 phenotypes of 13 inbred mouse strains have been assessed, and it was found that the Cmv1r resistance phenotype was restricted to the C57BL/6J and Ma/MyJ strains. We have further analyzed the linkage of Cmv1 to the NK gene complex (NKC) mapping to distal mouse chromosome 6 in 99 (BALB/c x C57BL/6J)F1 x BALB/c backcross mice using cloned gene probes and microsatellite markers from this region. No recombinants were observed between Cmv1 and the NKC-associated Ly49 and musNKR-P1 multigene families, nor the Kap locus, nor with 7 microsatellite markers, indicating that Cmv1 is closely linked (< 1 cM) to all of these markers. Analysis of the genotype of the MCMV-susceptible BXD8 RI strain around the NKC region revealed that it had C57BL/6J alleles at microsatellite markers immediately proximal and distal to Cmv1. This suggests that the Cmv1s phenotype of this strain is due to a germ-line mutation. Thus, the close linkage of Cmv1 to the Ly49 and musNKR-P1 multigene families suggests that it may represent an NK cell recognition structure encoded in the NKC region.

Animals↗
PubMed1996

Fine genetic mapping of the Hyp mutation on mouse chromosome X.

The hypophosphatemic (Hyp) mouse is the murine homolog of hypophosphatemic vitamin-D-resistant rickets (HYP) in human. Despite extensive investigations in the Hyp mouse, the pathophysiology of this X-linked dominant disorder remains unclear. As a first step toward cloning the Hyp gene, we have generated a high-resolution linkage map in the vicinity of the Hyp locus using two independent backcross panels segregating the Hyp mutation, one generated from an interspecific mating between C57BL/6J-Hyp/Hyp and Mus spretus and the other from an intrasubspecific mating between C57BL/6J-Hyp/Hyp and Mus musculus castaneus. Linkage analyses in 1101 backcross progeny using a total of 23 DNA markers favor the following gene order from the centromere: DXMitl3-(DXMit11, DXMit34)-(DXMit36, Alas2)-(Hyp, DXMit8O)-DXMi198-(DXMit28, DXMit33, DXMit7O)-Pdhal-DXMit2O. This study has localized Hyp to a region of approximately 1 cM flanked by the proximal markers DXMit36 and Alas2 and the distal marker DXMit98. One microsatellite marker, DXMit8O, was found to be very tightly linked to Hyp, as it was nonrecombinant with Hyp among all the progeny of both backcrosses corresponding to 1101 meioses.

Animals↗
PubMed1997

Molecular genetic mapping of the mouse male sterility and histoincompatibility (mshi) mutation on proximal chromosome 10.

The recessive male sterility and histoincompatibility (mshi) mutation in the mouse generates pleiotropic effects on histocompatibility and male reproduction, while female mutants appear to be reproductively normal. We have mapped the mshi mutation to mouse Chromosome (Chr) 10 by analysis of 126 progeny from an intraspecific backcross. Our analysis both places the male sterility and histoincompatibility controlled by mshi within a 20-cM interval between the markers D10Mit51/D10Mit212 and D10Mit170 and has allowed the ordering of several other microsatellite markers on Chr 10 that were previously unresolved. The high-resolution backcross panel we describe should facilitate the isolation of more tightly linked probe sequences and, ultimately, the molecular identification of the gene or genes affected by this interesting mutation.

Animals↗
PubMed2002

FISSR-PCR: a simple and sensitive assay for highthroughput genotyping and genetic mapping.

The recently developed Inter-Simple Sequence Repeat PCR (ISSR-PCR) or microsatellite primed PCR or Simple Sequence Repeat (SSR)-Anchored PCR technique detects polymorphic markers in a wide variety of genomes. Usually the ISSR primers are either 5' end-labeled with gamma[32P]ATP or one of the alpha[32P] labeled dNTPs is added to the PCR reaction and the PCR products are resolved on PAGE and autoradiographed. Alternatively, cold PCR products are resolved on agarose gel electrophoresis. In the present study, we show that informativity, sensitivity and speed of the ISSR-PCR can be substantially enhanced by adding fluorescent nucleotide in the PCR reaction followed by resolution of PCR products on an ABI 377 automated sequencer. The informativeness, measured as a number of detectable amplified fragments, was two-fold higher and the quantity of required template DNA is two-fold lower than the regular ISSR-PCR. We have termed this method as FISSR-PCR and show its usefulness in generating large number of species and varietal specific markers in plants, insects, parasites of insects and human and various infectious organisms. Further, we show that the FISSR markers are inherited and segregated in Mendelian fashion as demonstrated on a panel of 99 F2 offspring derived from a cross of two divergent silkworm strains. The FISSR-PCR marker assay could be a method of choice for large scale screening of varieties/cultivars and highthroughput genotyping in mapping of genomes where microsatellite information is scanty or absent.

Animals↗
PubMed1995

Genetic mapping of Xp22.12-p22.31, with a refined localization for spondyloepiphyseal dysplasia (SEDL).

Spondyloepiphyseal dysplasia tarda (SEDL) is an X-linked recessive disorder characterized in affected males by short stature resulting from a growth defect of the vertebral bodies. We have extended our earlier studies by analyzing 15 families with newly identified microsatellite DNA markers; analysis of recombination events with these markers indicates that the gene responsible for SEDL is located in Xp22 between DXS 16 and DXS 987 on an interval spanning approximately 2 Mb.

Chromosome Mapping↗
PubMed1993

Genetic mapping of the athymic nude (RNU) locus in the rat to a region on chromosome 10.

The nude trait in the rat is transmitted in an autosomal recessive manner and is associated with thymic aplasia, T-cell deficiency, and hairlessness. Congenic rats homozygous for the RNU (Rowett nude) locus are important models in the study of inflammatory disease, tumor growth, and transplant rejection. The RNU locus has not been previously mapped, and the nature of the gene product is unknown. To determine the map location of this gene, a single F344.rnu/rnu (athymic nude congenic Fischer rat) male congenic rat was bred with 3 LEW/N (NIH stock Lewis rat) female rats to produce F1 progeny. Twelve F1 brother-sister breeding pairs were established. Forty-nine phenotypically nude F2 offspring (198 total) were obtained. Linkage analysis done on F2 DNA revealed highly significant cosegregation between the nude phenotype and eight polymorphic markers located on Chromosome (Chr) 10. The tightest linkages were with: MYH3 (embryonic, skeletal myosin heavy chain) and SHBG (sex hormone-binding globulin), giving 2 point lod scores of 20.2, and 20.0, respectively. The map order and map distances, determined by multipoint linkage calculations, were: RR24-(16.1 cM)-MYH3-(3.5 cM)-SHBG-(4.7 cM)-RNU-(11.9 cM)-F16F2-(24.1 cM)-CLATP (citrate lyase ATPase)-(2.4 cM)-ACE (angiotensin converting enzyme)/PPY (pancreatic polypeptide)-(14.1 cM)-RR1023. The position of the RNU locus in the rat corresponds closely with that of the recently reported nu locus in the mouse. This finding suggests that the nude phenotype in the rat and the mouse arise from defects in homologous genes.

Animals↗
PubMed1987

Genetic mapping of two pairs of linked ribosomal protein genes in Saccharomyces cerevisiae.

We have used the 2 mu mapping method described by Falco and Botstein (1983) and tetrad analysis to map four ribosomal protein genes (two linked pairs) in S. cerevisiae. One pair (rp28-rp55 copy 1) is on chromosome XV, 14 cM proximal to ARG8. The other pair (rp55-rp28 copy 2) is 19 cM from the centromere on the left arm of chromosome XIV. To map copy 1 we used the E. coli beta-galactosidase gene rather than a yeast gene to mark the ribosomal protein chromosomal locus. This provided a more sensitive color screening assay for chromosome loss in the 2 mu method. It also removed the restriction that the mapping tester strains must be mutant for the plasmid marker.

Chromosome Mapping↗
PubMed1995

A high-resolution genetic map of mouse chromosome 15 encompassing the Dominant megacolon (Dom) locus.

Dominant megacolon (Dom) is one of four mutations in the mouse that can produce a phenotype similar to Hirschsprung disease in human. The Dom gene product is not known, and no candidate region has been defined for a possible human homolog. In this publication we report mapping the Dom locus with high definition, using several intra-and interspecific crosses and a set of 16 Chr 15-specific microsatellites flanking this locus.

Animals↗