Dissertations / Theses: 'Chromosone mapping'

1

Morroll, Shaun Michael. "Mapping of yeast artificial chromosomes from Arabidopsis chromosome 5." Thesis, University of Nottingham, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.308922.

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Åkesson, Eva. "Genetic mapping and association analysis in multiple sclerosis /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-174-1/.

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Stephens, Sarah H. "Fine mapping of the chromosome 15q13-14 schizophrenia linkage region /." Connect to full text via ProQuest. Limited to UCD Anschutz Medical Campus, 2008.

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Thesis (Ph.D. in Human Medical Genetics) -- University of Colorado Denver, 2008.
Typescript. Includes bibliographical references (leaves 112-128). Free to UCD Anschutz Medical Campus. Online version available via ProQuest Digital Dissertations;

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Brinkman-Mills, Polly. "Transcriptional mapping in human chromosome 22q11.2." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0015/MQ47011.pdf.

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Apostolou, Sinoula. "Physical mapping of human chromosome 16." Title page, contents and abstract only, 1997. http://web4.library.adelaide.edu.au/theses/09PH/09pha645.pdf.

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6

He, Bing. "Susceptibility gene mapping in multiple sclerosis /." Stockholm, 1998. http://diss.kib.ki.se/search/diss.se.cfm?19980608he.

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7

Söderhäll, Cilla. "Gene mapping of atopic dermatitis /." Stockholm : [Karolinska institutets bibl.], 2001. http://diss.kib.ki.se/2001/91-7349-088-1/.

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Holm, Sofia. "Molecular genetic studies of psoriasis susceptibility in 6p21.3 /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-225-X.

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9

Dutton, Elizabeth R. "Mapping studies on mouse distal Chromosome 2." Thesis, University of Oxford, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.299401.

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Creavin, Treasa Agnes Della Geraldine. "Transcriptional mapping of human chromosome 16p12.3-p12.2." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.321891.

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11

Mazaheri, Mona. "Radiation Hybrid Mapping of Barley Chromosome 3H." Diss., North Dakota State University, 2014. https://hdl.handle.net/10365/27454.

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Assembly of the barley (Hordeum vulgare L.) genome requires high resolution maps for aligning contig-based physical maps along chromosomes. Genetic maps lack accurate information on the physical position of almost half of the barley genome located in recombination-poor regions. Radiation hybrid (RH) mapping is an alternative approach, which is based on radiation-induced chromosomal deletions. In this study, an RH population for barley chromosome 3H was developed. Genotyping 373 3H-RH lines with 113 markers resulted in an RH map with an average resolution of 2.22 Kb. Compared to an analogous genetic map, the 3H-RH map resolution was 9.53-X higher, reaching to >262.40-X better resolution in the centromeric region. We suggest that RH maps would facilitate assembly of the barley genome. For future RH studies of the barley genome, an optimum genotyping platform, consisting of 400,536 barley-specific repeat junction markers (RJMs), was developed.
Frank Bain Dissertation Fellowship
Charles and Linda Moses Presidential Graduate Fellowship
North Dakota State University. College of Agriculture, Food Systems and Natural Resources

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12

Liu, Jian. "Deletion mapping of human 3P in major epithelial malignancies and fine localization of candidate tumor suppressor genes /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-577-8/.

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Kedra, Darek. "Characterization of candidate disease genes from human chromosomes 11g13 and 22q /." Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3792-3/.

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Khodaei-O'Brien, Shideh. "Molecular studies of multiple endocrine neoplasia type 1 (MEN1) /." Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4312-5/.

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15

Hinkley, Craig S. (Craig Steven). "Gene Dosage Study on Human Chromosome 22." Thesis, North Texas State University, 1986. https://digital.library.unt.edu/ark:/67531/metadc500617/.

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A gene dosage study was conducted on a rare complete trisomy 22 human fibroblast cell line utilizing three lysosomal enzymes, ∝-iduronidase, ∝-galactosidase B, and arylsulfatase A, whose genes are located on chromosome 22 and two control enzymes, ,β-hexosaminidase A and -- fucosidase, with genes not on chromosome 22. A gene dosage effect was clearly demonstrated for an early passage number of the fibroblasts; however, later passage numbers gave inconclusive results. This study suggests that gene dosage studies must be carefully designed to be conducted only on early, matched passage number cells. ∝-fucosidase gave anomalous results most likely due to pleiotropic effects. The present gene dosage study confirmed the trisomic nature of the cell line studied and suggests that this type of study may be a useful diagnostic tool for small deletions, additions, or unbalanced translocations.

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Good, David Andrew, and n/a. "Genetic Loci for Paget's Disease of Bone." Griffith University. School of Biomolecular and Biomedical Science, 2003. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20040319.125358.

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Paget's disease of the bone is a skeletal disorder of unknown cause. This disease is characterised by excessive and abnormal bone remodelling brought about by increased bone resorption followed by disorganised bone formation. Increased bone turnover results in a disorganised mosaic of woven and lamellar bone at affected skeletal sites. This produces bone that is expanded in size, less compact, more vascular, and more susceptible to deformity or fracture than normal bone. Symptoms of Paget's disease may include bone pain, bone deformity, excessive warmth over bone from hypervascularity, secondary arthritis, and a variety of neurologic complications caused in most instances by compression of the neural tissues adjacent to pagetic bone. Genetic factors play a role in the pathogenesis of Paget's disease but the molecular basis remains largely unknown. The identification of the molecular basis of Paget's disease is fundamental for an understanding of the cause of the disease, for identifying subjects at risk at a preclinical stage, and for the development of more effective preventive and therapeutic strategies for the management of the condition. With this in mind, the aim of this project is to identify genetic loci, in a large pedigree, that may harbour genes responsible for Paget's disease of bone. A large Australian family with evidence of Paget's disease was recruited for these studies (Chapter 3). This pedigree has characterised over 250 individuals, with 49 informative individuals affected with Paget's disease of bone, 31 of whom are available for genotypic analysis. The pattern of disease in these individuals is polystotic, with sites of involvement including the spine, pelvis, skull and femur. Although the affected individuals have a severe early-onset form of the disease, the clinical features of the pedigree suggest that the affected family members have Paget's disease and not familial expansile osteolysis (a disease with some similarities to Paget's disease), as our patients have extensive skull and axial skeletal involvement. The disease is inherited as an autosomal dominant trait in the pedigree with high penetrance by the sixth decade. Due to the large size of this family and multiple affected members, this pedigree is a unique resource for the detection of the susceptibility gene in Paget's disease. The first susceptibility loci for Paget's disease of bone have been mapped by other investigators to chromosome 6p21 (PDB1) and 18q21.1-q22 (PDB2) in different pedigrees. Linkage analysis of the Australian pedigree in these studies was performed with markers at PDB1: these data showed significant exclusion of linkage, with LOD scores < - 2 in this region (Chapter 4). Linkage analysis of microsatellite markers from the PDB2 region excluded linkage with this region also, with a 30 cM exclusion region (LOD score < -2.0) centred on D18S42 (Chapter 4). This locus on chromosome 18q21.1-q22 contains a serine protease (serpin) cluster with similarities to chromosome 6p21. Linkage analysis of this region also failed to provide evidence of linkage to this locus (Chapter 4). These data are consistent with genetic heterogeneity of Paget's disease of bone. A gene essential for osteoclast formation encoding receptor activator of nuclear factor-kB (RANK), TNFRSF11A, has been previously mapped to the PDB2 region. Mutations in the TNFRSF11A gene have been identified segregating in pedigrees with Familial Expansile Osteolysis and early onset familial Paget's disease, however, linkage studies and mutation screening have excluded the involvement of RANK in the majority of Paget's disease patients. For the Australian pedigree, mutation screening at the TNFRSF11A locus revealed no mutations segregating with affected individuals with Paget's disease (Chapter 4). Based on these findings, our hypothesis is that a novel susceptibility gene relevant to the pathogenesis of Paget's disease of bone lies elsewhere in the genome in the affected members of this pedigree; this gene should be identifiable using a microsatellite genome-wide scan followed by positional cloning. A genome-wide scan of the Australian pedigree was carried out, followed by fine mapping and multipoint analysis in regions of interest (Chapter 5). The peak 2-point LOD scores from the genome-wide scan were LOD = 2.75 at D7S507 and LOD = 1.76 at D18S70. Two additional regions were also considered for fine mapping: chromosome 19p11-q13.1 with a LOD of 1.58 and chromosome 5q35-qter with a LOD of 1.57. Multipoint and haplotype analysis of markers flanking D7S507 did not support linkage to this region (Chapter 5). Similarly, fine mapping of chromosome 19p11-q13.1 failed to support linkage to this region (Chapter 5). Linkage analysis with additional markers in the region on chromosome 5q35-qter revealed a peak multipoint LOD score of 6.77 (Chapter 5). A distinct haplotype was shown to segregate with all members of the family, except the offspring of III-5 and III-6. Haplotype analysis of markers flanking D18S70 demonstrated a haplotype segregating with Paget's disease in a large sub-pedigree (descendants of III-3 and III-4) (Chapter 5). This sub-pedigree had a significantly lower age at diagnosis than the rest of the pedigree (51.2 + 8.5 vs. 64.2 + 9.7 years, p = 0.0012). Linkage analysis of this sub-pedigree demonstrated a peak two-point LOD score of 4.23 at marker D18S1390 (q = 0.00), and a peak multipoint LOD score of 4.71, at marker D18S70. An implication of these data is that 18q23 harbours a novel modifier gene for reducing the age of onset of Paget's disease of bone. A number of candidate Paget's genes have previously been identified on chromosome 18q23, including the nuclear factor of activated T cells (NFATc1), membrane-associated guanylated kinase (MAGUK) and a zinc finger protein. Candidate gene sequencing of these genes in these studies has failed to identify mutations segregating with affected family members in the sub-pedigree linked to chromosome 18q23 (Chapter 6). More recently, a mutation in the gene encoding the ubiquitin-binding protein sequestosome 1 (SQSTM/p62) has been shown to segregate with affected members of Paget's disease families of French-Canadian origin. In this study, a single base pair deletion (1215delC) was identified as segregating with the majority of affected members in the pedigree (Chapter 6). This deletion introduces a stop codon at amino acid position 392 which potentially results in early termination of the protein and loss of the ubiquitin binding domain. The three affected members of the family that do not share the affected haplotype do not carry a mutation in the coding region of SQSTM/p62. Screening of affected members from 10 further Paget's disease families identified the previously reported P392L mutation in 2 (20%) families. No SQSTM1/p62 coding mutations have been found in the remaining 8 families or in 113 aged matched controls. In conclusion, this project has identified genetic loci and mutations that segregate with individuals affected with Paget's disease. Further investigation of the functional significance of the genetic changes at these loci is expected to lead to a better understanding of the molecular basis of this disease.

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17

Coyle, Elizabeth. "Mapping and mutational analysis of chromosome 11q12-13." Thesis, University of Edinburgh, 1995. http://hdl.handle.net/1842/20919.

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This thesis describes a) the isolation and mapping of new markers from human chromosome 11q12-13 and b) the mutational analysis of a gene from this region as a candidate for an inherited deafness syndrome. A number of markers were concentrated in a sub region of 11q13 which had been linked to several important disorders, and these were used to isolate YACs. Thus the formation of a cloned DNA map of the region was initiated. In parallel I examined the Olfactory Marker Protein (OMP) gene as a candidate for Usher Syndrome Type IB, by DNA sequencing and mutational analysis of affected individuals. Usher syndrome is characterised by deafness and retinitis pigmentosa. In Type I, vestibular dysfunction is also a feature of the disorder. The disorder is genetically heterogeneous and for each subtype several genetic loci have been linked in individual populations: Type IB has been linked to 11q13. A stereociliary defect was proposed, and the mapping of OMP to the linked region, its expression in olfactory nasal cilia and the CNS, and the mapping of the mouse OMP gene to the synthetic region on mouse chromosome 7 very close to Shaker-1, a possible mouse homologue of Usher syndrome type I, justified close examination of OMP as a candidate for both disorders. A human genomic clone was therefore obtained and sequenced, several different methods of mutation detection compared, and the value of the chemical mismatch cleavage technique demonstrated. At the same time, comparative mapping was carried out by mapping candidates from the Shaker-1 nonrecombinant region on the somatic cell hybrid panel. Variants of the OMP gene were identified, but were formally excluded as candidates when a gene located very close to OMP was shown by others to be mutated in Shaker-1 mice and USHIB patients.

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18

Bradley, Maria. "Genetic studies of atopic dermatitis /." Stockholm : [Karolinska institutets bibl.], 2001. http://diss.kib.ki.se/2001/91-7349-085-7/.

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19

Li, Fang-Yuan. "Genetic study of autosomal dominant progressive external ophthalmoplegia and familial myasthenia gravis : linkage analysis, candidate gene cloning and mutation detection /." Stockholm, 2001. http://diss.kib.ki.se/2001/91-628-4695-7/.

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20

Maslen, G. Ll. "Molecular analysis of the mammalian X-chromosome." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260723.

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21

Slape, Christopher Ian. "Molecular characterisation of translocations involving chromosome band 1p36 in acute myeloid leukaemia." Title page, table of contents and abstract only, 2002. http://web4.library.adelaide.edu.au/theses/09PH/09phs6313.pdf.

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"October 2002" Bibliography: leaves 159-198. This thesis describes the mapping of the breakpoints of three different chromosome rearrangements, all involving 1p36, in acute myeloid leukaemia (AML) patients, and an investigation into the molecular outcomes of these rearrangements.

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Solinas, Toldo Sabina. "Chromosome mapping in cattle by fluorescence in situ hybridization /." [S.l.] : [s.n.], 1993. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=10301.

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23

Zimmer, Régis. "Micromanipulation and physical mapping of the chicken Z chromosome." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq24435.pdf.

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Fraser, J. Lee A. "Transcription mapping of the pericentromeric region of chromosome 10." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/MQ31207.pdf.

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25

Wixon, Joanne. "Physical and transcriptional mapping in human chromosome band 6p23." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.363758.

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Cummings, James Rowland Fraser. "Linkage Disequilibrium Mapping of Chromosome 19 on Crohn's Disease." Thesis, University of Oxford, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.531666.

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Malas, Stavros. "Genetic and physical mapping studies on mouse chromosome 2." Thesis, University College London (University of London), 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.283659.

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Derry, Jonathan Michael James. "Genetic and physical mapping of the mouse X chromosome." Thesis, University of Cambridge, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.239109.

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Heyns, I. C. "Mapping of chromosome arm 7DL of Triticum aestivum L." Thesis, Stellenbosch : University of Stellenbosch, 2005. http://hdl.handle.net/10019.1/1584.

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Thesis (MSc (Genetics))--University of Stellenbosch, 2005.
The Russian wheat aphid, Diuraphis noxia (Mordvilko), is a serious insect pest of wheat and barley. It affects the quality and yield of grain by sucking plant sap from the newest growth whilst toxic substances are injected that destroy plant tissue. The Russian wheat aphid also acts as a vector of plant viruses. The cultivation of aphid resistant cultivars is the preferred control strategy and nine resistance genes, designated Dn1 to Dn9, have been identified. Another undesignated gene, Dnx, was found in the wheat accession PI220127. Mapping of the resistance genes relative to known markers will improve their use in breeding programs. The dominant RWA resistance gene, Dn5, was identified in the accession PI294994 and mapped to chromosome arm 7DL. However, recent reports have placed Dn5 on ...

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Gras, Konrad. "Mapping of Chromosome Dynamics over the Bacterial Cell Cycle." Thesis, Uppsala universitet, Institutionen för cell- och molekylärbiologi, 2018. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-353718.

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The replication of DNA, its compaction and segregation in dividingcells are challenges which all organisms are faced with. Ensuringthat these processes occur without error is essential for thesurvival of the organism. While the major mechanisms governingchromosome replication and segregation have been elucidated ineukaryotic organisms, analogous processes and their details inprokaryotic organisms have been more challenging to analyse. Inorder to understand the processes behind the localisation of thechromosome during cell division, this project has aimed atanalysing the dynamics of 13 fluorescently labelled loci over thecell cycle of Escherichia coli. The results of this project can beused for further analysis of the chromosome in a large-scale studywhere more loci are analysed to map the dynamics of the wholechromosome.The fluorescent labelling was achieved by introducing the parSsequence at the chosen sites with lambda-Red recombination andexpression of ParB fused to the fluorescent protein mCherry. Thesequence was successfully introduced at eight different positionsin eight separate strains. The introduced parS/ParB system wasconfirmed to result in fluorescent foci by fluorescence microscopyimaging of the strains on agarose pads. Three of these strainswere analysed in a microfluidic PDMS chip platform withfluorescence microscopy. Microfluidic systems provide an advantageof capturing large amounts of cells and making it possible toanalyse them continuously in the same conditions. Combining thesesystems with bright-field, phase contrast and fluorescenceimaging, the growth rates of the cells and dynamics of thefluorescent foci were successfully analysed over several hours.

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31

Hsu, Ssucheng Jeff 1964. "Physical and genetic mapping on mouse proximal chromosome 18." Diss., The University of Arizona, 1998. http://hdl.handle.net/10150/282617.

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An 8-Mb yeast artificial chromosome (YAC) contig has been constructed spanning 9 cM on mouse proximal chromosome 18. The contig consists of 49 YAC clones that cover roughly 15% of the chromosome. The map was assembled based on the presence or absence of 38 DNA microsatellites, from proximal DI8Mit109 through distal D18Mit68. The physical order of those microsatellite STSs have been assigned. The locations of 21 known genes including markers near twirler (Tw) and the recently isolated Niemann-Pick type C1 (Npc1), formerly designated as spm (sphingomyelinosis), are delimited on this physical map. Mouse Niemann-Pick disease type C1 (Npc1) is an autosomal recessive lipid storage disorder. We generated a high resolution linkage map in the 2.24 cM Npc1 critical region by typing 8 polymorphic markers in 2322 meioses. A minimal set of overlapping yeast artificial chromosome (YACs) has been assembled. The YAC 313-B-8 which covers this whole region, has been used to construct a cosmid library. Three cosmid contigs were built and one of them contained the Npc1 locus. Two (CA)n microsatellites were identified and characterized from the YAC derived cosmids. The most proximal cosmid contig overlaps with the markers near twirler gene (Tw). These identified YACs and cosmid clones will be an important resource for mouse geneticists wishing to further characterize the Npc1 gene and identify Tw and other genes in this region. The physical map and genetic linkage map were integrated to study the recombination frequencies in this particular mouse genome region. On average, it showed a recombination ratio of cM/Mb > 1.1. However, there is no recombination in the 300 Kb Npc1 critical region. We believe that the 703 bp deletion and 824 bp insertion of nonhomologous sequences in the mutation of Npc1 inhibits the occurrence of recombination in the region. These results confirm previous studies showing that recombination in mice is sensitive to heterozygous deletions or insertions of DNA fragments.

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32

Fratini, Antonio. "Fragile sites on human chromosome 16 : a linkage analysis study /." Title page, table of contents and summary only, 1988. http://web4.library.adelaide.edu.au/theses/09PH/09phf844.pdf.

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Laval, S. H. "Molecular analysis of mammalian sex chromosomes." Thesis, University of Oxford, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.302954.

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Palma, Federica Di. "Analysis and mapping of bovine MHC class I gene." Thesis, University of Reading, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.248145.

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Gill, Clare Alexandra. "Use of an ovine bacterial artificial chromosome library for the study of Bovidae genomes." Title page, table of contents and abstract only, 1999. http://web4.library.adelaide.edu.au/theses/09ANP/09anpg475.pdf.

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Yang, Fan. "Optimization of Cytogenetic and Physical mapping of Culicinae genomes." Thesis, Virginia Tech, 2010. http://hdl.handle.net/10919/76948.

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Understanding chromosome structure and genome organization of Culicine mosquitoes can potentially contribute to the development of novel approaches to vector control. However, because of highly repetitive nature of the Aedes and Culex genomes, the structure of their polytene chromosomes is damaged by ectopic contacts that make the analysis difficult. Mitotic chromosomes from imaginal discs of 4th instar larvae of Aedes aegypti were tested as a source for the physical genome mapping for this mosquito. Chromosomes in imaginal discs are 10 times more abundant than chromosomes in nervous ganglia, and they do not accumulate chromosomal mutation as cell line chromosomes do. Prometaphase chromosomes in imaginal discs of Ae. aegypti are 4-5 times longer than metaphase chromosomes and can provide higher resolution for physical mapping. Cold temperature (+16°C) was proven to increase the number of the chromosomes. Hypotonic solution treatment of live larvae was proven to elongate chromosomes and improve banding patterns. We differentially stained these mitotic chromosomes with Giemsa and YOYO-1 to revile the banding pattern. We applied fluorescent in situ hybridization (FISH) procedure developed for human chromosomes to Ae. aegypti chromosomes. A strain from Culex pipiens, Cx. quinquefasciatus and their hybrids from the natural population in Virginia was successfully colonized in the laboratory. This strain can be used as a reliable source for cytogenetic studies.
Master of Science in Life Sciences

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37

Xu, Chun. "Candidate genes and chromosomal loci in multiple sclerosis /." Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3433-9/.

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38

Xiang, Fengqing. "Genetic studies of neurological disorders : Rett syndrome and HD-like familial prion disease /." Stockholm, 2001. http://diss.kib.ki.se/2001/91-628-4882-8/.

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Wong, Chi Cheung Andrew. "Transcriptional mapping in a terminal microdeletion of human chromosome 22q." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/NQ34859.pdf.

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Howell, Gareth Rhys. "Physical, transcriptional and comparative mapping on the human X chromosome." Thesis, Open University, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.394787.

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Daly, Maria Catherine. "Chromosome 3 deletion mapping in human small cell lung cancer." Thesis, University of Cambridge, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.304095.

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42

Nie, Ying. "Positional mapping for blood pressure loci on rat chromosome 9." University of Toledo Health Science Campus / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=mco1434993505.

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43

Bailey, David M. D. "Genome mapping in a search for a sex determining gene." Thesis, University of Cambridge, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.361752.

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Meaney, Paul James. "Mapping the Plasmodium falciparum genome with yeast artificial chromosomes." Thesis, University of Edinburgh, 1995. http://hdl.handle.net/1842/12640.

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Yeast Artificial Chromosome cloning vectors, with their capacity to maintain up to 1 Mb of cloned DNA in a stable form, have proved extremely useful in mapping the genomes of higher eukaryotes. These vectors possess features which can circumvent some of the problems associated with classical molecular manipulation in Plasmodium falciparum. The research presented in this thesis is aimed at contributing to genome mapping in P. falciparum. The primary objective is the construction of a complete, detailed YAC- based physical map of chromosome 6, with a resolution of 10 Kb. To accomplish this, an 1100 YAC library of the P. falciparum isolate HB3 was constructed. The library contains clones with an average insert size of 100 Kb. Insert DNA is stable when cultured over 100 generations and the library is predicted to have a 4/5 fold genome redundancy, corresponding to 90% of the genome. Chromosome 6 specific YAC's have been isolated and three contigs initiated. Overlapping YAC's have been identified by using Sequence Tagged Site markers obtained from the 5 and 3 ends of each YAC by Inverse PCR. A total of 700 Kb of P. falciparum DNA has been cloned and this has been extensively mapped with seven restriction enzyme. Maps for all available YAC's will be presented. In addition, an attempt has been made to evaluate the degree of stage specific gene expression of cloned DNA within each YAC. The implications of these findings for genome mapping in P. falciparum will be discussed in the thesis.

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45

Sundholm, James, and n/a. "Analysis of Specific Migraine Candidate Genes Mapping to Human Chromosome 1." Griffith University. School of Health Science, 2003. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20030829.153348.

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Migraine, comprised of migraine with aura (MA) and migraine without aura (MO), is a painful neurovascular disease, affecting approximately 16% of the general population. It is characterised by a wide variety of symptoms including headache, nausea and vomiting, and photo- and phonophobia. The disorder is complex involving not only multiple genes, but also specific environmental factors, which can induce attacks in genetically predisposed individuals. Hyperhomocysteinaemia is a known risk factor for cerebrovascular, peripheral vascular and coronary heart disease. The Methylenetetrahydrofolate Reductase (MTHFR) enzyme is involved in homocysteine metabolism. Furthermore, it has been reported that a homozygous mutation (677C to T; Ala to Val) in the 5,10-MTHFR gene is associated with an elevation in plasma homocysteine levels (Frosst et al., 1995). This common mutation in the MTHFR gene has recently been associated with migraine with aura in a Japanese cohort (Kowa et al., 2000). The present study was designed to determine the prevalence of the MTHFR C677T mutation in Australian patients with migraine and to determine whether this mutation is associated with the disease in Caucasians. A large case-control study, consisting of 270 patients with migraine (167 with aura and 103 without aura), and 270 normal matched controls was investigated. Genotypic results indicated that the prevalence of the homozygous (T/T) genotype in migraine sufferers (15%) was higher than that of controls (9%) (P = 0.084). Furthermore, the frequency of the mutant (T/T) genotype in individuals with MA (19%) was significantly higher than in controls (9%) (P = 0.006). Interestingly, the risk of MA was ~2.5-fold higher in suffers possessing the homozygous variant (OR = 2.52, CI: 1.42 - 4.47, P = 0.0012). To confirm the MTHFR allelic association with MA, family-based tests were performed in an independent pedigrees group, where only those with MA were considered affected. Results from both the Pedigree Disequilibrium Test (PDT) and Family-Based Association Test (FBAT) analysis revealed slight, although not significant (PDT test, P = 132; and FBAT test, P = 0.390), over-transmission of the mutant allele (T) from parents to affected offspring. However, despite the MTHFR variant having a high heterozygosity (0.48), there were a limited number of informative transmissions for the MTHFR variant in the pedigree group resulting in reduced power for these tests. In conclusion, our results support the trends reported in the Japanese migraine study and suggest that the homozygous 677T gene variant causing mild hyperhomocysteinaemia, is a genetic risk factor for migraine, and indicate that further studies investigating the role of this gene are warranted. Mutations in various ion channel genes are responsible for neurovascular and other neurological disorders. Inherited ion channel mutations or "channelopathies" are increasingly found to be the cause of various neurological disorders in humans. Wittekindt and colleagues (1998) reported that the calcium-activated potassium channel (hKCa3) gene is a good candidate for schizophrenia and bipolar disorder (BD), as well as for other neurological disorders such as migraine. The hKCa3 gene is a neuronal small conductance calcium-activated potassium channel, which contains a polyglutamine tract, encoded by a polymorphic CAG repeat in the gene. The hKCa3 gene encodes a protein of 731 amino acids containing two adjacent polyglutamine sequences in its N-terminal domain separated by 25 amino acids. The C-terminal polyglutamine sequence is highly polymorphic in length (Austin et al., 1999). hKCa3 plays a critical role in determining the firing pattern of neurons via the generation of slow after-polarization pulses and the regulation of intracellular calcium channels (Kohler et al., 1996). Three distinct mutations in the a1 calcium channel gene have been shown to cause SCA-6, episodic ataxia-2 and familial hemiplegic migraine (FHM) (Ophoff et al., 1996). The hKCa3 gene contains a highly polymorphic CAG repeat that was initially mapped (Chandy et al., 1997) to a schizophrenia locus on chromosome 22 (Pulver et al., 1994). Recently Austin et al (1999) re-mapped hKCa3 and found it to reside on chromosome 1q21, a region that has been linked to FHM (Austin et al., 1999), a rare subtype of MA (Ducros et al., 1997; Gardner et al., 1998), and a region recently showing genetic linkage to typical migraine (Lea et al., 2002). The hKCa3 polymorphism results in small variations in polyglutamine number, similar to those that occur in the calcium channel a1a subunit gene (CACNA1A), which is encoded by CAG expansions and thought to cause Spinocerebellar Ataxia Type 6 via loss of channel function (Austin et al., 1999). Given the recent linkage of FHM to the region of chromosome 1q21, to which hKCa3 resides, and also linkage of typical migraine to this region, a large case-control study investigating this hKCa3 CAG marker and consisting of 270 migraine and 270 stringently matched healthy controls was undertaken. Our results indicated that there was no statistically significant difference in allele distributions for this marker between migraine and non-migraine patients (P >0.05). No significant difference in the allelic distribution was observed in the MA or MO groups when compared to controls (P >0.05) and there was no significant difference in CAG repeat length distribution between the migraine group and controls (P = 0.92), or between the MA and MO groups (P = 0.72) collectively. Hence, the CAG repeat in this gene does not show expansion in migraine. Overall, our results provide no genetic evidence to suggest that the hKCa3 CAG repeat polymorphism is involved in migraine aetiology in Australian Caucasians. Thus the involvement of the hKCa3 gene in migraine is not likely, although the hKCa3 gene remains an important candidate for other neurological disorders that may be linked to the 1q21.3 chromosomal region.

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Sadeghzadeh, Behzad. "Mapping of chromosome regions associated with seed zinc accumulation in barley." University of Western Australia. School of Earth and Geographical Sciences, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0204.

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[Truncated abstract] Zinc deficiency in crops is the most widespread micronutrient deficiency, with about 50% of the cereal-growing areas worldwide containing low levels of plant-available Zn. Zinc plays multiple key roles in different metabolic and physiological processes; its deficiency in crops reduces not only grain yield, but also the nutritional quality of grains. Insufficient micronutrient intake, particularly Zn and Fe, afflicts over 3 billion people in the world, mainly in developing countries. Increasing the amount of Zn in food crops can contribute to improving the Zn status of people. Furthermore, Zn-dense seeds have agronomic benefits, resulting in greater seedling vigour, bigger root system and higher crop yield when sowed to soils with low plant-available Zn. Enhancing nutrient content and nutritional quality of crops for human nutrition is a global challenge currently, but it was mostly ignored during the breeding process in the past. There is a significant genotypic variation for seed Zn accumulation in several crops (including barley) which could be exploited in the breeding programs to produce genotypes with higher seed Zn concentration and content. However, the progress in Zn efficiency until now has mainly relied on conventional plant breeding approaches that have had limited success. Therefore, reliable alternative methods are required. Enhancing mineral nutrition through plant biotechnology may be a sustainable and beneficial approach in developing Zn-dense seeds in the staple crops. ... This DNA band was sequenced and converted into a simple sequence-specific PCR-based marker, which was designated as SZnR1 (seed Zn-regulator1). The developed marker is very easy to score, is inexpensive to run and amenable for a large number of plant samples. The successful development of SZnR1 molecular marker linked to chromosome region associated with seed Zn concentration and content using MFLP in this study illustrates the advantage of this technique over some other DNA fingerprinting methods used for identification of molecular markers for marker-assisted selection (MAS). In conclusion, the greater Zn efficiency of Sahara over Clipper under sufficient Zn supply may be attributed to its higher uptake of Zn. It appears that soil-based pot experiments under controlled condition may offer potential improvements over field experiments in screening for seed Zn accumulation. Shoot and seed Zn concentration and content can be used to diagnose the Zn statues of barley genotypes, and may be a useful selection criterion for Zn efficiency in large populations like doubled-haploid populations aimed at developing molecular markers for Zn efficiency. Identified QTLs influencing seed Zn concentration were repeatable in the field and glasshouse conditions, suggesting their robustness across environments as well as their value in marker-assisted selection. The developed PCR-based marker SZnR1 and other molecular markers associated with the QTLs on the short and long arms of chromosome 2H have the potential to be used for marker-assisted selection in breeding for Zn-dense seed in barley.

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Stafford, Amanda Newland. "Physical mapping within human chromosome 11q12-q13 including the atopy locus." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.239248.

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Williams, Gareth Owen. "Mapping studies of the centromeric region of the human Y chromosome." Thesis, University of Oxford, 1998. http://ora.ox.ac.uk/objects/uuid:c471a22f-e52b-452a-8714-bfcd9610da44.

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Mapping studies of the centromeric region of the human Y chromosome Construction of a map of a human centromeric region is very important in order to understand the organisation of this essential part of the chromosome. A YAC contig map has been assembled of the pericentric 10 Mb of the human Y chromosome, giving coverage of Yp from the large X-Y homologous region through to the alphoid satellite of the centromere, and from the alphoid DNA to the proximal unique sequences on Yq. The Yp map has one remaining gap between TSPY1 and the AMELY region, while two gaps separate the satellite region on Yq from the other two contigs. After constructing the map, the known genes were localised to the region. One Yq gene, DFFRY, was discounted as a potential anti-Turner syndrome gene by analysis of rearranged Y chromosomes. Detection of a block of duplicated sequence on Yp led to the confirmation of the existence of an inversion polymorphism, which was then found to be correlated with a major subclass of sex-reversed individuals, who have X-Y chromosomal breakpoints within the inverted region. These results not only give a far more extensive and detailed map of this region than before, but also show that understanding the organisation of the region has important consequences for a number of genetic disorders.

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Priestley, Matthew David. "Detailed mapping of a congenital heart disease gene in chromosome 3p25." Thesis, University of Birmingham, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.270058.

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Greenham, Jaimie Alexanda. "The identification and integration of transcripts mapping to human chromosome 16p12.2." Thesis, University College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.286479.

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Dissertations / Theses on the topic 'Chromosone mapping'

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