Dissertations / Theses: 'Mice – Genetics'

1

McGowan, Kelly Ann. "Genetics of skin color in mice /." May be available electronically:, 2008. http://proquest.umi.com/login?COPT=REJTPTU1MTUmSU5UPTAmVkVSPTI=&clientId=12498.

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2

Bhanji, Tania. "Elastin in zebrafish and mice." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111938.

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The extracellular matrix is a vital component of the cardiovascular system, in that, it not only provides structural support but also plays a critical role in the maintenance of cellular stability. One of the major components of the vascular matrix is elastin, which confers vessels with the specialized property of stretch and recoil. Elastin deficiency has been implicated in many vascular diseases and determined experimentally to be a negative regulator of smooth muscle cell proliferation. In zebrafish, two elastin genes have been identified, which are actively expressed during development. Based on this finding, protein production and spatial localization for the two elastin proteins was studied by immunohistochemistry with specific antibodies. Results revealed a global distribution for elastin 1 in the ventral aorta and swim bladder, whereas elastin 2 was preferentially localized to the bulbus arteriosus indicating a possible specialized function of elastin 2 in this structure. This observation, and the unique physiological property of this structure, suggests a possible reason for the preservation of both elastin genes during evolution.
In the second part of this study, elastin-null mice were studied to uncover the impact of the loss of elastin on the expression of other elastic fiber-associated proteins. The expression of fibrillin-1, the major component of microfibrils, was not altered in the absence of elastin, implying that elastin is not necessary for the formation of microfibrils. On the other hand, both fibulin-2 and -5 were upregulated in the absence of elastin, suggesting that expression of these genes are controlled by elastin. Overall, this study highlights the importance of elastin in evolution, as well as its potential role in the regulation of expression of other matrix molecules.

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3

Byers, Shannon L. "Use of Inbred Strains of Mice to Study the Genetics and Biology of Sperm Function." Fogler Library, University of Maine, 2006. http://www.library.umaine.edu/theses/pdf/ByersSL2006.pdf.

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4

Gini, Beatrice. "The genetics of family interactions in mice." Thesis, University of Manchester, 2015. https://www.research.manchester.ac.uk/portal/en/theses/the-genetics-of-family-interactions-in-mice(afdad740-ef76-403c-b4fc-738a3470cffe).html.

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Parents and offspring engage in conflict over the amount of resources provisioned by parents, because parents wish to distribute resources equally between all offspring, while each offspring attempts to secure a greater than average share of resources for itself. Parents are responsible for the act of provisioning, yet they need to be sensitive to signals of hunger from their offspring (begging) and therefore they can be manipulated by cheating offspring into provisioning more than the parental optimum. Both parents and offspring evolve strategies to cope with this conflict and, because the payoff of each strategy depends on the behaviour of the interacting party, parents and offspring co-evolve pairs of compatible strategies. While these dynamics have been studied in detail from a game-theoretical and phenotypic perspective, little is known about the genetics underlying parental and offspring strategies. In this study, I used a panel of recombinant inbred mouse lines to investigate the genetics of provisioning and begging. The results clearly show that some areas of the genome are associated with particular strategies in each individual, and also that the genome of offspring can be linked to maternal behaviour through indirect genetic effects. They also show that provisioning and growth are co-adapted in these mice, and that linkage disequilibrium is the mechanism maintaining co-adaptation in this case. Importantly, the genotype of mothers interacts with the environment created by pups in highly significant and complex ways. Finally, I describe an area of the genome associated with sex ratio, and find that a male-biased sex ratio causes mothers to intensify provisioning. All findings are discussed with regards to their implications for evolutionary models.

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Bell, Cindy Lea. "Transport studies in primary cultures of mouse renal epithelial cells." Thesis, McGill University, 1986. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=75363.

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The Hyp (hypophosphatemic) mouse, a murine homologue of X-linked hypophosphatemia (XLH) in man, is a Mendelian disorder of phosphate (Pi) homeostasis. The mutant genotype is characterized by abnormal Pi transport at the brush border membrane (BBM) of the proximal tubule and a defect in renal metabolism of vitamin D$ sb3$. The exact nature of these defects has not been elucidated.
In order to determine if the defect is intrinsic to the renal cell or dependent upon an extrinsic humoral factor, I established primary cultures of renal epithelial cells from normal and Hyp mouse kidney. The cultures demonstrated several differentiated properties of epithelial cells of the renal proximal tubule, the site of the Pi transport defect in the Hyp mouse.
Primary cultures initiated from Hyp mice had decreased Pi transport (expressed as an uptake ratio, Pi/$ alpha$-MG), and increased production of 24,25 dihydroxyvitamin D$ sb3$. These results provide evidence for the intrinsic nature of the primary defect in the Hyp mouse.
This appears to be the first time that expression of a mutant transport gene has been demonstrated in cultured renal cells.

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Chau, Hien Nguyet 1977. "Renal calcification in Npt2 knockout mice." Thesis, McGill University, 2002. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=78338.

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Mice homozygous for the disrupted renal type 11a sodium/phosphate (Na/Pi) cotransporter gene, Npt2, (Npt2 KO) exhibit renal Pi wasting and hypercalciuria, predisposing factors for renal stone formation. We observed that Npt2 KO mice, but not wild-type littermates form renal stones. The renal stones were evident in newborn, weanling and adult mice and composed of calcium (Ca) and Pi. The presence of renal calcification correlated with the absence of Npt2 gene expression and the presence of genes responsible for the synthesis (1alpha-hydroxylase) and catabolism (24-hydroxylase) of 1,25-dihydroxyvitamin D, whose elevated levels contribute to the hypercalciuria and renal calcification in Npt2 KO mice. The renal calcification was associated with increased osteopontin (OPN) mRNA expression and colocalized with OPN, the latter associates with renal stones in vivo and inhibits Ca mineralization in vitro). These data demonstrate that hyperphosphaturia and hypercalciuria, secondary to Npt2 gene disruption, are sufficient for the development of renal calcification.

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7

邱大安 and Tai-on Yau. "Regulation of the mouse hoxb-3 gene in the neural expression domains during embryogenesis." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2001. http://hub.hku.hk/bib/B31242601.

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8

Husbands, Sandra D. "Tolerance and immunity in transgenic mice." Thesis, University College London (University of London), 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.303680.

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9

Devine, Jill Christine. "POPULATION GENETICS OF GOLDEN MICE (OCHROTOMYS NUTTALLI) AND WHITE-FOOTED MICE (PEROMYSCUS LEUCOPUS)." OpenSIUC, 2012. https://opensiuc.lib.siu.edu/theses/943.

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Golden mice (Ochrotomys nuttalli) are generally an elusive and rare species throughout their geographic range in the southeastern United States. They are considered to be habitat specialists that prefer dense understory consisting of shrubs and vines. Golden mice are less vagile, and likely disperse shorter distances than other sympatric species such as the white-footed mouse (Peromyscus leucopus). Conversely, white-footed mice are considered habitat generalists that inhabit a variety of habitat types, are more vagile, and disperse farther than golden mice. Because of this it is likely that golden mice have a lower genetic diversity and are more genetically subdivided than white-footed mice. In southern Illinois, golden mice are on the periphery of their range, which is one of the reasons they are on the state-threatened list in Illinois. It has been hypothesized that populations on the periphery of a species range will have more population structure and lower genetic diversity than populations in the core of the range. Tissue samples for golden mice and white-footed mice were collected from 24 sites throughout southern Illinois and 24 sites throughout the golden mouse core range. I analyzed 13 and 10 microsatellite markers as well as 594 and 624 base pairs of the mitochondrial control region for golden mice and white-footed mice, respectively, to characterize and compare the genetic diversity and population structure of both species. Overall haplotype diversity (0.76) and nucleotide diversity (0.20%) was lower in golden mice compared to white footed mice (0.99 and 1.97%). Results of an AMOVA using the mitochondrial control region revealed more subdivision among the 3 populations of golden mice (Φst = 0.099, P < 0.001) than among the 3 populations of white-footed mice (Φst = 0.058, P < 0.001). Microsatellite loci showed a similar trend with overall FST values of 0.027 (P < 0.001) for golden mice and 0.004 (P = 0.137) for white-footed mice. I intended to compare golden mouse individuals from southern Illinois and the core of the range, but too few individuals were collected from the core. More samples need to be collected throughout the core of the range to better understand the population genetics of golden mice in the core of the range compared to the periphery.

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10

Shek, Kim Fung. "Identification of cis-regulatory elements in mouse Mab21l2 gene by comparative genomics /." View abstract or full-text, 2010. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202010%20SHEK.

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11

Champigny, Marc. "Expression of stem-loop binding protein during murine oogenesis and pre-implantation development." Thesis, McGill University, 1998. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=21522.

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The goal of the work presented here was to investigate the hypothesis that cytoplasmic SLBP is required for translation of somatic H1 mRNA, and their translational repression is due to a lack of SLBP in the cytoplasm of oocytes, and early cleavage-stage embryos. To this end, the expression of SLBP in murine oocytes and pre-implantation embryos was characterized by RT-PCR, Western blotting, and immunocytochemical. techniques.
mRNA encoding SLBP was detected throughout oogenesis and pre-implantation development, from small growing oocytes to the late blastocyst stage. SLBP protein was found in the nucleus and cytoplasm of growing and fully-gown prophase I-arrested oocytes. SLBP accumulated to extremely high levels during meiotic maturation in a process requiring translation. The protein remained abundant both in the nucleus and cytoplasm throughout the 1- and 2-cell stages. SLBP was depleted in 4-cell embryos in a process independent of DNA replication, and was not detected again until the late 8-cell stage. From the late 8-cell stage to the early blastocyst stage, SLBP was detected exclusively in the cytoplasm. Interestingly, in late blastocysts, SLBP was translocated to the nucleus. (Abstract shortened by UMI.)

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12

關仲天 and Chung-tin Kwan. "Studies of the regulation of mouse Hoxb-3 gene." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1998. http://hub.hku.hk/bib/B31237150.

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13

Tang, Ling-fung Paul, and 鄧凌鋒. "Dissecting the genetics of complex trait in mouse: an attempt using public resources and in-houseknockout." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B43572170.

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14

Behnam, Yousif Toma. "DNA hypomethylation and gene expression in mice." Thesis, University of Southampton, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.296518.

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15

Yang, Lanjian 1976. "Effect of DNA methyltransferase 1 on transmission ratio distortion and epigenetic inheritance." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=116080.

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Epigenetic modification of DNA plays an important role in gene regulation. During gametogenesis and early embryogenesis epigenetic states are reset to ensure embryonic-specific gene expression patterns after fertilization. However, certain genomic regions may resist epigenetic reprogramming. This may result in transgenerational epigenetic inheritance. Earlier, a grandparental origin dependent (GPO) transmission ratio distortion (TRD) of alleles in the distal region of mouse chromosome 12 had been found (Croteau et al ., 2002). The distorted region overlaps with the imprinted region of chromosome 12. The mechanism underlying this TRD is unknown, and we hypothesized that it was due to failure to reset imprints in the imprinted region in a proportion of germ cells. Such an imprint resetting failure would represent a particular case of transgenerational epigenetic inheritance. DNA (Cytosine-5) methyltransferase 1 (DNMT1) plays a key role in the maintenance of epigenetic states in mammalian genomes. To test the role of DNA methylation and DNMT1 in the genesis of TRD and its relationship to epigenetic inheritance we investigated the effect of Dnmt1 loss-of-function mutations using two mouse models: GPO (grandparental origin dependent)-TRD (transmission ratio distortion) and epigenetic inheritance at the agouti locus. Here, we report that Dnmt1 mutations have a modifying parental effect on the transmission of grandparental chromosome 12 alleles. However, the same Dnmt1 mutation did not affect the agouti coat color inheritance patterns in mice that inherited the Avy (agouti viable yellow) mutant allele from the father. Our results suggest that Dnmt1 is a trans-acting modifier of allelic transmission and support the role of epigenetic states in the genesis of TRD.

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16

HuÌˆbner, Roland Karl Peter. "Chromosomal and biochemical variation in wild mice from Switzerland : relevance for models of chromosomal evolution in European house mice." Thesis, University of Oxford, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.316879.

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17

Rambau, Ramugondo Victor. "Molecular genetics of Rhabdomys subspecies boundaries : phylogeography of mitochondrial lineages and chromosomal fluorescence in situ hybridization." Thesis, Stellenbosch : Stellenbosch University, 2003. http://hdl.handle.net/10019.1/53504.

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Thesis (PhD)--University of Stellenbosch, 2003.
ENGLISH ABSTRACT: The geographic genetic population structure and evolutionary history of the African four-striped mouse, Rhabdomys pumilio, was investigated using mitochondrial (mtDNA) cytochrome b gene (1140 bp) and control region (994 bp) sequences and a combination of cytogenetic banding techniques (G- and C-banding), and fluorescence in situ hybridization. Two cytotypes (2n = 46 and 2n = 48) were identified by cytogenetic analysis. No evidence of diploid number variation within populations was found nor were there differences in gross chromosome morphology, or subtle interchromosomal rearrangements at levels detected by ZOO-FISH. The comparative painting data (using the complete suite, N = 20, of Mus musculus chromosome specific painting probes) show that 10 mouse chromosomes have been retained as chromosomal arms, or intact chromosome blocks within the R. pumilio genome, six produced double signals, while the remaining four hybridized to three or more R. pumilio chromosomes. In total, the 20 mouse chromosome paints detected 40 segments of conserved synteny. Their analysis revealed eight R. pumilio specific contiguous segment associations, a further two that were shared by R. pumilio and other rodents for which comparable data are available, the Black (Rattus rattus) and Norwegian (Rattus nONegicus) rats, but not by the Chinese hamster, Cricetulus grise us. The results suggest that mouse chromosomes 1, 10, and 17 have undergone extensive rearrangements during genome evolution in the murids and may be useful markers for enhancing our understanding of the mode and tempo of chromosome evolution in rodents. Following initial studies using control region sequences, the phylogeographic appraisal of R. pumilio was done using cytochrome b gene sequences. Analyses based on a variety of analytical procedures resulted in the detection of two major mtDNA lineages that correspond roughly to the xeric and mesic biotic zones of southern Africa. One clade comprises specimens with 2n = 48, and the other representatives of two cytotypes (2n = 48 and 2n = 46). The mean sequence divergence (12.0%, range 8.3% -15.6%) separating the two mtDNA clades is comparable to among-species variation within murid genera suggesting their recognition as distinct species, the prior names for which would be R. dilecfus and R. pumilio. Low sequence divergences and the diploid number dichotomy within the mesic lineage support the recognition of two subspecies corresponding to R. d. dilecfus (2n = 46) and R. d. chakae (2n = 48). The data do not support subspecific division within the nominate, R. pumilio. Molecular dating places cladogenesis of the two putative species at less than 5 million years, a period characterised by extensive climatic oscillations which are thought to have resulted in habitat fragmentation throughout much of the species' range.
AFRIKAANSE OPSOMMING: Die geografiesebevolkingsstruktuur en evolusionêre verwantskappe binne die Afrika streepmuis, Rhabdoys pumilio, is ondersoek deur middel van mitochondriale ONS volgordebepaling van die geenfragment sitochroom b (1140 basispare) en die reguleerstreek (994 bp) in kombinasie met sitogenetiese tegnieke (G- en Cbandkleuring en f1uoreseerende in situ hibridisasie). Twee sitotipes (2n = 46 en 2n = 48) is geidentifiseer deur sitogenetiese analasie. Geen bewys van variasie in die 2n chromosoomgetal binne bevolkings is gevind nie. Verder is daar ook geen verskil in die morfologies struktuur van chromosome aanwesig binne bevolkings nie. Vergelykende data (verkry met behulp van die N = 20 Mus musculus chromosoomspesifiekepeilers) dui daarop dat 10 muis chromosome behoud gebly het as chromosoomarms of chromosoomblokke binne die R. pumilio genoom. Ses peilers het dubbel seine gelewer terwyl die oorblywende vier peilers gehibridiseer het aan drie of meer R. pumilio chromosome. In totaal het die 20 muischromosoomverwe 40 konserwatiewe segmente geidentifiseer. Die analise dui agt R. pumilio spesifieke aaneenlopende segmentassosiasies aan, met 'n addisionele twee wat deur R. pumilio en ander muisagtiges vir wie vergelykende data beskikbaar is, byvoorbeeld die swart (Rattus rattus) en Noorweegse (R. norvegicus) rot maar nie die Chinese hamster, Cricetulus grise us, gedeel word. Die resultate stel voor dat muischromosoom 1, 10 en 17 ekstensiewe herrangskikkings ondergaan het gedurende die genoom evolusie binne die Muridae en dat hulle waarskynlik waardevolle merkers kan wees om beide die patroon en tempo van chromosome evolusie in muisagtiges verder te kan verstaan. Die filogeografiese verwantskappe binne R. pumilio is ondersoek deur middel van ONS volgordebepalings van die reguleerstreek asook sitochroom b. Die resultate van hierdie studie het twee divergente mitochondriale ONS eenhede ontdek wat gekorreleer kan word met xeriese en mesiese klimaatsones binne suidelike Afrika. Een groep bestaan uit diere met 2n = 48, terwyl die ander genetiese groep twee sitotipes (2n = 46 en 2n= 48) insluit. 'n Gemiddelde genetiese divergensie van 12.0% (varieer tussen 8.3% - 15.5%) verdeel die twee mtDNS-groepe en is vergelykbaar met tussenspesievariasie binne ander muisagtige genera, wat moontlik daarop dui dat twee verskillende spesies teenwoordig is; die voorgestelde name is R. di/ectus en R. pumilio. Lae genetiese divergensie binne die mesiese groep versterk die moontlike teenwoordigheid van twee subspesies, R. d. di/ectus (2n = 46) en R. d. chakae (2n = 48). Die data verleen egter nie steun aan die divisie binne R. pumilio nie. Molekulêre datering van die twee spesies dui daarop dat die divergensie ten minste 5 miljoen jaar gelede plaasgevind het. Die periode was gekarakteriseer deur ekstensiewe klimaatsossilasies, wat gely het tot habitat fragmentasie in die spesie se verspreidingsgebied.

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18

Seymour, Rosemarie. "Mutations in the Mouse Sharpin Gene Cause the Chronic Proliferative Dermatitis Phenotype." Fogler Library, University of Maine, 2008. http://www.library.umaine.edu/theses/pdf/SeymourR2008.pdf.

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19

Le, Tissier Paul Roussel. "The biochemical genetics of purine catabolism in mice." Thesis, University of Reading, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.236393.

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20

Macdonald, Karen Beth. "The genetics and embryopathology of exencephaly in SELH/Bc mice." Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/27983.

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This project was the first study of the genetics and embryo-pathology of exencephaly in a partially inbred mouse stock, SELH/Bc. Exencephaly was found in 17% of SELH fetuses. Analysis of day 8-9 gestation embryos indicated that SELH embryos were collectively normal in general development, but delayed in neural tube closure relative to overall or general development compared to two normal strains of mice, ICR/Be and SWV/Bc. Exencephaly was observed to be caused by a failure of fusion of the cranial neural folds in the mesencephalon region in SELH. All SELH embryos appeared to be abnormal in their pattern of cranial neural tube closure. They fail to make initial contact at the prosencephalon/mesencephalon junction region of the cranial neural folds (the first fusion in the cranial neural folds in normal embryos). SELH embryos, fused their anterior neural folds via an alternate (possibly passive) mechanism compared to normal strains of mice (SWV/Bc, and ICR/Be), by fusing the folds in a "zipper-like" fashion from the rostral base of the prosencephalon. This closure of the neural tube in genetically liable embryos by an abnormal sequence of events suggests a new model for anterior neural tube closure failure. Liability to exencephaly appeared to be fixed in the SELH stock. Of the 53 SELH males tested, all produced exencephaly. SELH animals were found to be heterogeneous in the frequency of exencephaly they produced, indicating that there are still genes segregating in the stock which affect the ability of embryos to complete anterior neural tube closure. Exencephaly in SELH does not appear to be caused by an autosomal dominant, sex-linked dominant or recessive, or simple autosomal recessive single gene, although F2, BCl, and BC2 exencephaly frequencies (after an outcross to ICR/Be) suggest that only a small number of genes are involved. A marked excess of female exencephalics was observed in SELH, F2, BCl, and BC2 fetuses.
Medicine, Faculty of
Medical Genetics, Department of
Graduate

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21

Ahmed, F. A. W. "Pleiotropic effects of coat-colour mutants in mice." Thesis, University of Essex, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.375647.

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Tinch, Alan E. "The genetics of muscle growth in chickens and mice." Thesis, University of Edinburgh, 1990. http://hdl.handle.net/1842/13134.

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DIAS, VIVIANE L. "Aspectos da resistencia a infeccao experimental com Trypanosoma cruzi." reponame:Repositório Institucional do IPEN, 2010. http://repositorio.ipen.br:8080/xmlui/handle/123456789/9609.

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Dissertacao (Mestrado)
IPEN/D
Instituto de Pesquisas Energeticas e Nucleares - IPEN-CNEN/SP

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Kim, Iksoo Phillips Carleton J. "Gene flow, genetic population structure, and biogeography of the leaf-eared mouse, Phyllotis xanthopygus, dwelling in natural habitat islands." Normal, Ill. Illinois State University, 1998. http://wwwlib.umi.com/cr/ilstu/fullcit?p9835913.

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Thesis (Ph. D.)--Illinois State University, 1998.
Title from title page screen, viewed July 5, 2006. Dissertation Committee: Carleton J. Phillips (chair), Elmer C. Birney, Angelo P. Capparella, Sabine S. Loew, Charles F. Thompson. Includes bibliographical references (leaves 61-74) and abstract. Also available in print.

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McClellan, Kelly Anne. "Murine oocyte loss occurs during fetal development." Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=79047.

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Recently, the timing of oocyte loss during murine development has been brought into question as authors using mouse vasa homologue (MVH) as a germ cell marker did not observe a loss of oocytes during fetal life. Instead the major loss was observed in the days following birth, after chromosome pairing has occurred.
In this study the controversy was addressed by establishing a new and reliable method to quantify murine oocytes in meiotic prophase, as well as to determine the gestation age and meiotic prophase stage of oocyte loss. Earlier limitations were overcome through the use of Germ Cell Nuclear Antigen-1 (GCNA-1) antibody as a germ cell specific marker, and the novel addition of a cytospin centrifugation step to the method. Progress through meiotic prophase was examined in chromosome spread preparations where meiotic stages were assessed using an antiserum against synaptonemal complex (SC) proteins. Quantification was accomplished by counting the number of GCNA-1 immunoreactive cells in chromosome spread preparations and estimated in histological sections using the ratio estimation model. (Abstract shortened by UMI.)

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Jeffries, Sean Joseph. "Imprint erasure and DNA demethylation in mouse development." Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608949.

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Mao, Jian-Hua. "Stochastic modelling of tumorigenesis in p53 deficient transgenic mice." Thesis, University of Glasgow, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.286124.

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Argyropoulos, George. "Molecular and genetic investigations of testicular development in mice." Thesis, University of Essex, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.280829.

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Demczuk, Suzanne. "Genetic analysis of the maternal factors controlling the survival of trisomy 16 mouse fetuses." Thesis, McGill University, 1991. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=60479.

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The BxH recombinant inbred strains of mice were used to undertake a genetic analysis of the maternal factors controlling the survival of trisomy 16 fetuses. The data presented indicate that the prevalence of trisomic fetuses on day 15 of gestation varies significantly with the genetic background of the mother. The strain difference in the frequency of trisomy appears to be the result of selective elimination of trisomic fetuses. Various statistical methods to elucidate the genetic architecture of the trait from the recombinant inbred strains data indicate that the number of loci involved in the selection process ranges from one to five. Linkage association with two loci have been found; however, with a low probability level (p = 0.292).

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Trasler, Tessa A. "Genetic control of the survival of trisomy 19 fetuses in mice." Thesis, McGill University, 1987. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=66103.

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31

鄭智強 and Chi-keung Cheng. "Structural organization of the mouse testin gene and characterization of its promoter sequence." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31224106.

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32

Dingler, Felix. "Investigations into origin and fate of uracil in the mouse genome." Thesis, University of Cambridge, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708713.

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33

Asante, Emmanuel A. "Biochemical genetics of lipid metabolism in chickens and mice." Thesis, University of Edinburgh, 1988. http://hdl.handle.net/1842/11520.

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Caron, Judith 1973. "Genetics of host resistance to chronic Salmonella infection in mice." Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=85895.

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Salmonella cause a broad spectrum of diseases in humans ranging from asymptomatic carriage to life-threatening sepsis. The disease outcome depends partly on the host genetic background.
The contribution of genes controlling the late phase of a Salmonella infection was studied using a model based on the inoculation of a sublethal dose of S. Enteritidis in 129S6 and C57BL/6J mice. C57BL/6J mice were able to eliminate completely S. Enteritidis from their RES, whereas 129S6 mice could not. Linkage analysis of 302 (C57BL/6J X 129S6) F2 progeny identified three QTLs, Ses1, Ses2, and Ses3. They were associated with disease susceptibility in 129S6 mice, and their estimated effects on bacterial clearance were greater in females. A statistical interaction was detected between Ses1 and Ses2. The model included the QTLs, the interaction and sex as a covariate, and explained 32% of the phenotypic variance suggesting that unidentified modifiers contributed to the phenotype.
A two-locus epistasis QTL linkage analysis conducted separately in the F2 females and males identified additional QTLs with individual effects and epistasic QTLs associated with the Salmonella carrier state of 129S6 mice. The model for females included Ses3 and two significant interactions (Ses1-D7Mit267 and Ses1-DXMit48 ) accounting for 47% of the total phenotypic variance. The model for males included Ses1.1, three interactions (Ses1-D9Mit218, D2Mit197-D4Mit2 and D3Mit256-D13Mit36) and explained 47% of the phenotypic variance.
We constructed congenic mice carrying the Ses1.1, Ses1, Ses2 and Ses3 regions to validate their existence in vivo and to study their impact on Salmonella clearance (129.136). Double congenic mice Ses1/Ses2 were constructed to test functionally the statistical interaction between these QTLs. Phenotypic analysis confirmed that Ses1 and Ses1.1 contribute to bacterial clearance.
The candidacy of Nramp1 as the gene underlying Ses1 was evaluated using Nramp1-deficient mice. 129S6-Nramp1tm1Mcg mice have a significantly lower bacterial load compared to 129S6 mice, suggesting that Nramp1 influences the S. Enteritidis clearance during the late phase of infection. We observed that the 129S6 mice mounted an early and strong TH1 response, whereas the 129S6-Nramp1 tm1Mcg mice mounted an earlier and more vigorous TH 2 response that seems to improve the late phase Salmonella clearance.

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35

Everett, Clare Alexandra. "Robertsonian translocations and their effect on the fertility of mice." Thesis, University of Oxford, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.357568.

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Ciciotte, Steven. "Characterization of CRE Recombinase Expression in Erythroid Tissues of Transgenic Mice." Fogler Library, University of Maine, 2005. http://www.library.umaine.edu/theses/pdf/CiciotteS2005.pdf.

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37

麥小珊 and Siu-shan Suzanne Mak. "Analysis of transgenic mice with ectopic Hoxb-3 expression in rhombomere 4." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31223175.

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38

Fu, Germaine 1976. "Mouse oocytes and embryos with or without the H10 gene : linker histone subtypes and development performance." Thesis, McGill University, 2000. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=33399.

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H1 histones are potentially significant to nuclear reprogramming during the oocyte-to-embryo transition. One characteristic distinguishing the H1 subtypes is that the somatic H1 histones are found primarily in dividing cells, whereas the H10 subtype is predominantly found in differentiated cells. The H1 complement in mouse oocytes and preimplantation embryos from wild-type and H10-/- animals was investigated.
Immunocytochemistry of wild-type cells demonstrated that H10 was predominant in oocytes while somatic H1 began accumulating in the 2-cell embryo. In H10-/- cells H10 was not detected, but, surprisingly, somatic H1 was detected beginning at the 1-cell stage. Radiolabeling of wild-type and H10-/- cells revealed that somatic H1 synthesis intensified after meiotic maturation, and therefore prior to its detection in embryos. The functional study found that loss of H10 impaired oogenesis but enhanced embryogenesis. The patterns of H1 immunodetection and synthesis are integrated, and the significance of H1 composition in development is discussed.

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39

Moase, Connie E. (Connie Evelyn). "Cell interactions in abnormal neural tube and neural crest cell development of splotch mice." Thesis, McGill University, 1991. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=70336.

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Early identification of mutant embryos prior to the manifestation of a defect facilitates the study of dysmorphogenesis. The In(l)lRk inversion was used as a cytogenetic marker to distinguish embryonic day 9 (D9) splotch (Sp) and splotch-delayed $(Sp sp{d})$ mouse mutants from heterozygous and wild-type littermates, and cellular aspects of abnormal neurulation and NCC migration were examined before inherent neural tube defects (NTDs) and deficiencies in neural crest cell (NCC) derivatives developed. In vitro analysis of NCC emigration from D9 neural tube explants revealed a delay in the release of NCCs from mutant neural tubes compared to controls, suggesting that the primary effect of the mutation was intrinsic to the neuroepithelium. Immunofluorescent localization of the neural cell adhesion molecule (N-CAM) antibody in situ demonstrated an increased intensity of antibody fluorescence in mutant tissue compared to controls, and further characterization by immunoblot analysis showed an altered embryonic N-CAM profile in both Sp and $Sp sp{d}$ mutants at D9 of gestation. The importance of N-CAMs in mediating cellular organization and communication has been well documented, supporting the idea that an alteration in this adhesion mechanism could result in the types of defects seen in splotch locus mouse mutants.

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40

Neale, Sondra-Ann. "Characterization of the neural cell adhesion molecule N-CAM in splotch mutant mouse embryos." Thesis, McGill University, 1993. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=69646.

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Cell adhesion molecules are known to play crucial roles in a variety of developmental processes. The neural cell adhesion molecule N-CAM is strongly implicated in neurulation and neural crest cell (NCC) migration and was thus studied in splotch (Sp) neural tube defect mutant embryos. At the 20 somite-stage of gestation day 9, Sp N-CAM was found to contain polysialic acid (PSA) side chains which are normally only present beginning at gestational day 11. Younger embryos at 12 and 14 somites also showed the presence of PSA on N-CAM, which was absent in controls. Enzymatic removal of PSA from N-CAM resulted in isoforms which migrated identically to PSA-free N-CAM isoforms in SDS-polyacrylamide gels. The post-translational modification of N-CAM appears to be the primary target of the Sp gene. In view of N-CAM's importance during development, an alteration at a critical stage is likely to result in the cascade of abnormalities seen in Sp mutants.
A new genotyping assay was also implemented for examination of N-CAM in Sp and other related wildtype strains.

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41

McLay, David W. "Developmental regulation and molecular nature of an activity in murine oocytes that transfers histones onto sperm DNA." Thesis, McGill University, 2001. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=38235.

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At fertilization, the remodelling of the sperm nucleus into the male pronucleus is critical for normal development. Morphological and functional changes to the nucleus are underpinned by biochemical changes in the chromatin composition, most notably the removal of sperm specific protamines and assembly of histones onto the paternal DNA. This exchange is controlled by oocyte factors, as exemplified in Xenopus by nucleoplasmin. Though mammalian factors remain unidentified, a functional assay based on antibodies recognizing core histones has been developed to test the activity in oocytes that transfers histones onto sperm DNA, named histone transfer activity (HTA). The assay was applied to growing and maturing murine oocytes to determine when during oogenesis HTA develops, and to probe potential regulatory mechanisms. Fully-grown oocytes develop HTA upon maturation, in a protein-synthesis dependent manner. Large, growing oocytes also develop HTA upon entry into M-phase. Small growing meiotically incompetent oocytes, ones that do not spontaneously enter M-phase, do not develop HTA, though this can be overcome by culture of oocytes to meiotic competence, or by treatment with strontium to induce intracellular calcium oscillations. Taken together these findings form a model of how HTA develops throughout oogenesis. Finally, an attempt is made to identify a potential mammalian HTA factor. Transcripts for two remodelling factors, mNAP and Npm3, are identified in the murine oocyte, and injection of anti-sense oligonucleotides reveals that Npm3 plays a significant role in the deposition of histories and the remodelling of sperm chromatin at fertilization. Combined with the findings of the HTA assay, the data forms a testable model of how Npm3 may be regulated throughout oogenesis.

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42

Zhang, Xiao-Qun. "Functional Studies on the PDGFR α gene promoter and effects of autocrine PDGF-A stimulation in vivo." Doctoral thesis, Uppsala universitet, Institutionen för genetik och patologi, 2001. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-1455.

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Platelet-derived growth factor receptor α (PDGFRα) plays an important role during embryogenesis. After implantation, the patterns of expression of Pdgfrα and its ligand Pdgf-A undergo an "autocrine-paracrine transition", in that Pdgf-A becomes expressed in the ectoderm and epithelia, while Pdgfrα is expressed in the adjacent mesenchymal tissue. In human tumors, such as malignant glioma, both PDGF and PDGFRα are overexpressed within the same tissue, indicating that an autocrine PDGF loop is generated in the tumors. This thesis is focused on the in vivo functionality of the PDGFRα gene (PDGFRA) promoter, arid on the effect of autocrine PDGF-A stimulation in transgenic n-iice during embryogenesis. To test the in vivo promoter function of a human PDGFRA 2.2 kb 5' flanking fragment, we generated transgenic mouse lines and found that the 2.2 kb fragment was able to promote lacZ reporter gene expression in most of the endogenous Pdgfra expressing tissues. Absence of expression and "ectopic" expression of the transgenic lacZ were also observed. To investigate the autocrine PDGF effect, we produced autocrine PDGF-As (A short-chain) transient transgenic embryos. These transgenic embryos carried a 6 kb mouse Pdgfra 5' flanking sequence linked to a human PDGF-As cDNA. The pattern of expression of the PDGF-As transgene mRNA was similar to that of lacZ. Some of the transgenic embryos exhibited severe abnormal phenotypes, such as midline fusion defects in the cephalic and craniofacial region and small body size, and these embryos die at mid-gestation stage. These findings indicate that a paracrine pattern of expression and the dosage of PDGF are important for sustaining normal embryo development, especially with regard to the middline fusion in craniofacial regions. The possible signaling pathways that may be involved in regulating Pdgfra activity were also studied by comparison of patterns of mRNA expression of Gli, Ptc, and Paxl with that of Pdgfra. The results pointed to the possibility that the Shh signaling pathway may be involved in the regulation of Pdgfra expression for example during early bone and foregut development. The specific regulatory mechanisms may vary for different tissues.

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Meunier, Charles. "Genetic control of susceptibility to carcinogen-induced colorectal cancer in mice." Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=104532.

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Colorectal cancer (CRC) is a complex multi-step disease that involves both an intrinsic genetic component, and extrinsic environmental factors. Using a set of AcB/BcA recombinant congenic strains (RCS) derived from CRC-susceptible A/J and CRC-resistant C57BL/6J progenitors, we have identified and characterized a major locus on a 14Mb segment of chromosome 3, as controlling azoxymethane-induced susceptibility to tumorigenesis in AcB/BcA strains, the Colon cancer susceptibility locus 3 (Ccs3). In following studies, we further ascertained the close phenotype/genotype correlation in additional AcB/BcA strains, as well as in groups of backcross populations bearing unique recombinant chromosomes for the interval. We reduced the Ccs3 interval to a 2.2Mb segment, containing 13 annotated transcripts, one of these genes coding for the NFkB p105 protein. As it is involved in pathological inflammation in the gut, Nfkb1 is also expressed at high levels in A/J intestinal mucosa but at low levels in CRC tumors. Sequencing of the 13 positional candidates identified a copy number variant (CNV) consisting of a strain-specific deletion of a 54bp duplication sequence near the Nfkb1 exon/intron junction of exon 15. Loss of one of the duplicated 54 bp-repeat is associated with CRC susceptibility in A/J. Finally, we observed the presence of additional genetic effects influencing the Ccs3-mediated CRC phenotype in AcB/BcA strains. Hence, we performed a linkage analysis by whole genome-scanning on 208 (B6 X A/J)F2 mice. These studies validated the effect of Ccs3 [LOD = 4.89] and identified an additional locus on distal chromosome 9 [LOD = 3.76], denoted Colon cancer susceptibility 5 locus (Ccs5). Ccs5 modulates tumor multiplicity in F2 animals bearing at least one A/J-derived susceptibility allele at Ccs3, with A/J-derived Ccs5 susceptibility alleles being inherited in a recessive manner. In F2 mice, a strong additive effect is observed between susceptibility alleles at both loci. Therefore, the work in this thesis also identifies a two-locus system (Ccs3, Ccs5) that regulates predisposition to CRC in mice.
Le cancer colorectal (CRC) est une maladie complexe résultant de l'interaction de composantes génétiques et environnementales. Nous avons identifié, puis caractérisé, un important locus nommé Colon cancer susceptibility locus 3 (Ccs3) contrôlant la susceptibilité à l'induction de CRC des lignées AcB/BcA, Les lignées de souris AcB/BcA recombinantes (recombinant congenic strains (RCS)) sont dérivées de la lignée A/J (susceptible à l'induction de CRC) croisée sur la lignée C57Bl/6J (résistante à l'induction de CRC), Nous avons ensuite confirmé la corrélation entre le génotype/phénotype du locus Ccs3 de lignées AcB/BcA additionnelles, de même que la corrélation des groupes générés par rétrocroisement incluant certains animaux portant un chromosome recombinant pour la portion du locus Ccs3. Cette approche a réduit l'intervalle physique correspondant à Ccs3 à un segment minimum de 2.2Mb. Cette région contient 13 transcrits annotés, notamment celui encodant la protéine NFκB p105. Nous avons examiné l'expression du gène Nfkb1 : celui-ci est fortement exprimé dans la muqueuse intestinale des souris A/J mais très peu dans leurs tumeurs de côlon. Le séquençage des 13 gènes candidat a identifié une variation du nombre de copies (CNV) d'une duplication de 54pb spécifique à une lignée A/J près du site d'épissage 3' de l'exon 15 de Nfkb1. La perte d'une de ces copies est associée avec l'apparition de tumeurs intestinales chez la souris A/J. Enfin, nous avons utilisé une approche génétique d'association par balayage du génome entier sur un total de 208 souris (B6 x A/J)F2 qui a confirmé l'effet majeur de Ccs3 [LOD = 4.89], et a détecté un locus additionnel dans la portion distale du chromosome 9 [LOD = 3.76], identifié Colon cancer susceptibility locus 5 (Ccs5). Ccs5 module la multiplicité de tumeurs chez les animaux F2 porteurs d'au moins un allèle de susceptibilité A/J au locus Ccs3, héritée de manière récessive. Nous avons donc identifié un système de deux loci (Ccs3, Ccs5) contrôlant la prédisposition au cancer colorectal chez la souris.

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44

Pemberton, Kieran David. "An analysis of the human tissue factor gene in transgenic mice." Thesis, Imperial College London, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.299183.

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45

Yazbek, Soha Nabil. "Analysis of genetic susceptibility to type II diabetes in mice." Case Western Reserve University School of Graduate Studies / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=case1277326732.

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46

Salcedo, Tovah. "Population Genetics and Evolution of Innate Immunity in House Mice." Diss., The University of Arizona, 2009. http://hdl.handle.net/10150/194535.

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Whole-genome studies of rates of protein evolution show that genes underlying reproduction and immunity tend to evolve faster than other genes, consistent with the frequent action of positive selection. The evolution of immunity has been well-studied at the interspecific level, but much remains unknown about the population-level dynamics of immunity. This project described genetic variation at immunity and non-immunity loci as well as variation among levels of infection for diverse pathogens in a natural population of mice from Tucson. Analysis of autosomal and X-linked loci in the native range of Mus domesticus, the species from which Tucson mice are primarily descended, revealed low levels of variation consistent with a recent population expansion, resulting in a slight excess of rare alleles across the genome. Genetic variation among a set of classical inbred strains represented a small fraction of wild variation. An overlapping set of genes sequenced in mice from Tucson revealed that there is significant introgression from Mus castaneus. After controlling for gene flow, Tucson mice showed evidence of a mild bottleneck that produced a slight excess of intermediate frequency alleles, but did not result in a dramatic loss of genetic variability. Most of the 15 pathogens and parasites studied in Tucson were found at low to intermediate frequency, and most mice had one to three infections, suggesting that there are many opportunities for host-pathogen coevolution, and a possible role for coinfection. A study of Fv-4, which confers resistance to murine leukemia viruses, confirmed that the resistance allele originated in M. castaneus and is now found at intermediate frequency in Tucson after introduction through gene flow. Finally, a study of the recently duplicated Ceacam1 and Ceacam2 genes, previously shown to be involved in resistance to mouse hepatitis virus (MHV), revealed that a gene conversion event moved a suite of mutations from Ceacam2 to Ceacam1. An elevated rate of protein evolution showed that Ceacam2 had experienced positive selection after duplication. Interestingly, there was no association between MHV antibody presence and Ceacam1 genotype in Tucson. This project showed that gene flow and gene conversion mediated resistance to infections in wild mice.

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47

Holmes, Andrew. "Mechanisms and contexts of kin recognition in female house mice." Thesis, University of Liverpool, 2012. http://livrepository.liverpool.ac.uk/9259/.

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As relatives share genes that are identical by descent, organisms can gain additional fitness benefits by improving the reproductive success of known kin. There are a number of costs associated with close inbreeding, including an increased likelihood of the expression of recessive deleterious alleles and reduced survivorship. The ability to recognise kin therefore enables individuals to improve their inclusive fitness and avoid problems associated with close inbreeding. Female house mice (Mus musculus domesticus) will nest and nurse offspring communally. Choosing an appropriate nest partner is therefore important and competition between nesting females can result in reproductive inhibition and infanticide. Kin selection theory suggests that females could gain inclusive fitness benefits from nesting with relatives. This thesis explores the mechanisms of kin recognition in female house mice in the contexts of social partner choice and inbreeding avoidance. Female house mice recognised unfamiliar relatives, suggesting a phenotype matching mechanism for kin recognition. Females were presented with maternal and paternal half-siblings to investigate recognition template formation. Females nested with maternal but not paternal half-sisters, suggesting that female house mice may use a recognition template learnt from their mother for social partner choice decisions. However females avoided both maternal and paternal half-brothers suggesting that females may use a match-to-self mechanism for inbreeding avoidance. Female house mice were able to identify relatives from urine, suggesting that genetic markers are present in urine. To investigate the molecular markers of kin recognition mice were bred to control for the major histocompatibility complex (MHC) and major urinary proteins (MUPs). Females nested with females that matched for MHC or MUP type, suggesting that both gene families may be used for kin recognition between females. A non-significant trend was observed for females to avoid males that matched themselves for MUP type, but females showed no avoidance of males that matched for MHC type. A small pilot experiment investigated the physiological effects of female social environment. Housing with unfamiliar females resulted in short-term decreases in female body mass and urinary protein concentration but an increase in urinary creatinine concentration. Competition between unfamiliar females may have resulted in a decreased water uptake and an increase in scent marking which could explain the physiological changes observed. Together these results suggest that female house mice may use two mechanisms of kin recognition. For social partner choice females may use a match-to-maternal MHC and MUP type mechanism, whilst for inbreeding avoidance females may use a match-to-own MUP type mechanism. The possibility of a single species using two separate mechanisms suggests that kin recognition may be considerably more complex than previously thought.

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48

Bander, S. A. A. "Pre-zygotic interactions in mice : A genetic analysis." Thesis, University of Essex, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.380568.

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49

Shukri, N. M. "Genetic studies of male reproductive characteristics in mice." Thesis, University of Essex, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.383426.

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50

李彥霆 and Yin-ting Lee. "Molecular characterization of the insertional mouse mutant yellow submarine, Ysb." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2002. http://hub.hku.hk/bib/B31226279.

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Dissertations / Theses on the topic 'Mice – Genetics'

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