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Dissertationen zum Thema „Cell-Embryo“
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1
Spanos, Sophia. „Cell death during preimplantation embryo development“. Thesis, Imperial College London, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.398228.
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2
Chisholm, J. C. „Cell diversification in the mouse early embryo“. Thesis, University of Cambridge, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.384438.
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3
Ridyard, Marc Steven. „Cell adhesion-related signaling molecules in embryo development“. Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ46910.pdf.
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4
Anderson, Jon E. „Cell cycle regulation in the early porcine embryo /“. free to MU campus, to others for purchase, 2000. http://wwwlib.umi.com/cr/mo/fullcit?p9974607.
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5
Selleck, Mark Anthony James. „Hensen's node and cell commitment in the chick embryo“. Thesis, University of Oxford, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.293410.
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6
Storey, Kate Gillian. „Cell lineage and pattern formation in the earthworm embryo“. Thesis, University of Cambridge, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.346430.
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7
Hughes, Julian Richard. „mRNA localisation and cell polarity in the Drosophila embryo“. Thesis, University College London (University of London), 2005. http://discovery.ucl.ac.uk/1445657/.
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Asymmetric localisation of mRNA transcripts to specific sites within the cytoplasm is a widely employed mechanism for targeting of proteins and generating cell polarity. The mechanism and function of mRNA localisation has been extensively studied in Drosophila melanogaster, where, for example, the Egalitarian/Bicaudal- D/dynein complex mediates transport of mRNA transcripts, towards microtubule minus-ends, during oogenesis and in syncytial blastoderm embryos. However, it is not known whether the Egalitarian/Bicaudal-D/dynein mRNA transport machinery is required to localise mRNAs in somatic cell types in the Drosophila embryo. In this thesis, I show that the Egalitarian/Bicaudal-D/dynein complex is active in embryonic epithelial cells and neuroblasts and mediates asymmetric localisation of inscuteable, wingless and crumbs, but not miranda, mRNA transcripts, indicating that this is a general mechanism for mRNA localisation in Drosophila. I provide preliminary evidence that y-Tubulin mediates asymmetric miranda localisation. I have also explored the role of mRNA localisation in protein targeting in epithelial cells and neuroblasts, and find that asymmetric localisation of inscuteable and wingless, but not crumbs, mRNA transcripts is required to enhance the targeting of their protein products. I find that asymmetric localisation of wingless mRNA and protein is not required to support Wingless function in the embryo, although, Inscuteable activity is significantly reduced when inscuteable mRNA localisation is disrupted, and neuroblasts display defects in apico-basal polarity and metaphase spindle length. In conclusion, mRNA localisation acts to enhance protein targeting and activity in somatic cell types in the Drosophila embryo.
8
Prigent, Serena. „Biochemical regulation of cell mechanics in C. elegans Embryo“. Electronic Thesis or Diss., Sorbonne université, 2021. http://www.theses.fr/2021SORUS395.
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L’architecture et la dynamique du cortex d’Actine joue un rôle central dans la contractilité cellulaire et la morphogénèse des tissus. La modulation locale de la dynamique du réseau d’Actomyosine dépend majoritairement de la cascade d’activation de RhoA. Dans ma thèse, j’ai combiné des approches de microscopie quantitative en TIRFM, de l’imagerie en molécule unique, des simulations numériques et de la modélisation mathématique simple pour explorer l’architecture dynamique du réseau sous-jacent aux contractions pulsées dans un modèle simple : le jeune embryon de C. elegans. En se concentrant sur la Formine, élongateurs de l’Actine, nous avons observé que l’élongation de la F-Actine était catalysée par une population spécifique de Formines corticales – appelées Formines élongatrices – qui montrent une mobilité de type balistique. Nous avons ensuite montré que les Formines saturent les extrémités barbées disponibles et convertissent un gradient biochimique local de l’activité de RhoA en un réseau d’architecture polaire. Dans une seconde étude, en se concentrant sur la cinétique de la cascade d’activation de RhoA, nous avons développé un modèle numérique simple. Celui-ci tire profit des mesures des paramètres dynamiques de la Myosine, un effecteur terminal de la cascade d’activation de RhoA, pour prédire l’évolution temporelle de cette cascade. Je propose ici que ce modèle simple et générique – qui peut par essence s’adapter à n’importe quelle cascade – offre un cadre mathématique simple pour comprendre la dynamique temporelle des cascades d’activation, et le délai et changement dans la forme de la réponse qui peuvent être observés entre l’entrée et la sortieActin network architecture and dynamics play a central role in cell contractility and tissue morphogenesis. Local modulations of Actomyosin network dynamics depend largely on the activation of the RhoA activation cascade. In my thesis, I combined quantitative microscopy using TIRFM, single-molecule imaging, numerical simulations and simple mathematical modeling, to explore the dynamic network architecture underlying pulsed contractions in a simple model, the C. elegans early embryo. Focusing on the Actin elongator Formin, we observed that F-Actin elongation was catalyzed by a specific subpopulation of cortical Formins – termed elongating Formins – that displayed a characteristic ballistic mobility. My results also showed that Formin-mediated F-Actin elongation rate was dependent on the phase of the cell cycle and embryonic stage. We subsequently showed that elongating Formins saturate available barbed ends of Actin filaments, converting a local biochemical gradient of RhoA activity into a polar network architecture. In second study, focusing on the kinetics of the RhoA activation cascade, we developed and functionally challenged a simple numerical model. This model takes advantage of the measurements of the dynamical parameters of the Myosin, downstream effector of the RhoA activation cascade, to predict the temporal evolution of this cascade. I propose that this simple and generic model – which can in essence fit any activation cascade – offers a simple mathematical framework to understand the temporal dynamics of signaling cascades, and the delay and change in the shape of the response which can be observed between the input and the output of a cascade
9
Bloom, Theodora Leah. „Protein phosphorylation and cell diversification in the mouse early embryo“. Thesis, University of Cambridge, 1990. https://www.repository.cam.ac.uk/handle/1810/250962.
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This dissertation reports the results of studies into the control of compaction of the mouse preimplantation embryo. Compaction is a post-translationally controlled rearrangement of cell contacts and the cytoskeleton that occurs at the 8-cell stage of development. This re-arrangement seems to be necessary for the differentiation of the two cell types present in the blastocyst. Protein phosphorylation is a post-translational modification believed to be important in the modulation of cell shape and cytoskeletal assembly. It is therefore feasible to propose a role for protein phosphorylation in compaction. Two types of approach have been used to investigate the possible role of protein phosphorylation in compaction. Firstly, embryos have been treated with two drugs, 6-dimethylaminopurine (DMAP) and a phorbol ester (phorbol myristate acetate, PMA), each of which seems to affect both protein phosphorylation and compaction. DMAP is an adenine analogue and putative inhibitor of protein phosphorylation that was found to perturb the cell cycle of mouse embryos. In addition, DMAP caused rapid cellular flattening of 4-cell and 8-cell embryos. However, this flattening was not accompanied by cell polarisation and did not seem to be mediated by the cell adhesion molecule uvomorulin. It is therefore unlikely to be related directly to the flattening that occurs at compaction. Phorbol esters, such as PMA, are potent stimulators of the membrane-associated, Ca2+- and phospholipid-dependent protein kinase, protein kinase C (PKC). Incubation in medium containing PMA had some effects on the cytoskeleton of oocytes and early embryos but caused severe, widespread disassembly of the cytoskeleton and reversal of flattening in 8-cell embryos. These effects of PMA, seen specifically at the 8-cell stage, may be related to the spatially restricted disassembly of the cytoskeleton that occurs naturally during compaction at the 8-cell stage. This interpretation provides indirect evidence for a possible role for PKC activity, and hence protein phosphorylation, in the process of compaction. The relationship between protein phosphorylation and the events occurring at the 8-cell stage has been examined more directly by labelling 4-cell and 8-cell embryos with [32P]orthophosphate and examining the phosphoproteins obtained by one and two-dimensional gel electrophoresis. By synchronising groups of embryos precisely to successive cleavage divisions prior to labelling, changes in phosphoprotein profile associated with passage through the 4-cell and 8-cell stages have been described. While many of the 32P-labelled phosphoproteins detectable after electrophoresis in one or two dimensions are similar at each stage examined, there are some changes associated specifically with passage through the 8-cell stage which may be related to the cell flattening and polarisation occurring at this time. In addition, the profile of 8-cell embryos differed according to the duration of pulse-labelling with [32Pjorthophosphate or the inclusion of "chase" periods. Finally, several treatments that affect features of compaction, including exposure to DMAP and PMA, have been used to assess the link between the observed changes in phosphoprotein profile and the events of compaction. Embryos were also incubated in protein synthesis inhibitors, which cause premature cell flattening in 4-cell embryos and in Ca2+-free medium, which prevents intercellular flattening and delays polarisation of 8-cell blastomeres. In each case, the relative labelling intensity of some of the phosphoproteins characteristic of untreated 8-cell embryos was altered. The behaviour of these phosphoproteins suggests that they may be important in the mechanism by which cells flatten and polarise or in the maintenance of flattened, polarised, cells; they now provide a focus for future study.
10
李燕柳 und Yin-lau Lee. „Embryotrophic effects of Vero cell on preimplantation mouse embryo development“. Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1999. http://hub.hku.hk/bib/B31223023.
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11
Lee, Yin-lau. „Embryotrophic effects of Vero cell on preimplantation mouse embryo development /“. Hong Kong : University of Hong Kong, 1999. http://sunzi.lib.hku.hk/hkuto/record.jsp?B2168747X.
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12
Jesuthasan, Suresh. „Two modes of cell movement in the zebrafish embryo : neural crest cell migration and epiboly“. Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.240465.
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13
Lambert, Justin David. „Patterning a mollusc embryo: The roles of cell lineage and cell signaling in Ilyanassa obsoleta“. Diss., The University of Arizona, 2001. http://hdl.handle.net/10150/279869.
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The experiments reported here describe mechanisms of cell fate specification in the embryo of the snail Ilyanassa obsoleta. During early cleavage, the animal-vegetal axis of the embryo is subdivided by a stereotyped series of asymmetric cell divisions that produce sets of cells with similar cleavage patterns and developmental fates. Here I show that, during these cell divisions, mRNAs for multiple patterning genes co-localize with particular centrosomes and are partitioned into specific cells during cleavage. The movement of the mRNAs to the centrosomes requires the microtubule cytoskeleton, and the subsequent movement, from the centrosome to a region on the cortex, requires actin filaments. These events localize different mRNAs to distinct sets of cells with similar developmental fates. In experimentally produced cells with two interphase centrosomes, mRNAs accumulate on the appropriate centrosome, indicating that the patterned accumulation of mRNAs is controlled at the level of individual centrosomes. In a second phase of cell fate specification, one cell in the embryo (called 3D) induces several ectodermal fates in target cells. Here I show that this signaling event involves two conserved cell signaling pathways, the MAPK pathway and the Dpp/BMP2&4 pathway. MAPK activation is detected first in 3D, and then in the cells that are predicted to require the signal. Ablation of 3D prevents the activation in the responding cells, and blocking MAPK activation with a specific inhibitor prevents the differentiation of the structures that require induction by 3D. My results indicate that 3D induces MAPK activation in the responding cells and that this is required for normal patterning. I examined embryos of several other molluscs and representatives of related protostome phyla and found that, in embryos with equal spiral cleavage, MAPK was activated in 3D, but not in the responding cells. The Ilyanassa ortholog of the secreted ligand Dpp (IoDpp) is expressed in the 3D macromere. Treatment of embryos with a closely related ligand (human BMP4) induces a high frequency of extra eyes in intact embryos, and rescues the lack of eyes in embryos where 3D is not specified. These results suggest that 3D specifies multiple fates by parallel Dpp and MAPK-activating signals.
14
Takeda, Hiroyuki. „Commitment of cell fate in embryo of the zebrafish, Danio rerio“. Laboratory of Freshwater Fish Stocks Bioscience Center Nagoya University, 1994. http://hdl.handle.net/2237/13791.
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15
Jaligam, Vanaja. „Developmental cell death in the midline glia cells of Drosophila embryo“. College Park, Md. : University of Maryland, 2004. http://hdl.handle.net/1903/1467.
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Thesis (M.S.) -- University of Maryland, College Park, 2004.Thesis research directed by: Dept. of Cell Biology and Molecular Genetics. Title from t.p. of PDF. Includes bibliographical references. Published by UMI Dissertation Services, Ann Arbor, Mich. Also available in paper.
16
Butler, L. C. „Analysis of cell behaviours underlying germband extension in the Drosophila embryo“. Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.597164.
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Germband extension (GBE) in the early Drosophila embryo provides a simple system in which to study convergence and extension, a type of tissue remodelling common in development. During GBE the embryonic trunk (“germband”) extends in the anterior-posterior (AP) axis, and narrows in the dorso-ventral (DV) axis. I have quantitatively analysed cell and tissue behaviours during GBE. Our collaborators have developed novel algorithms to measure the continuous impact of cell intercalation and cell shape change on tissue deformation. Here I apply these algorithms to describe the behaviours contributing to GBE. I find that wild type embryos not only undergo cell intercalation, but also cell shape change which accounts for up to 50% of the extension rate during the fast phase of GBE. I find that this cell shape change is elevated in AP patterning mutants that have a defect in cell intercalation, and that this elevation accounts for the initial rapid pulse of extension in these mutants. Regional analysis of these cell behaviours in wild type and AP patterning mutants indicate that cell intercalation is regionally autonomous, but that cell shape change is controlled at a more global level. An external force may be present during early GBE, stretching cells in the AP axis if they fail to intercalate properly. Additionally, I have examined the impact that other morphogenetic movements of gastrulation have on GBE. Mutant analysis shows that the ventral furrow affects the rate but not overall extent of tissue deformation, while the posterior midgut invagination appears to be required only for correct displacement of the tissue as it deforms, and not for tissue deformation itself, at least during early GBE. Thus, the amount of tissue extension, the rate at which it occurs, and the tissue displacement by which it is accommodated are separable phenomena.
17
Rashidi, Hassan. „Developing the chick embryo model to study mesenchymal stem cell differentiation“. Thesis, University of Nottingham, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.659205.
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Human mesenchymal stem cells have attracted significant attention during the last decade as a versatile tool for cell therapy, gene therapy and tissue engineering. The existence of mesenchymal stem cells in adult tissues and their capacity for differentiation into multiple lineages are major benefits for clinical applications, circumventing the ethical and safety concerns surrounding the use of embryonic stem cells. It has been long established that mesenchymal stem cells have the potential to differentiate into mesenchymal lineages such as bone, cartilage and adipose tissue. Recent studies have uncovered the potential of mesenchymal stem cells to differentiate into endodermal and ectodermal derivatives, suggesting a greater plasticity than originally envisaged. In the current study, a novel approach using the chick embryo was developed to investigate the differentiation potential of bone marrow-derived human mesenchymal stem cells when exposed to developmental signals in vivo. In order to investigate the suitability of the chick embryo as a host, mesenchymal stem cells were first transplanted into fore- and hind limb of stage 17 chick embryos. Expression of differentiation markers were subsequently analysed using immunocytochemistry and molecular analysis. Expression of osteogenic-specific genes such as alkaline phosphatase, RUNX2 and osteocalcin was observed in human mesenchymal stem cells grafted into wing and limb buds of the chick embryo. To investigate the extra-mesodermal differentiation potential of mesenchymal stem cells, expression of lineage-specific genes was subsequently analysed after grafting mesenchymal stem cells into the chick neural crest. Mesenchymal stem cells showed extensive migration through head mesenchyme after injection into the chick neural crest. Injected cells also significantly up-regulated neural crest specific markers such as SLUG, FOXD3 and MITF, suggesting differentiation toward neural crest cell lineages.
18
Moss, Lara. „β1 integrin and neural stem cell maintenance in the chicken embryo“. Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608606.
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19
Encalada, Sandra Elizabeth. „Regulation of cell cycle timing in the early Caenorhabditis elegans embryo /“. view abstract or download file of text, 2003. http://wwwlib.umi.com/cr/uoregon/fullcit?p3102163.
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Thesis (Ph. D.)--University of Oregon, 2003.Typescript. Includes vita and abstract. Includes bibliographical references (leaves 159-180). Also available for download via the World Wide Web; free to University of Oregon users.
20
Challen, C. „Studies on the components of the cell-cell extruded cytosolic complex in chick embryo fibroblast cells“. Thesis, University of Newcastle Upon Tyne, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.234410.
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21
Saiz, Nestor. „Regulation of cell fate and cell behaviour during primitive endoderm formation in the early mouse embryo“. Thesis, University of Manchester, 2012. https://www.research.manchester.ac.uk/portal/en/theses/regulation-of-cell-fate-and-cell-behaviour-during-primitive-endoderm-formation-in-the-early-mouse-embryo(d40bb786-85ed-4efd-af64-aab331df98e8).html.
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The preimplantation stages of mammalian development are dedicated to the differentiation of two extraembryonic epithelia, the trophectoderm (TE) and the primitive endoderm (PrE), and their segregation from the pluripotent embryonic lineage, the epiblast. The TE and PrE are responsible for implantation into the uterus and for producing the tissues that will support and pattern the epiblast as it develops into the foetus. PrE and epiblast are formed in a two step process that involves random cell fate specification, mediated by fibroblast growth factor (FGF) signalling, and cell sorting through several mechanisms. In the present work I have addressed aspects of both steps of this process. Chimaera assays showed that epiblast precursors transplanted onto a recipient embryo rarely differentiate into PrE, while PrE precursors are able to switch their identity and become epiblast. Transient stimulation or inhibition of the FGF4-ERK pathway in the chimaeras can modify the behaviour of these cells and restore the plasticity of epiblast precursors. This work shows that epiblast precursors are refractory to differentiation signals, thus ensuring the preservation of the embryonic lineage. I have also found that atypical Protein Kinase C (aPKC) is a marker of PrE cells and that pharmacological inhibition of aPKC impairs the segregation of PrE and epiblast precursors. Furthermore, it affects the survival of PrE cells and can alter the subcellular localisation of the PrE transcription factor GATA4. These data indicate aPKC plays a central role for the sorting of the PrE and epiblast populations and links cell position within the embryo to PrE maturation and survival. Lastly, I have found that aPKC can directly phosphorylate GATA4 in vitro. Knockdown of GATA4 affects cell position within the embryo, whereas aPKC knockdown reduces the number of GATA4-positive cells. These results indicate GATA4 plays an important role in cell sorting during preimplantation development and suggest phosphorylation by aPKC could determine its presence in the nuclei of PrE cells. My work, in the light of the current knowledge, supports a model where the earliest cell fate decisions during mammalian development depend on cellular interactions and not on inherited cell fate determinants. This robust mode of development underlies the plasticity of the preimplantation embryo and ensures the formation of the first mammalian cell lineages, critical for any further progression in mammalian development.
22
Dhawan, Anil. „The role of oocyte- and embryo-secreted factors in cumulus cell differentiation and their relationship to embryo quality and developmental competence“. Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0028/MQ52295.pdf.
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23
Wongtawan, Tuempong. „Epigenetic and chromatin reprogramming in mouse development and embryonic stem cells“. Thesis, University of Edinburgh, 2010. http://hdl.handle.net/1842/8048.
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It is well established that epigenetics and chromatin modifications are important factors that can govern gene activity and nuclear architecture. They are also proven to be essential for normal embryonic development and cell differentiation. One important event during mouse development is the establishment of epigenetic reprogramming which is believed to be essential for normal growth and development, however; the mechanism is still poorly understood. The general objective of this PhD study was to investigate the profiles and mechanisms of epigenetic and chromatin modifications during normal mouse development and in embryonic stem cells. Mouse pre- and postimplantation embryos and ES cells were used in experiments employing a range of different methodologies. The dynamics of epigenetic DNA and histone methylation were captured using laser confocal immunofluorescent microscopy and western blotting. The activity of epigenetic modifiers was monitored by real-time PCR and candidate genes were validated using siRNA technology. The present studies demonstrate that heterochromatin markers H3K9me3, H3K9me2, H4K20me2, H4K20me3, HP1α and HP1β are reprogrammed during early development. Demethylation of H3K9me2, H3K9me3 and H4K20me3 took place at two-cell stage and remethylation occurred at four-cell stage except for H4K20me3. The reestablishment of H4K20me3 was initially observed in early postimplantation embryos in extraembryonic tissue, specifically in the mural trophectoderm. In embryonic tissue, H4K20me3 was not clearly detected until in mid to late postimplantation development. The mechanism of H3K9me2 and H3K9me3 demethylation might be due to either an imbalance of epigenetic modifiers or the presence of Jmjd2a and Jmjd1a histone demethylase postfertilisation. We have also report evidence that HP1α and Suv4-20h are required in heterochromatin before the recruitment of H4K20me3 during mouse development and in ES cells. Therefore H4K20me3 removal was believed to involve the lack of prerequisite heterochromatin complexes such as HP1α and Suv4-20h enzymes. Furthermore, the presence and levels of H4K20me3 and HP1α might be strongly associated with cell differentiation and tissue maturation in mouse in vivo development but not in vitro early differentiated ES cells. Surprisingly, the results showed that chromatin modifications and their modifiers in ES cells are different from ICM and epiblast. Chromatin modifications H4K20me3 and HP1α were absent from ICM and epiblast, but were detected in ES cells. Notably, H4K20me3 and HP1α were established after early incubation of ICM into ES cell medium, but this change was not dependent on the presence of serum and leukaemia inhibiting factor. Epigenetic modifier Jmjd2a but not Jmjd1a was found in ICM. Conversely, Jmjd1a is highly expressed in ES cells while Jmjd2a was inactivated. In addition, the present studies revealed the substantial role of histone demethylases in development, as it may be important for epigenetic reprogramming. The results demonstrated that inhibition of demethylase Jmjd2a and Jmjd1a caused preimplantation embryos to arrest at the twocell stage while Jmjd2c deficient embryos failed to reach blastocyst. Thus it is possible that Jmjd2a and Jmjd1a were essential for epigenetic reprogramming while Jmjd2c is critical for cell fate establishment during blastocyst formation. In conclusion, the global chromatin signature in ES cells differs from ICM and epiblast; heterochromatin reprogramming occurs at two-cell stage; maturation of heterochromatin occurs at postimplantation; and histone demethylases Jmjd1a, Jmjd2a and Jmjd2c are important in preimplantation development. Results from the present studies could provide crucial information for developmental biology and stem cell research, and provide as a model for improvement of reproductive biotechnologies such as somatic cell reprogramming, and diagnosis of epigenetic abnormalities in early development.
24
Jędrusik, Agnieszka Józefa. „Dissecting origins and consequences of cell heterogeneity in the early mouse embryo“. Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609543.
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25
Kravtsova, Natalia. „Theoretical Investigation of Cell Polarity Initiation in the Early C. Elegans Embryo“. The Ohio State University, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=osu1397254117.
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26
Leung, Chuen Yan. „Connecting the dots : timing, polarity & cell fate in the mouse embryo“. Thesis, University of Cambridge, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708629.
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27
Sedelmeier, Oliver [Verfasser], und Sebastian Johannes [Akademischer Betreuer] Arnold. „EMT and cell invasion during germ layer formation in the mouse embryo“. Freiburg : Universität, 2016. http://d-nb.info/1139210882/34.
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28
Senft, Anna Dorothea. „Investigating TGFβ signals in cell fate specification in the early mouse embryo“. Thesis, University of Oxford, 2016. http://ora.ox.ac.uk/objects/uuid:d9365934-8a34-4f4f-8a38-8aa221b94977.
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TGFβ signalling via Smad transcription factors is essential for axis patterning and subsequent cell fate specification during mammalian embryogenesis. However, the cellular and molecular mechanisms have been difficult to characterise in vivo due to early embryonic lethality of mouse mutants and redundant functional activities. Here I show that combined deletion of closely related Smad2 and Smad3 in mouse embryonic stem cells impairs induction of lineage specific gene expression during differentiation, while extra-embryonic gene expression is up-regulated. Preliminary data suggest that the underlying mechanism of this differentiation defect reflects the inability of Smad2/3-/- cells to establish lineage priming. Collectively, these findings identify novel downstream target genes controlled by Smad2/3 and an absolute requirement for Smad2/3 during embryonic differentiation. TGFβ signalling via Smad1 and Smad4 is essential for induction of the transcription factor Blimp1 required for primordial germ cell specification. The direct upstream regulators of Blimp1 are unknown, but T-box factors have recently been suggested to play a role. In a second project, I performed tissue- specific ablation of the T-box transcription factor Eomes as well as components of the TGFβ signalling pathway in either the visceral endoderm or the epiblast to examine tissue-specific functions for Blimp1 induction. I show that Eomes and Smad2 functions in the visceral endoderm as well as Eomes function in the epiblast are dispensable for Blimp1 induction, but rather are required to restrict Blimp1 induction to posterior epiblast cells. In contrast, epiblast-specific Smad4 or Smad1 mutants fail to robustly induce Blimp1 in the epiblast. My preliminary analysis suggests that competence to induce primordial germ cell fate is dependent on the interplay of Smad2/Eomes functions in the visceral endoderm and Smad1/4 functions in the epiblast. Collectively, this thesis provides insight into the transition from pluripotency to cell fate specification in the mammalian embryo that is impossible to obtain from human embryos in vivo.
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Davis, Aaron Patrick. „Apoptotic and Epigenetic Induction of Embryo Failure Following Somatic Cell Nuclear Transfer“. DigitalCommons@USU, 2013. https://digitalcommons.usu.edu/etd/1941.
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Somatic cell nuclear transfer (SCNT) is a useful tool for selective breeding, conservation, and production of transgenic animals. Despite the successful cloning of several species, high rates of embryo failure following SCNT prevent the wide-scale use of the technique. Embryos produced through cloning have a higher incidence of developmental arrest, decreased developmental potential, frequent implantation failures, and increased incidence of abortion. The objective of this dissertation research was to characterize the factors that lead to SCNT failures by examining epigenetic and apoptotic pathways that can negatively influence the development of cloned preimplantation embryos. Aberrant genome reprogramming is generally considered to be a key factor in the failure of SCNT embryo development. Therefore, we used bisulfite pyrosequencing technology to compare DNA methylation patterns of several genes critical for embryonic development (POU5F1, NANOG, SOX2, and KLF4) in SCNT and in vitro fertilized (IVF) blastocyst stage embryos. The methylation profiles obtained from these experiments indicate that methylation patterns of the POU5F1 gene were undermethylated compared to IVF embryos, suggesting reprogramming did occur, but that the reduced methylation was inappropriate for the blastocyst stage. Furthermore, aberrant methylation profiles were detected for SOX2 and NANOG, suggesting that problems of genome reprogramming following SCNT can be gene-specific or localized. Because high rates of apoptosis are associated with failure of preimplantation embryos, we compared the activation of the P53-mediated apoptosis pathway in individual IVF and SCNT preimplantation embryos at multiple developmental stages. This pathway is activated in response to cell stress and genomic instability, and in response to the expression of genes associated with somatic cell reprogramming. Evidence from gene expression and immunohistochemistry analyses suggests that the P53 pathway is frequently active in SCNT embryos. Also, we detected expression of several factors known to induce apoptosis more frequently and at higher levels in SCNT embryos. Collectively, the work presented here illuminates some of the molecular consequences of incomplete or inappropriate genome reprogramming in cloned embryos. The identification of these factors may lead to interventions that target the apoptosis pathway during preimplantation development and increase SCNT success rates.
30
Kang, Youn-Jung. „Cell adhesion and signalling at implantation“. Thesis, University of Oxford, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.711653.
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31
Glover, Hannah Jacquilyn. „L-proline-induced transition of mouse ES cells to a spatially distinct primitive ectoderm-like cell population primed for neural differentiation“. Thesis, The University of Sydney, 2018. http://hdl.handle.net/2123/20576.
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Naïve mouse embryonic stem cells (mESCs) derived from the preimplantation mouse blastocyst self-renew in the presence of LIF and BMP4. These cells are pluripotent, meaning they have the ability to differentiate into the ~200 cell types of the developing embryo and adult. Naïve mESCs are one discrete state along a pluripotency continuum – delimited by ground-state mESCs as the earliest cell population, followed by naïve mESCs, and with EpiSCs as the most ‘primed’ population. The amino acid L-proline has novel growth factor-like properties during development - from improving blastocyst development to driving neurogenesis. Addition of 400 μM L-proline to naïve mESCs produces a pluripotent cell population between naïve mESCs and EpiSCs. These cells, named early primitive ectoderm-like (EPL) cells, recapitulate in vivo development of the pre-implantation inner cell mass to the postimplantation primitive ectoderm. EPL cells maintain expression of the naïve marker Rex1 and upregulate expression of the primitive ectoderm genes Dnmt3b and Fgf5. This thesis identifies mechanisms underpinning L-proline-mediated differentiation to EPL cells, including a complex self-regulating signalling network involving the MAPK, Fgfr, PI3K and mTOR pathways. Statistical models were used to understand the contributions of individual signalling pathways to changes in colony morphology, cell number, gene expression, proliferation and apoptosis. Other mechanisms underpinning the naïve mESCs-to-EPL cell transition were explored, including DNA methylation, histone acetylation, proline synthesis and metabolism. In addition to expressing primed pluripotency genes, EPL cells upregulate genes associated with neurogenesis, whereas EpiSCs express genes associated with cardiovascular development. When mapped to the 7.0 dpc embryo, EPL cells and EpiSCs represent spatially distinct cell populations. This suggests that after cells transition from naïve mESCs, they diverge and are fated to become either ectoderm (from EPL cells), or mesendoderm (from EpiSCs). This thesis also explored whether L-proline plays an underappreciated role in existing neural differentiation protocols. mESCs cultured in custom N2B27 medium without L-proline had reduced selective cell death resulting in a larger yield of Sox1+ neurectoderm.
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Jurisicova, Andrea. „Programmed cell death during mammalian preimplantation embryo development, genetic regulation and developmental consequences“. Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ35200.pdf.
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Stephens, Tricia. „CHARACTERIZATION OF PIGMENT CELL SPECIFIC GENES IN THE SEA URCHIN EMBRYO (STRONGYLOCENTROTUS PURPURATUS)“. Master's thesis, University of Central Florida, 2007. http://digital.library.ucf.edu/cdm/ref/collection/ETD/id/2692.
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In sea urchin development, cell fate specification appears by the 60-cell stage embryo when several embryonic territories are recognized: the small micromeres, the large micromeres which will generate primary mesenchyme cells, the vegetal2 layer that will give rise to pigment cells, immunocytes, and muscle cells, the vegetal1 layer, as well as the oral and aboral ectoderm. A Delta-Notch signaling event is required for the differential specification of mesodermal cells that will give rise to secondary mesenchyme cells (SMCs). SMCs produce four cell types: pigment cells, blastocoelar cells, circumesophageal muscle cells, and coelomic pouch cells. Pigment cells are the first to be specified. During primary invagination at the gastrula stage, eight pigment cell progenitors delaminate from the archenteron into the blastocoel. By the pluteus stage, approximately 30 pigment cells are embedded in the ectoderm. Pigment cells produce echinochrome, a napthoquinone pigment. Previously, several genes in the sea urchin embryo were isolated that are expressed specifically in pigment cell precursors during the blastula stage. The goal of this research was to characterize a subset of these genes, which are highly similar to: the polyketide synthase gene (Pks), a sulfotransferase gene (Sult), three different members of the flavin-containing monooxygenase gene family (Fmo), and the transcription factor glial cells missing (Gcm). Polyketide synthases (PKSs) are a large family of multifunctional proteins mainly found in bacteria, fungi, and plants. They are responsible for the biosynthesis of a variety of polyketide compounds including antibiotics and mycotoxins. In the sea urchin, SpPks is required for echinochrome biosynthesis. Flavin-containing monooxygenases (FMOs) are NADPH-dependent flavoproteins mainly found in bacteria, plants, and higher metazoan. They are responsible for catalyzing the oxidation of several compounds including the detoxification of xenobiotics and activation of numerous metabolites. It is known that SpFmo1 is required for echinochrome biosynthesis. Sulfotransferases are found from bacteria through higher eukaryotes. These enzymes catalyze the sulfate conjugation of several substrates resulting in either compound detoxification or bioactivation.M.S.
Department of Biology
Sciences
Biology MS
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Porchet, Nicolas. „Role of signaling pathays in cell-fate specification in the early mouse embryo“. Thesis, Université de Paris (2019-....), 2019. http://www.theses.fr/2019UNIP7096.
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Lors du développement précoce de l’embryon de souris, divers évènements de spécification des destins cellulaires induisent la formation du blastocyste pré-implantatoire. Ces évènements sont majoritairement contrôlés par l’action de voies de signalisation activées via la fixation de molécules signal à la membrane de la cellule. L’activité de ces voies de signalisation permet la régulation de la transcription de gènes cible responsable de l’acquisition d’une identité cellulaire et de son arrangement sous forme de tissu. Ici je m’intéresse aux rôles des voies ACTIVINE/NODAL et βCATENIN dans la spécification de ces identités cellulaires lors de la formation du blastocyste de sourisDuring the early mouse embryogenesis, cell-fate specification events result in the formation of the pre-implantation blastocyst. Those events are mainly regulated by the action of signaling cascades activated upon fixation of the signaling molecules at the cell membrane. The activity of these signaling pathways allow the transcriptional regulation of a specific pool of genes responsible for cell-fate decisions and the formation of tissues. Here, I am interested in the roles of both ACTIVIN/NODAL and βCATENIN signaling pathways in the specification of cell identities during the maturation of the mouse blastocyst
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廖佩珊 und Pui-shan Liu. „An investigation on the embryotrophic effect of human oviductal cell on mouse embryo development“. Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1996. http://hub.hku.hk/bib/B31235098.
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Shearer, Joanne Lesley. „Phospholipase C signalling pathways during the first cell cycle of the sea urchin embryo“. Thesis, University of Newcastle Upon Tyne, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.297530.
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Corujo, Simon Elena. „Wnt/β-catenin signalling facilitates cell fate decision making in the early mouse embryo“. Thesis, University of Bath, 2018. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.761022.
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At embryonic day 3.5 (E3.5), inner cell mass (ICM) cells co-express the transcription factors NANOG and GATA6. Between E3.5 and E4.5, cells of the ICM differentiate into epiblast (Epi) and primitive endoderm (PrE). These two lineages are distinguished by the differential expression of the previously coexpressed transcription factors; Epi cells express NANOG while PrE cells express GATA6. FGF/ERK signalling is responsible for Epi and PrE differentiation but it does not explain the initial co-expression of both factors and how the mutually exclusive expression arises. β-catenin is the downstream effector of Wnt signalling, and it is also found in the membrane forming a complex with E-cadherin. Depending on it subcellular location, β-catenin has been associated with pluripotency and differentiation of mESCs, whose origin is the mouse embryo. My hypothesis was that changes in both cellular pools of β-catenin are involved in ICM differentiation. To characterize Wnt/β-catenin role during preimplantation development, I applied quantitative immunofluorescence analysis (QIF) together with chemical and classical genetics in in vitro and in vivo models. I found that high membrane β-catenin levels are associated with Epi cells from E4.0 stage, while nuclear β-catenin levels are higher in co-expressing cells at E3.5 and PrE precursors at E4.0. My results indicate that increases in nuclear β-catenin levels allow the ICM cells to be specified earlier, determined by an earlier appearance of mutually exclusive expression of GATA6 and NANOG in vitro and ex vivo. Moreover, increased β-catenin levels promote specification towards PrE fate, observed by the presence of higher percentages of PrE cells. Conversely, a decrease in β-catenin levels result in slower ICM specification into Epi and PrE. Finally, modulation of FGF/ERK signalling in mouse embryos, which is the main pathway in this cell fate choice, led to changes in β-catenin subcellular location and levels. Altogether, my results are consistent with a role for Wnt/β-catenin signalling facilitating PrE fate acquisition concomitantly with FGF/ERK signalling.
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Liu, Pui-shan. „An investigation on the embryotrophic effect of human oviductal cell on mouse embryo development /“. Hong Kong : University of Hong Kong, 1996. http://sunzi.lib.hku.hk/hkuto/record.jsp?B17538452.
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Daniel, Pablo Gabriel. „The Influence of Embryo Cell Culture Systems on Pretransfer Development of Early Ovine Embryos“. DigitalCommons@USU, 1989. https://digitalcommons.usu.edu/etd/4061.
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The complete requirements for early embryo development in vitro of the ovine and other domestic species remain unknown. Many studies have concentrated on new media, supplementation, and gas atmosphere formulations.
A newer approach is to coculture early embryos with different cell types to provide the physico-chemical requirements for their development.
In this study, oviduct epithelial (OEC) and dissociated embryo cell (DEC) growth were tested in minimum essential media (MEM) and RPMI. Media were supplemented with fetal calf serum (FCS) and equine derived serum (EDS). Fetal calf serum supported maximum cell confluence in OEC collected on day 3 and day 13 post-estrus. Although at a slower growth rate, DEC developed faster in FCS-supplemented media. Cell growth was slower for EDSsupplemented media in all treatments.
As a result, FCS-supplemented media were used to evaluate early embryo growth in various coculture systems. In MEM + OEC, 67% of 1- to 1 0- cell embryos developed to the hatched blastocyst stage (following 8 days of culture). In MEM+DEC, 66% hatched after the same time period. In control treatments (no exogenous cell layers), all embryos degenerated. When early embryo development was compared between St.Croix and Targhee-type breeds in MEM+OEC and RPMI+OEC, no significant differences were observed. The improved results obtained with coculture systems may provide an important method for assessing the viability of embryos following micromanipulation techniques (such as splitting, gene transfer, or following long periods of freezing). The nature of the beneficial action of these coculture systems remains unknown.
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Stander, Cornelia Steynberg. „An ultrastructural and light microscopic study of melanocyte differentiation in chick embryos“. Master's thesis, University of Cape Town, 1991. http://hdl.handle.net/11427/27149.
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The embryonic source and chemical nature of those factor/s directing the in vivo differentiation of melanocytes from crest cells are as yet unknown. To begin to address this issue, it is important to establish exactly when and where these signa/s first exert their effects. Therefore, in the present study, overtly differentiated melanocytes containing melanin were quantitated in developing Black Australorp X New Hampshire Red chick embryos. In contrast to previous studies, it was found that embryos synthesize melanin from as early as Day 5 of development, and that at this stage, the melanocytes are predominantly dermally located. Between 5 and 8 days, the numbers of both dermal and epidermal melanocytes increase, after which the dermal melanocyte population declines rapidly while the number of epidermal melanocytes continues to increase. These findings suggest that premelanocytes do not have to be epidermally located to initiate terminal differentiation and implicate the dermis as a possible source of melanocyte inducing factor/s. The next step was to examine stages of development prior to the onset of pigment production. For this reason, tyrosinase was purified for use as antigen in the production of a polyclonal antibody. The antibody was tested for specificity by western blotting, - immunocytochemistry and immunoinhibition procedures. Lack of specificity was demonstrated, rendering it unsuitable as an antibody marker for early melanocytes. Fowl melanocytes are thought to differentiate into either eumelanosome- or pheomelanosome synthesizing cells. To test the validity of this concept, embryonic skin of the red/black cross breed were screened for possible mixed type melanocytes by electron microscopy. The melanocytes contained melanosomes with a matrix of irregularly arranged filaments amongst typical eumelanogenic melanosomes. This suggests that these chick melanocytes may synthesize both eumelanosomes and pheomelanosomes in single cells. In a further study on pure breeding New Hampshire Reds, it was found that the melanocytes contained a mixture of typical and less typical pheomelanosomes. Outer membrane indentations in the latter melanosome type suggest that tyrosinase may enter these pheomelanosomes by a mechanism related to that proposed for the melanosomes of goldfish.
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Ishikawa, Yuji, Takako Yasuda, Keiko Maeda, Atsuko Matsumoto und Kouichi Maruyama. „Apoptosis in neural tube during normal development of medaka“. Laboratory of Freshwater Fish Stocks Bioscience and Biotechnology Center Nagoya University, 2007. http://hdl.handle.net/2237/13834.
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Whitaker, Brian Daniel. „Exogenous γ-Glutamyl Cycle Compound Supplementation to In Vitro Maturation Medium and the Effects on Subsequent In Vitro Fertilization and Culture Parameters of Porcine Oocytes and Their Impact on Embryo Viability“. Thesis, Virginia Tech, 2002. http://hdl.handle.net/10919/33924.
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High concentrations of intracellular glutathione enhance the in vitro production of porcine embryos. Six experiments were conducted to study the effects of varying concentrations of different supplements to the in vitro maturation (IVM) medium on in vitro fertilization (IVF) and in vitro culture (IVC), and evaluate subsequent embryo viability. In Exp. 1, 2, 3, and 4, porcine oocytes were matured in either 3.3 mM cysteine, 150 μM cysteamine, 3.3 mM cysteine and 150 μM cystemaine; 1.0 mM glycine, 2.5 mM glycine, 5.0 mM glycine; 1.0 mM L-glutamate, 2.5 mM L-glutamate, 5.0 mM L-glutamate; and 3.3 mM L-α-aminobutyrate, 25 μM β-mercaptoethanol, 3.3 mM cysteine and 25 μM β-mercaptoethanol, or 3.3 mM L-α-aminobutyrate and 25 μM β-mercaptoethanol. After IVM (44 h), concentrations of intracellular glutathione (GSH) were determined using a colorimetric assay based on absorbency. The supplements that elicited significantly (P < 0.05) the greatest increase in GSH concentrations were 3.3 mM cysteine, 1.0 mM L-glutamate, 3.3 mM L-α-aminobutyrate, and 3.3 mM L-α-aminobutyrate with 25 25 μM β-mercaptoethanol. In Exp. 5, oocytes matured with 3.3 mM L-α-aminobutyrate and 25 μM β-mercaptoethanol had a significantly less (P < 0.05) occurrence of polyspermy and greater occurrence of MPN formation during IVF compared to the other treatment groups and a significantly greater percentage (P < 0.05) of embryos reaching the 2 cell developmental stage by 48 h post-IVF and blastocyst stage of development by 144 h post-IVF compared to the other treatment groups. In Exp. 6, treatment had no effect on the time of cell death. The times at which embryo mortality was significantly the greatest (P < 0.05) were located within the middle of IVC. The approximate time of the onset of cell death occurred between 24 to 42 h post-IVF with the greatest occurrence around 36 h. These results suggest that supplementing 3.3 mM L-α-aminobutyrate and 25 μM β-mercaptoethanol into the IVM medium 1) increases intracellular GSH concentrations by the end of IVM, 2) decreases the occurrence of polyspermy during IVF, 3) increases the MPN formation during IVF, and 3) increases embryo development parameters during IVC. Supplementation to the maturation media does not have an effect on cell death during embryo development. The onset of cell death appears to occur between 24 to 42 h post-IVF with the greatest occurrence around 36 h post-IVF. In order to increase the success of in vitro derived porcine embryos and offspring, the basic fundamentals of the system need to be fully understood.Master of Science
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Pickles, Jessica Chiara. „Mechanisms of senescience bypass in cells derived from the Syrian hamster embryo cell transformation assay“. Thesis, Brunel University, 2014. http://bura.brunel.ac.uk/handle/2438/10526.
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Recent European legislation has enforced a reduction in the use of animal models for safety assessment purposes and carcinogenicity testing. The Syrian hamster embryo cell transformation assay (SHE CTA) has been proposed as a suitable animal alternative, but its implementation into test batteries has been delayed. This is due to concerns regarding the assay’s endpoint subjectivity and, moreover, the model’s relevance to carcinogenicity remains mostly unexplored. Senescence is an essential barrier against uncontrolled cell proliferation and its evasion is necessary for clonal evolution and tumour development. Carcinogenesis can be modelled by reproducing underlying mechanisms leading to senescence bypass. In this project, the SHE CTA was performed using the known mutagen and human carcinogen, benzo(a)pyrene, and the resulting SHE colonies were analysed. It was found that morphological transformation (MT) does not guarantee senescence bypass and cell immortalisation, but increases the likelihood of MT-derived cells subsequently acquiring unlimited growth potential. A limited number (between 10 and 20 %) of MT colonies produced cell clones capable of sustained proliferation and in most cases secondary events were necessary for the evasion of senescence barriers. With regard to mechanisms, p53 point mutations were present in 30 % of immortal B(a)P-induced MT colony-derived cells and located within the protein’s DNA binding domain. No p16 mutations were identified. Expression of p16 mRNA was commonly silenced or markedly reduced by a combination of mechanisms including monoallelic deletion, promoter methylation and BMI-1 overexpression. Taking advantage of the recently available Syrian hamster genomic sequence information generated by the Broad Institute, the coding regions of the Syrian hamster CDKN2A/B locus were shown to have good homology to human nucleotide sequences and confirmed the exonic structures of SH p16, ARF and p15. The findings further implicate the importance of p16 in regulating senescence while providing a molecular evaluation of SHE CTA-derived MT clones.
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Guedes, Maria Susana Ramos Ferreira. „The mex-1 gene and specification of germ cell identity in the Caenorhabditis elegans Embryo“. Doctoral thesis, Porto : Edição do Autor, 1998. http://hdl.handle.net/10216/64557.
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Ehrman, Lisa Ann. „MOLECULAR REGULATION OF ANTERIOR AND POSTERIOR CELL FATES IN THE PRIMITIVE STREAK STAGE AVIAN EMBRYO“. University of Cincinnati / OhioLINK, 2001. http://rave.ohiolink.edu/etdc/view?acc_num=ucin998398595.
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Yoon, Yeonsoo. „Morphogenetic Requirements for Embryo Patterning and the Generation of Stem Cell-derived Mice: A Dissertation“. eScholarship@UMMS, 2013. http://escholarship.umassmed.edu/gsbs_diss/679.
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Cell proliferation and differentiation are tightly regulated processes required for the proper development of multi-cellular organisms. To understand the effects of cell proliferation on embryo patterning in mice, we inactivated Aurora A, a gene essential for completion of the cell cycle. We discovered that inhibiting cell proliferation leads to different outcomes depending on the tissue affected. If the epiblast, the embryonic component, is compromised, it leads to gastrulation failure. However, when Aurora A is inactivated in extra-embryonic tissues, mutant embryos fail to properly establish the anteroposterior axis. Ablation of Aurora A in the epiblast eventually leads to abnormal embryos composed solely of extra-embryonic tissues. We took advantage of this phenomenon to generate embryonic stem (ES) cell-derived mice. We successfully generated newborn pups using this epiblast ablation chimera strategy. Our results highlight the importance of coordinated cell proliferation events in embryo patterning. In addition, epiblast ablation chimeras provide a novel in vivo assay for pluripotency that is simpler and more amenable to use by stem cell researchers.
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Tsou, Meng-Fu Bryan. „The mechanisms of spindle positioning in asymmetric cell divisions of the early C. elegans embryo /“. For electronic version search Digital dissertations database. Restricted to UC campuses. Access is free to UC campus dissertations, 2003. http://uclibs.org/PID/11984.
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Guedes, Maria Susana Ramos Ferreira. „The mex-1 gene and specification of germ cell identity in the Caenorhabditis elegans Embryo“. Tese, Porto : Edição do Autor, 1998. http://catalogo.up.pt/F?func=find-b&local_base=UPB01&find_code=SYS&request=000086736.
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Zhu, Meng. „Investigating the mechanisms and the temporal regulation of the first cell polarity establishment in the mouse embryo“. Thesis, University of Cambridge, 2019. https://www.repository.cam.ac.uk/handle/1810/288353.
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Embryonic cells of many species polarise and the cell polarity is often important for the normal developmental progression. In the mouse embryo, the prototype of epithelial cell polarity, namely apico-basal polarisation, become established at the 2.5 days' post-fertilisation, when the embryos are at the 8-cell stage. The formation of apical domain is necessary and sufficient for the first segregation of extra-embryonic and embryonic cell lineages, as well as the following up morphogenetic transitions, such as the blastocyst formation. This study aims to explore the molecular pathways triggering the first cell polarity establishment in the mouse embryo, and to reveal the mechanism that programmes the timing of this event in the mouse embryo. The results showed that cell polarity establishment during the 8-cell stage development can be divided into two major phases: in the first phase actomyosin complex became polarised to the cell-contact free surface; and in the second phase apical proteins recruited to the actomyosin enriched cell-contact free cortex, they further became centralised in the cell-contact free surface, excluding the local actomyosin meshwork, resulting in the formation of actomyosin ring. The activation and assembly of actomyosin meshwork during the first phase, but not its contractility, was essential for apical protein recruitment. Factors responsible for actin cytoskeleton reorganisation included Phospholipase C (PLC) - Protein Kinase C (PKC) pathway components, they directly activated actomyosin in the first phase through the Rho proteins such as RhoA. Further results showed that the apical protein centralisation step required a proximate transcriptional input that was induced by two transcription factors, Tfap2c and Tead4. RNAi and Genetic depletion of these two factors prevented apical protein centralisation and the final apical domain assembly. The protein expression profile indicated that Tfap2c and Tead4 expression, and therefore their activity, were induced by zygotic genome activation. Significantly, overexpression of Tfap2c, Tead4, together with constitutively activated Rho proteins were sufficient to advance the timing of apical domain formation, indicating that the timer of cell polarity establishment at the 8-cell stage is set by the Rho proteins activation, and the zygotic transcriptional accumulation of Tfap2c and Tead4. Together, these results characterised the molecular events during the cell polarity establishment at the 8-cell stage mouse embryo, and identified the timing regulation of this event.
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Gustafsson, Sofia. „Cannabinoids as modulators of cancer cell viability, neuronal differentiation, and embryonal development“. Doctoral thesis, Umeå universitet, Farmakologi, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-51560.
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Cannabinoids (CBs) are compounds that activate the CB1 and CB2 receptors. CB receptors mediate many different physiological functions, and cannabinoids have been reported to decrease tumor cell viability, proliferation, migration, as well as to modulate metastasis. In this thesis, the effects of cannabinoids on human colorectal carcinoma Caco-2 cells (Paper I) and mouse P19 embryonal carcinoma (EC) cells (Paper III) were studied. In both cell lines, the compounds examined produced a concentration- and time-dependent decrease in cell viability. In Caco-2-cells, HU 210 and the pyrimidine antagonist 5-fluorouracil produced synergistic effects upon cell viability. The mechanisms behind the cytocidal effects of cannabinoids appear to be mediated by other than solely the CB receptor, and a common mechanism in Caco-2 and P19 EC cells was oxidative stress. However, in P19 EC cells the CB receptors contribute to the cytocidal effects possibly via ceramide production. In paper II, the association between CB1 receptor immunoreactivity (CB1IR) and different histopathological variables and disease-specific survival of colorectal cancer (CRC) was investigated. In microsatellite stable (MSS) cases there was a significant positive association of the tumor grade with the CB1IR intensity. A high CB1IR is indicative of a poorer prognosis in MSS with stage II CRC patients. Paper IV focused on the cytotoxic effects of cannabinoids during neuronal differentiation. HU 210 affected the cell viability, neurite formation and produced a decreased intracellular AChE activity. The effects of cannabinoids on embryonic development and survival were examined in Paper V, by repeated injection of cannabinoids in fertilized chicken eggs. After 10 days of incubation, HU 210 and cannabidiol (without CB receptor affinity), decreased the viability of chick embryos, in a manner that could be blocked by α-tocopherol (antioxidant) and attenuated by AM251 (CB1 receptor antagonist). In conclusion, based on these studies, the cannabinoid system may provide a new target for the development of drugs to treat cancer such as CRC. However, the CBs also produce seemingly unspecific cytotoxic effects, and may have negative effects on the neuronal differentiation process. This may be responsible for, at least some of, the embryotoxic effects found in ovo, but also for the cognitive and neurotoxic effects of cannabinoids in the developing and adult nervous system.