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At least 1,081 records · Page 60Linked to original sources
PubMed2000

Physical and genetic mapping of IDDM8 on chromosome 6q27.

Genome-wide mapping studies have provided evidence of a type 1 diabetes susceptibility gene (IDDM8) that is located on chromosome 6q27. However, association studies of IDDM8 have so far been negative. The purpose of this investigation was to determine a linkage disequilibrium (LD) map in the chromosome 6q27 region and to better localize IDDM8. A physical map of nearly 1 Mb containing the chromosome 6 telomere was constructed, and polymorphic markers spanning this region were defined. Haplotypes composed of the markers in LD were tested for association with type 1 diabetes in 266 families. A microsatellite marker allele and multiple haplotypes were associated with IDDM8, which suggests localization of this type 1 diabetes susceptibility gene to the terminal 200 kb of chromosome 6.

Adult↗
PubMed1979

Genetic mapping of toxin regulatory mutations in Vibrio cholerae.

We have mapped a regulatory site mediating the hyperproduction of cholera toxin in mutants of Vibrio cholerae strain 569B. Mutations in this locus, called htx, result in the hypertoxinogenic phenotype, as measured by the ganglioside filter assay and immunoradial diffusion. Transposon-facilitated recombination was used to construct improved genetic donors in 569B parental and hypertoxinogenic mutant strains. Subsequent mapping by conjugation indicated that the htx locus was closely linked to the rif, str, and ilv loci of V. cholerae. Analysis of recombinants from these crosses suggested the following gene order: thy str htx rif ilv arg. The close genetic linkage of htx to rif (as high as 98%) resulted in a high comutation frequency of these two loci by nitrosoguanidine mutagenesis. Transfer of the htx mutant locus from a hypertoxinogenic donor to several unrelated Tox+ strains of V. cholerae caused a detectable elevation of toxin production in the recipients. These results suggest that toxin production in diverse strains of V. cholerae is controlled by a common regulatory mechanism in which the htx gene product plays a significant role.

Cholera Toxin↗
PubMed1988

Genetic mapping of the Wiskott-Aldrich syndrome with two highly-linked polymorphic DNA markers.

The Wiskott-Aldrich syndrome (WAS) is an X-linked recessive genetic disease in which the molecular defect is unknown. In 15 families with WAS, seven restriction fragment length polymorphic loci from the X chromosome were used to map the disease locus. Of the eight intervals studied, the likelihood of the WAS gene lying between DXS7 (Xp11.3) and DXS14 (Xp11) was at least 128 times higher than that for any other interval. The most likely gene order is DXS84-OTC-DXS7-WAS-DXS14-DXS1-PGK-DXYS1. Close genetic linkage to DXS7 and DXS14 permits accurate prenatal diagnosis and carrier detection with greater than 98% confidence in fully informative WAS families.

DNA↗
PubMedDate not supplied

A sibling-pair based approach for mapping genetic loci that influence quantitative measures of reading disability.

Family and twin studies consistently demonstrate a significant role for genetic factors in the aetiology of the reading disorder dyslexia. However, dyslexia is complex at both the genetic and phenotypic levels, and currently the nature of the core deficit or deficits remains uncertain. Traditional approaches for mapping disease genes, originally developed for single-gene disorders, have limited success when there is not a simple relationship between genotype and phenotype. Recent advances in high-throughput genotyping technology and quantitative statistical methods have made a new approach to identifying genes involved in complex disorders possible. The method involves assessing the genetic similarity of many sibling pairs along the lengths of all their chromosomes and attempting to correlate this similarity with that of their phenotypic scores. We are adopting this approach in an ongoing genome-wide search for genes involved in dyslexia susceptibility, and have already successfully applied the method by replicating results from previous studies suggesting that a quantitative trait locus at 6p21.3 influences reading disability.

Chromosome Mapping↗
PubMed1996

Genetic mapping and chromosome localization of the rat mitochondrial glycerol-3-phosphate dehydrogenase gene, a candidate for non-insulin-dependent diabetes mellitus.

The mitochondrial FAD-dependent glycerol-3-phosphate dehydrogenase (mtGPD) plays an important role in the regulation of insulin secretion and has been postulated as a candidate responsible for the pathogenesis of non-insulin-dependent diabetes mellitus (NIDDM) in humans as well as in rodent models of NIDDM. Recent molecular genetic studies of the Goto-Kakizaki (GK) rat model of NIDDM have identified loci linked to NIDDM. To elucidate whether rat mtGPD might play a role in the pathogenesis of NIDDM, the rat mtGPD gene (Gpd2) was cloned, and a genetic marker for Gpd2 was developed. The gene mapped to the region of rat chromosome 3 that contains a region linked to NIDDM in the GK rat. Fluorescence in situ hybridization was also carried out to verify the map position.

Animals↗
PubMed1995

Construction of genetic maps using distance geometry.

The techniques of distance geometry, which generate coordinates from observed interpoint distances, have been applied to the problem of determining the relative positions of linked genetic loci from observed interlocus distances. Only the most precise data needed to join the loci are used, with missing distances substituted by sums of precise intermediate distances. Good initial positions (and therefore the order) of loci on a linear map are obtained in an operation of complexity O(N3). The method can therefore be used to generate good initial framework maps for the large numbers of markers encountered in current mapping projects. The locus positions can be subsequently refined to maximize the agreement with the originally observed distances, taking account of the weights of individual interlocus distances. By choosing only small distances from which to construct the map, the method reduces any error due to an incorrect choice of mapping function. It also prevents undue expansion of the map due to error-prone markers, since such markers are accommodated in higher dimensions. The method estimates the error in the positions of individual markers on the final map and identifies well- and ill-defined regions of the map.

Algorithms↗
PubMed2000

Genetic mapping of the Tsw locus for resistance to the Tospovirus Tomato spotted wilt virus in Capsicum spp. and its relationship to the Sw-5 gene for resistance to the same pathogen in tomato.

The Tsw gene conferring dominant resistance to the Tospovirus Tomato spotted wilt virus (TSWV) in Capsicum spp. has been tagged with a random amplified polymorphic DNA marker and mapped to the distal portion of chromosome 10. No mapped homologues of Sw-5, a phenotypically similar dominant TSWV resistance gene in tomato, map to this region in C. annuum, although a number of Sw-5 homologues are found at corresponding positions in pepper and tomato. The relationship between Tsw and Sw-5 was also examined through genetic studies of TSWV. The capacity of TSWV-A to overcome the Tsw gene in pepper and the Sw-5 gene in tomato maps to different TSWV genome segments. Therefore, despite phenotypic and genetic similarities of resistance in tomato and pepper, we infer that distinct viral gene products control the outcome of infection in plants carrying Sw-5 and Tsw, and that these loci do not appear to share a recent common evolutionary ancestor.

Capsicum↗
PubMed1992

Genetic mapping of the integrin alpha 1 gene (Vla1) to mouse chromosome 13.

The integrin alpha 1 chain (Vla1) associates with the beta 1 chain to form a heterodimer that functions as a dual laminin/collagen receptor in neural cells and hematopoietic cells. We have used an interspecies backcross gene-mapping technique to map the Vla1 gene to the distal end of chromosome 13 in the mouse genome. The Vla1 locus is located 3.5 cM distal to Ctla-3 and 7.8 cM distal to Htrla. We have further characterized this locus in recombinant inbred (RI) mice by examining the strain distribution patterns of nine genomic DNA restriction fragment length variants detected with alpha 1 cDNA probes. The RI gene mapping did not show linkage to previously mapped genes or mutants in the AXB, BXA, or AKXD RI sets and therefore defines a new genetic marker for the distal end of chromosome 13 in these RI sets.

Animals↗
PubMed2003

High-resolution genetic map of X-linked juvenile-type granulosa cell tumor susceptibility genes in mouse.

SWR/Bm (SWR) female mice spontaneously develop early-onset ovarian granulosa cell (GC) tumors that can progress to metastatic carcinoma and thus provide a model system for human, juvenile-type GC tumors. In SWR mice, GC tumor susceptibility is an inherited, polygenic trait that appears at a low frequency. A dramatic increase in tumor frequency occurs when the autosomal SWR genetic complement is combined with the X-linked Gct4 allele of the mouse strain SJL/Bm (SJL). The modifier effect of the SJL Gct4 allele (Gct4(J)) also shows a strong parent-of-origin effect, occurring only when the Gct4(J) allele is paternally inherited. To genetically localize Gct4, we generated seven congenic mouse strains (SWR.SJL-X1 through -X7) that contained a defined segment of the SJL X chromosome (Chr) on the SWR autosomal strain background and mapped Gct4 to a 3 cM region. To better define the location of Gct4, we created an additional congenic strain (SWR.CAST-X) that contains most of the genetically polymorphic Chr X from the strain CAST/Ei. From crosses of the SWR.CAST-X and SWR.SJL-X congenic strains, we derived males carrying unique combinations of SJL-X and CAST-X segments. Progeny testing subsequently revealed a second SJL-derived, GC tumor frequency modifier gene, Gct6, located 6.5 cM distal to Gct4 on Chr X. In summary, we have mapped two modifier genes on the mouse Chr X that cause high-frequency, juvenile-type GC tumor development in female mice. The identity of these genes will provide a solid foundation for determination of tumor susceptibility genes in human cases of juvenile-type GC tumors.

Animals↗
PubMed1985

Genetic mapping of Caenorhabditis elegans collagen genes using DNA polymorphisms as phenotypic markers.

In Caenorhabditis elegans collagens comprise a dispersed family of 40-150 genes, the majority of which probably code for collagen proteins found in the animal's cuticle. The conserved (Gly-X-Y)n triple helix coding sequence of collagen genes has facilitated the isolation of a large number of C. elegans collagen genes by recombinant DNA methods. We have begun a study of the chromosomal organization of these genes by screening laboratory strains of C. elegans for DNA polymorphisms in the regions surrounding collagen genes. Polymorphisms near seven genes have been identified and have been used as phenotypic markers in genetic crosses to assign the genes to linkage groups II, III, IV, and X. Four genes are shown by multifactor crosses to map to a 2-3 map unit interval between unc-24 and unc-22 on chromosome IV.

Animals↗
PubMed1999

Physical and genetic map of the genome of Vibrio parahaemolyticus: presence of two chromosomes in Vibrio species.

We constructed a physical map of the genomic DNA (5.1 Mb) for Vibrio parahaemolyticus strain AQ4673 by combining 17 adjacent NotI fragments. This map shows two circular replicons of 3.2 and 1.9 Mb. Pulsed-field gel electrophoresis (PFGE) of undigested genomic DNA revealed two bands of corresponding sizes. Analysis both by NotI digestion and by Southern blot of the two isolated bands confirmed the existence of two replicons. The presence of genes for 16S rRNA on both the replicons indicates that the replicons are chromosomes rather than megaplasmids. The two bands were also seen after PFGE of undigested genomic DNA of V. parahaemolyticus strains other than AQ4673, and of strains belonging to other Vibrio species, such as V. vulnificus, V. fluvialis and various serovars and biovars of V. cholerae. It is noteworthy that V. cholerae O1 strain 569B, a classical biovar, was also shown to have two replicons of 2.9 and 1.2 Mb, which does not agree with a physical map proposed in a previous study. Our results suggest that a two-replicon structure is common throughout Vibrio species.

Chromosome Mapping↗
PubMed1985

Genetic mapping of endogenous RD-114 retroviral sequences of domestic cats.

The RD-114 family of endogenous retroviral sequences in domestic cats has been shown to consist of approximately 20 copies of genetically divergent virogenes per haploid genome. The chromosomal localization for four endogenous sequences (RDV1-4) was accomplished by correlating the occurrence of specific feline chromosomes with diagnostic viral DNA fragments in a panel of cat X rodent somatic cell hybrids. Analysis of the hybrid panel revealed that endogenous RD-114 sequences are dispersed on multiple cat chromosomes, that certain proviral segments are polymorphic with respect to the presence or absence of virus, and that a restriction fragment characteristic of inducible RD-114 resides on a single feline chromosome (B3), probably at a single locus.

Animals↗
PubMed1986

Rett syndrome: lack of association with fragile site Xp22 and strategy for genetic mapping of X-linked new mutations.

The hypothesis of X-linked new mutations which might cause early abortions of hemizygous male fetuses and a dominant phenotype in heterozygous females seems the most likely genetic explanation of the Rett syndrome. This hypothesis can be reconciled with the normal sex ratio observed in sibships of patients and with the rare recurrence of this disorder in sibs or half-sibs. The latter observation can be explained by germinal mosaicism in one of the two parents. Since in 14 patients no association was found with any particular fragile site or chromosome rearrangement, we propose to map the mutated gene (or loci) on the X through a strategy based on the reconstruction of X-linked haplotypes consisting of DNA polymorphisms, and on the identification of possible crossovers in affected sisters.

Cell Line↗
PubMed2006

[Genetic mapping of rice gene OsALB23 regulating chloroplast development].

The biogenesis of chloroplast from proplastid is the prerequisite of photosynthesis. Using electron microscope, we found that rice albino mutant Osalb23 had no thylakoid inside the chloroplast, only some empty vesicles could be observed (Fig. 2). Genetics analysis showed that albino phenotype was controlled by a single recessive locus. Using map-based cloning technique, OsALB23 has been mapped to a region of 280 kb between molecular markers R2M501 and R2M502 on chromosome 2 (Fig. 4). Homologous analysis indicated that this region contained six chloroplast protein genes.

Chloroplasts↗
PubMed1995

Physical and genetic map of the genome of Campylobacter upsaliensis.

A physical map of Campylobacter upsaliensis ATCC 43954 was constructed from DNA fragments generated by SalI (5' G/TCGAC), NarI (5' GG/CGCC) and BssHII (5' G/CGCGC) restriction digests separated using pulsed-field gel electrophoresis. The size of the C. upsaliensis genome was approximately 2000 kb, providing evidence of the largest Campylobacter genome sized to date. Twenty-one fragments created from these restriction digests were assembled into a physical map using a combination of complementary methods including cross-Southern hybridization, hybridization fingerprint analysis and hybridization with homologous and heterologous (from Campylobacter jejuni) gene probes. The position of ten genetic loci, including that of the iron-uptake regulatory (fur) gene, were localized to the physical map. A genomic library of C. upsaliensis ATCC 43954 was constructed in lambda Gem-11 vector. Fifty thousand recombinants with an average size of 16 kb represent a library about 200 times the size of the genome. Using C. jejuni DNA probes, clones representing C. upsaliensis flaA, fur and ftsZ genes were isolated and localized to the physical map.

Blotting, Southern↗
PubMed2003

Molecular tagging and genetic mapping of the disease resistance gene RppQ to southern corn rust.

Southern corn rust (SCR), Puccinia polysora Underw, is a destructive disease in maize ( Zea mays L.). Inbred line Qi319 is highly resistant to SCR. Results from the inoculation test and genetic analysis of SCR in five F(2) populations and five BC(1)F(1 )populations derived from resistant parent Qi319 clearly indicate that the resistance to SCR in Qi319 is controlled by a single dominant resistant gene, which was named RppQ. Simple sequence repeat (SSR) analysis was carried out in an F(2) population derived from the cross "Qi319x340". Twenty SSR primer pairs evenly distributed on chromosome10 were screened at first. Out of them, two primer pairs, phi118 and phi 041, showed linkage with SCR resistance. Based on this result, eight new SSR primer pairs surrounding the region of primers phi118 and phi 041 were selected and further tested regarding their linkage relation with RppQ. Results indicated that SSR markers umc1,318 and umc 2,018 were linked to RppQ with a genetic distance of 4.76 and 14.59 cM, respectively. On the other side of RppQ, beyond SSR markers phi 041 and phi118, another SSR marker umc1,293 was linked to RppQ with a genetic distance of 3.78 cM. Because the five linkage SSR markers (phi118, phi 041, umc1,318, umc 2,018 and umc1,293) are all located on chromosome 10, the RppQ gene should also be located on chromosome 10. In order to fine map the RppQ gene, AFLP (amplified fragment length polymorphism) analysis was carried out. A total 54 AFLP primer combinations were analyzed; one AFLP marker, AF1, from the amplification products of primer combination E-AGC/M-CAA, showed linkage with the RppQ gene in a genetic distance of 3.34 cM. Finally the RppQ gene was mapped on the short arm of chromosome 10 between SSR markers phi 041 and AFLP marker AF1 with a genetic distance of 2.45 and 3.34 cM respectively.

Basidiomycota↗
PubMedDate not supplied

Genetic mapping of X-linked loci involved in skewing of X chromosome inactivation in the human.

We have analyzed X-chromosome inactivation patterns in lymphocytes of 264 females from 38 families not known to have any genetic disease. Quantitative measures of X-inactivation showed strong sister-sister correlation in the degree of departure from equal numbers of cells having each X chromosome active, suggesting heritability of this phenotype. Strong sister-sister correlation was also observed for the fraction of cells having the same parent's X chromosome active, consistent with the possibility that this trait might be controlled by a cis-acting, X-linked gene. We used a sib-pair approach to determine whether X-inactivation phenotype was linked to loci in any region of the X chromosome. Both quantitative and discrete measures of X-inactivation phenotype showed evidence of linkage to markers in the region of the X inactivation center (XIC). The quantitative measure of X-inactivation phenotype used in our study also showed linkage to loci at Xq25-q26. This study provides the first evidence for X-linked inheritance of X chromosome inactivation phenotype derived from linkage analysis in phenotypically normal human families.

Base Sequence↗
PubMed1978

Location of non-temperature-sensitive genes on the genetic map of herpes simplex virus type 1.

By constructing crosses involving the genes coding for the enzyme deoxypyrimidine kinase and for resistance to the drug phosphonoacetic acid, it has been possible both to extend the genetic analysis of HSV-1 such that the eight possible progeny genotypes which arise from a three-factor cross can be identified and also to precisely locate the gene for the plaque-morphology marker syn, the gene for deoxypyrimidine kinase dPYK and the gene for resistance to phosphonoacetic acid PAAr.

Chromosome Mapping↗