Dissertations / Theses on the topic 'Mice embryology; mice genetics'
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1
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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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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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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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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Moase, Connie E. (Connie Evelyn). "Histopathology of, and retinoic acid effects in, biochemically identified splotch-delayed mouse embryos." Thesis, McGill University, 1986. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=66099.
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Hurtubise, Patricia. "Intracellular signalling during murine oocyte growth." Thesis, McGill University, 2000. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=31239.
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During the growth phase of oogenesis, mammalian oocytes increase several hundred-fold in volume. Although it is known that ovarian granulosa cells send growth promoting signals, neither these external signals nor the transduction pathways that become activated in the oocyte are known. Therefore, the presence and the activity of candidate signaling pathways in growing murine oocytes were investigated. By immunoblotting, the MAP kinases, ERK1 and ERK2, as well as their activating kinase MEK, were detected in oocytes at all stages of growth. However, using a phospho-specific anti-ERK antibody, no immunoreactive species were detectable in isolated granulosa cells or oocytes at any stage of growth, except metaphase II. Phosphorylated ERK was also present, although in smaller quantities, in oocyte-granulosa cell complexes at the later stages of growth. Furthermore, when ovarian sections were stained with an anti-ERK antibody, the protein was found to be highly concentrated in the cytoplasm of oocytes at all stages of growth, with lower levels in the nucleus. Another member of the MAP kinase family, Jun kinase (JNK), was investigated. By immunoblotting, JNK was detected in growing oocytes. Experiments using an anti-JNK antibody on ovary sections revealed the protein to be uniformly distributed in non-growing and growing oocytes with no evidence of preferential nuclear localization. These results imply that an interaction between the oocyte and the granulosa cells may be required to generate phosphorylated ERK. They also imply that growth signals probably are not relayed through ERK, but do not exclude a role for Jun kinase in mediating oocyte growth.
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O'Leary, Debra Alison. "Characterisation of gene structure and function of the ETS transcription factor Gabpα in mouse." Monash University, Centre for Functional Genomics and Human Disease, 2003. http://arrow.monash.edu.au/hdl/1959.1/9445.
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Nowacka, Lidia. "Muscle gene transfer studies of a 27-BP segment of the troponin I fast gene IRE enhancer." Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111563.
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The fast-skeletal-muscle-fiber-specific expression of the troponin I(fast) (TnIfast) gene is driven by an Intronic Regulatory Element (IRE) located within the first intron of the gene. The IRE is a 148 bp transcriptional enhancer that contains several known and suspected cis-regulatory elements. These include the E-box, the closely-spaced MEF2 site and CACT box, the CACC site, and the CAGG element. Previous loss-of-function studies performed using the quail TnIfast IRE suggest that its activity depended on the MEF2 and CACT elements. The goal of my thesis research was to determine whether the MEF2 and CACT sites were not only necessary, but also sufficient, to support IRE activity. I prepared head-to-tail multimers of a 27-bp IRE segment that consisted largely of the near-adjacent MEF2 and CACT elements and did not contain any other known/suspected elements. These multimers were cloned upstream of a reporter gene consisting of the minimal promoter of the quail TnIfast gene linked to sequences encoding human placental alkaline phosphatase. The transcriptional capabilities of the constructs were assessed by gene transfer into the mouse soleus muscle in vivo by intramuscular injection/electroporation, and histochemical analysis of reporter enzyme plap expression including quantitative microdensitometry. I found that expression of these constructs was readily detectable and that it was markedly reduced by prior mutation of the CACT and, especially, of the MEF2 sites. These data indicate that the short DNA segment containing MEF2 and CACT elements is sufficient to drive expression in skeletal muscle and confirms the functional importance of these specific elements.Although constructs containing the wild-type IRE 27-bp region were expressed, there was little preferential expression in fast fibers, in contrast to expression driven by the complete 148-bp IRE. Thus my results indicate that the MEF2 and CACT elements are not sufficient to drive fast fiber-type-specific expression, and suggest that additional elements outside of the 27-bp region tested are also necessary for fiber-type-specificity.
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Glaser, Juliane. "Functional characterization of the imprinted Liz/Zdbf2 locus in mice : from the early embryo to adult physiology." Electronic Thesis or Diss., Sorbonne université, 2018. http://www.theses.fr/2018SORUS243.
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L’empreinte parentale est un mécanisme de régulation épigénétique qui réduit l’expression d’environ 120 gènes à une seule dose parentale. L’expression monoallélique dépend de marques différentielles de méthylation de l’ADN, établies dans l’ovocyte et le spermatozoïde et maintenues après fécondation dans l’individu en développement. Chez les mammifères, les gènes soumis à empreinte sont essentiels au développement embryonnaire et à certaines fonctions comportementales et physiologiques après la naissance. Définir les mécanismes de régulation et la fonction des gènes soumis à empreinte est une question cruciale en biologie du développement et en pathologie. Mon travail de thèse a concerné l’étude fonctionnelle du locus Zdbf2 chez la souris. Zdbf2 est un gène exprimé paternellement, conservé chez l’humain, mais dont la fonction était inconnue. J’ai pu démontrer que l’activation de Zdbf2 dans le cerveau de souris pré-pubères dépend d’un signal épigénétique indélébile mis en place dès les premiers jours de développement embryonnaire. Cette programmation précoce de Zdbf2 assure une croissance normale du nouveau-né. Mes résultats indiquent de plus que la dose, mais pas l’origine parentale de Zdbf2 est essentielle. Ces découvertes ont été possibles par la création de divers modèles mutants avec des variations de la dose de Zdbf2 dans l’axe hypothalamo-hypophysaire. Ce travail met en lumière la fonction cruciale d’un gène soumis à empreinte, de sa régulation dans l’embryon précoce à son rôle sur la physiologie adulteGenomic imprinting refers to the epigenetic mechanism by which approximately 120 genes are expressed in a parent-of-origin manner. This parental asymmetry in gene expression is mediated through differential profiles of DNA methylation established in the oocyte and the sperm and maintained after fertilization in the developing individual. In mammals, imprinted genes are essential for normal embryo development as well as behavioral and physiological functions after birth. Clarifying the regulation and the function of those genes is thus fundamental in the field of developmental biology and health. During my PhD, I functionally characterized the imprinted Zdbf2 locus in mice. Zdbf2 is a paternally expressed gene, conserved from mouse to human, whose biological function was unknown. I revealed that Zdbf2 activation in the post-natal brain requires an indelible epigenetic signal that is established during the first days of embryogenesis. Additionally, I provided in vivo evidence that early programming of Zdbf2 is essential for proper growth after birth. By generating multiple CRISPR-mediated genetic mutants with varied doses of Zdbf2 in the hypothalamo-pituitary axis, I finally demonstrated that Zdbf2 is a growth-promoting gene, with a dose-sensitive effect and acting independently of its parental origin. Altogether, my work shed light onto the crucial function of a mammalian imprinted gene, from its regulation in the early embryo to its role in adult physiology
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Poirier, Luc. "The degradation of the stem-loop binding protein at the late 2-cell stage of mouse embryogenesis /." Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=80351.
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The efficient processing of replication-dependent histone mRNA requires the Stem-Loop Binding Protein (SLBP). SLBP is also involved in regulating histone mRNA half-life, their nucleocytoplasmic transport, and their translation. Unlike somatic cells, where SLBP protein accumulates only in S-phase, SLBP protein is present throughout the first two embryonic cell cycles in mice. We report here that in late 2-cell mouse embryos there is a substantial, proteasome-dependent decrease in SLBP throughout the cell. Based on chromosome morphology, the degradation of SLBP protein in late 2-cell embryos is most likely a late G2-phase event. The degradation of SLBP protein is not simply a zygotic clock event, but requires development to the late 2-cell stage. Furthermore, SLBP protein degradation in 2-cell mouse embryos requires cyclin-dependent kinase (Cdk) activity, DNA replication, and zygotic genome activation. A model for SLBP protein degradation is proposed based on observations made in both early mouse embryos and somatic cells.
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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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Chan, Siu-yuen. "Effects of prostaglandins on peri-implantation development of mouse embryos /." [Hong Kong : University of Hong Kong], 1989. http://sunzi.lib.hku.hk/hkuto/record.jsp?B12730191.
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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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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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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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Joyce, Bradley. "Elucidating the molecular mechanisms underlying cell movements during early embryogenesis." Thesis, University of Oxford, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.589616.
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The anterior visceral endoderm (AVE) is a specialised subpopulation of the visceral endoderm (VE), a single layer simple epithelium that surrounds the extra-embryonic ectoderm and epiblast of the egg cylinder stage embryo. Initially induced at the distal tip of the egg cylinder, AVE cells undergo a stereotypic migration towards the prospective anterior, stopping at the interface between the underlying epiblast and extra-embryonic ectoderm (ExE). Previous research has shown that membrane enrichment of Dvl2 is present in the VE overlying the epiblast (Epi-VE). In this thesis I confirm the presence of planar cell polarity (pep) signalling in this region by assaying the subcellular localisation of additional core pep proteins Vangl2 and Daaml. I show that null embryos of the Nodal antagonist Lefty1 exhibit ectopic membrane enrichment of Dvl2 and a previously unreported AVE over-migration phenotype. Furthermore, using pharmacological inhibition of Nodal signalling I show that the TGF~ protein Nodal modulates pep signalling in the YE. Utilising DIe and confocal microscopy I perform detailed time-lapse analyses of the VE to quantify the dynamic cell behaviour and topology. Using this assay I show that wild-type embryos exhibit dynamic cell movement, which is regionally restricted to the Epi-VE. Analysis of Leftyl-/- and ROSA26lyn-Celsr-l mutants, both of which exhibit disrupted pep signalling and AVE over-migration phenotypes, indicates that normal VE dynamics and topology are disrupted. The results of this quantitation indicate that these mutants exhibit increased cell migration and neighbour exchange across the YE. These data show that regional restriction of movement is lost and results in the AVE over-migration phenotypes observed. Together these results show that regionally restricted pep signalling in the VE acts to modulate cell behaviour and topology, which in turn determines the regional restriction and normal end-point of AVE migration.
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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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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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Fuku, Eiji. "Studies on the preservation of mammalian embryos in the supercooled state." Thesis, McGill University, 1991. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=60523.
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Firstly, exposure of compacted morulae (CM) and early blastocysts (EB) to methanol (M) or glycerol (G) for 1 h at room temperature followed by culture in standard culture medium showed that the embryos tolerated up to 12 to 24% methanol or 24 to 48% glycerol. Next, the effects of stage of embryo (CM vs EB), preservation temperature and concentration of 1:1 M:G on embryo survival were tested. EB survived longer than CM under all conditions. Increased concentrations of cryoprotectants (M and G) increased the survival of supercooled embryos, but survival was decreased with the storage temperature. Replacing G with propanediol (P) significantly increased blastocyst survival at lower temperatures.Exposure for 1 h to $>$ 0.6 M of sucrose or trehalose at room temperature suppressed growth in culture, but dehydration in up to 0.4M sucrose before supercooling (in M:P) increased survival at $-$5 or $-$10$ sp circ$C, survival increasing with dehydration.
Finally, demi-embryos and intact embryos were cultured to the blastocyst stage, stored at $-$5$ sp circ$ for 48 h, then cultured for 24 h and transferred into pseudopregnant recipients.
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Chia, Gloryn Le Bin. "Investigating the role of Oct4 during lineage specification in the physiological context of mouse embryonic development." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.607990.
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Yu, Hing-Sing. "Studies on the toxicity and teratogenicity of cadmium on mouse pre-embryos in vitro and in vivo with special reference to their subsequent development /." [Hong Kong] : University of Hong Kong, 1987. http://sunzi.lib.hku.hk/hkuto/record.jsp?B1221579X.
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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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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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Hübner, 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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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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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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Cheong, Wan-yee Ana, and 張韻怡. "A study on the embryotrophic action of the complement component-3 derivative (iC3b) in the preimplantation mouse embryo development." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B44231994.
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Fung, Chun-kit. "An investigation on the effects of glutamine in culture meida on the preimplantation mouse embryo /." Hong Kong : University of Hong Kong, 1999. http://sunzi.lib.hku.hk/hkuto/record.jsp?B21629821.
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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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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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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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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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Tian, Xiao Ying. "The study of Chinese herbal medicine in embryonic development of mice." HKBU Institutional Repository, 2009. http://repository.hkbu.edu.hk/etd_ra/1071.
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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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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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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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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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Chan, Siu-yuen, and 陳小圓. "Effects of prostaglandins on peri-implantation development of mouse embryos." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1989. http://hub.hku.hk/bib/B30257256.
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Fung, Chun-kit, and 馮俊傑. "An investigation on the effects of glutamine in culture meida on the preimplantation mouse embryo." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1999. http://hub.hku.hk/bib/B31222560.
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余慶聲 and Hing-Sing Yu. "Studies on the toxicity and teratogenicity of cadmium on mouse pre-embryos in vitro and in vivo with special reference to theirsubsequent development." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1987. http://hub.hku.hk/bib/B31231457.
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Alexandrova, Stoyana. "In vivo behaviour of embryonic stem cells in early mouse embryo development." Thesis, University of Cambridge, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708686.
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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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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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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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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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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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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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Schmidt, Kristie. "The Mechanism of Obesity in Rai1+/- Mice." VCU Scholars Compass, 2010. http://scholarscompass.vcu.edu/etd/135.
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Smith-Magenis syndrome (SMS) is a genetic disorder caused by a deletion or mutation of the retinoic acid induced 1 (RAI1) gene on chromosome 17p11.2 that results in haploinsufficiency. SMS patients with a deletion account for 90% of the cases, while the other 10% have a mutation in RAI1. The syndrome is characterized by cognitive impairment, craniofacial abnormalities, sleep disturbances, developmental delay, obesity, and behavioral phenotypes. SMS is thought to affect 1:25,000 live births, although due to similar infantile phenotypes with Down syndrome and Prader-Willi syndrome, SMS may be mis- or under-diagnosed. In a study of 54 children, it was shown that by age 12, females with SMS are in the 90th weight percentile, while males reach the 90th percentile by age 14. It was also shown that viii teens and adults with Smith-Magenis syndrome commonly present with truncal obesity. In order to keep SMS patients healthy, to reduce the risk for future health problems associated with obesity, and to more fully understand the role of Rai1 in Smith-Magenis syndrome, it is first necessary to understand the mechanism by which SMS patients become obese. Mouse models of SMS provide a powerful tool for looking at potential mechanisms of obesity related to the haploinsufficiency of Rai1. Obesity in Smith-Magenis syndrome may result from a combination of I) behavioral, II) metabolic, and III) signaling mechanisms in which the haploinsufficiency of Rai1 causes deviations in critical pathways responsible for energy intake and expenditure. Data suggest that the Rai1+/- mice are obese and hyperphagic. Data also demonstrate that Rai1+/- mice do not have symptoms of metabolic syndrome associated with their obesity. Signaling mechanisms are deviated from normal in Rai1+/- mice, including leptin levels and the expression of Pomc, Mc4r, Bdnf, and Agrp. Treatment with ampakine drug may increase expression of Bdnf and help to control obesity in Rai1+/- mice.
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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.