Rozprawy doktorskie: „Cellular differentiation”

1

Glover, Beverley Jane. "Cellular differentiation in plants". Thesis, University of East Anglia, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.338247.

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Brero, Alessandro. "Nuclear topology during cellular differentiation in mouse". Diss., [S.l.] : [s.n.], 2004. http://edoc.ub.uni-muenchen.de/archive/00002625/.

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Leahy, Rachel A. "Signal Transduction and Cellular Differentiation in Airway Epithelium". Kent State University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=kent1352673026.

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4

Yu, Lu. "Multiple signaling pathways cooperate to activate skeletal muscle differentiation /". View abstract or full-text, 2005. http://library.ust.hk/cgi/db/thesis.pl?BICH%202005%20YU.

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5

Chano, Laura. "Emdogain regulation of cellular differentiation in wounded rat periodontium". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/MQ63000.pdf.

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6

Parker, Emma. "The role of insulin-like growth factor binding proteins (IGFBPs) in the pathogenesis of pulmonary fibrosis". Thesis, Keele University, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.269130.

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7

Clarke, A. R. "Retroviral mediated expression of B-galactosidase in mouse cells". Thesis, University of Cambridge, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.303267.

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8

Dixon, Katherine. "Characterization of the Global and Locus-Specific Regulation of Gene Expression During Early Myogenic Differentiation". Thesis, Université d'Ottawa / University of Ottawa, 2016. http://hdl.handle.net/10393/35079.

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During cellular differentiation, gene expression is globally regulated through changes in the epigenome. How a single genome can give rise to a diversity of cell and tissue types remains a complex area of investigation, and here we sought to explore the molecular regulation of gene expression during the differentiation of skeletal muscle cells from committed myogenic progenitors. Using a systematic and integrated analysis of global transcriptional and epigenetic data, we characterized the regulation of gene expression in differentiating myoblasts and found that muscle-specific gene expression is regulated through differential activation of tissue-specific regulatory DNA elements by the myogenic transcription factor MyoD. In addition, the genome-wide localization of MyoD, and the mechanisms underlying its function in transcriptional regulation, varies between myogenic progenitors and differentiating myoblasts. Our study explores the recruitment and function of MyoD at regulatory elements of target genes and additionally describes a novel role for ligand-inducible signaling in the regulation of MyoD function and ultimately in myogenic differentiation.

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9

Berg, Tove. "C/EBP transcription factors in lung cellular differentiation and development /". Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-586-0/.

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10

Munkley, Jennifer. "The sub-cellular organisation of DNA replication factors during differentiation". Thesis, University of York, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.547361.

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11

Cowan, Joanne L. "Translational control during cellular stress and differentiation of C2C12 myoblasts". Thesis, University of Sussex, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.436824.

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12

Midgley, Adam Christopher. "Cellular mechanisms of myofibroblast differentiation and dysfunctions in wound healing". Thesis, Cardiff University, 2014. http://orca.cf.ac.uk/59241/.

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In wound healing and tissue repair, the presence of α-smooth muscle actin (α-SMA) containing myofibroblasts leads to wound closure and collagen-rich scar formation. This thesis investigated mechanisms of transforming growth factor-β1 (TGF-β1)-mediated differentiation and the dysfunctions involved in age-associated loss of differentiation. The loss of epidermal growth factor receptor (EGFR) and hyaluronan (HA) production, and diminished interaction of HA with its receptor CD44 (compromising its function) were the principal contributors to aged fibroblast resistance to differentiation. In response to TGF-β1, CD44 relocated to EGFR held in cholesterol-rich membrane-bound lipid rafts. This was HA-dependent, as hyaluronidase or 4-methylumbelliferone treatments restricted CD44 motility and prevented CD44-EGFR co-localisation. Additionally the intracellular signalling cascade was found to be a sequential phosphorylation of extracellular signal regulated kinase 1 & 2 followed by Ca2+/calmodulin kinase II. The activation of both proteins was required for differentiation. Elevated microRNA-7 (miR-7) expression was found in aged fibroblasts. Overexpressing miR-7 in young fibroblasts attenuated the expression of EGFR and inhibited differentiation. When miR-7 was inhibited, EGFR and hyaluronan synthase 2 expression, CD44 membrane motility, and TGF-β1-mediated differentiation in aged fibroblasts were restored. Activation of EGFR drove miR-7 promoter activity and expression in a JAK/STAT1 dependent manner. Treatments of aged fibroblasts with 17β-estradiol (E2) resulted in decreased miR-7 expression and, when TGF-β1 was added, restored the α-SMA-positive phenotype. E2 treatments had no impact on STAT1 phosphorylation; leading to the hypothesis that E2 regulation of inflammatory mediators may be involved. The data demonstrated different points of intervention for the promotion or prevention of TGF-β1-regulated myofibroblast differentiation. The interactions between HA-CD44 and EGFR were crucial elements in the differentiation process and the importance of miR-7 was apparent. The mechanisms shown here may have direct implications for modifying the wound healing response, particularly for developing therapeutic strategies to improve healing in the elderly.

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13

Nguyen, Khoi Thien. "Epigenetic determinants of cellular differentiation, transcriptional reprogramming, and human disease". Thesis, Massachusetts Institute of Technology, 2020. https://hdl.handle.net/1721.1/130186.

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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Biological Engineering, May, 2020
Cataloged from student-submitted PDF version of thesis.
Includes bibliographical references (pages 111-130).
Much of the diversity we observe in cellular and organismal phenotypes can be attributed to epigenetic and genetic variation. DNA provides the instructions for life, while epigenetic modifications regulate which parts of the genetic information contained in DNA can be read out in a given cell and how this information is interpreted. In recent years, epigenetic and genetic variation has been profiled on a large scale with sequencing-based assays, generating many datasets to be explored. In this thesis, I present three projects which apply computational techniques to identify and characterize epigenetic mechanisms that may contribute to the regulation of phenotypic variance. First, we mine a dataset charactering the epigenomes of diverse cell types in order to discover signatures of adult stem cell differentiation.
We identify a novel marker of the multipotent state, a chromatin state characterized by the histone marks H3K36me3 and H3K9me3, and describe biological processes that may be linked to the loss of this chromatin state in fully differentiated cell types. Next, I present what we learned from profiling the epigenetic state of cells before and after transplantation into Xenopus oocytes, a process that transcriptionally reprograms the cells. This analysis elucidates how the initial epigenetic state of a cell influences the success of cellular reprogramming and identifies transcription factors that help regulate this process. Finally, we integrate studies measuring the effects of genetic variants on disease with studies measuring the effects of genetic variants on transcriptional and epigenetic activity. This identifies specific mechanisms underlying disease processes, and demonstrates that transcriptional and epigenetic mechanisms may independently contribute to disease pathogenesis.
Together, these projects demonstrate the biological insights that can be gained from epigenetic profiling, and expand our understanding of the potential effects of epigenetic modifications.
by Khoi Thien Nguyen.
Ph. D.
Ph.D. Massachusetts Institute of Technology, Department of Biological Engineering

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14

Thulabandu, Venkata Revanth Sai Kumar. "REGULATION OF CELLULAR DIFFERENTIATION BY EZH2 DURING SKIN ANDMUSCLE DEVELOPMENT". Case Western Reserve University School of Graduate Studies / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=case1623415890187889.

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15

Herron, Matthew David. "Evolution of Multicellularity and Cellular Differentiation in the Volvocine Algae". Diss., The University of Arizona, 2009. http://hdl.handle.net/10150/196054.

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The evolution of multicellularity is an example of an evolutionary transition in individuality, in which a group of lower-level biological units (cells, in this case) emerges as a higher-level unit (the multicellular organism) with its own fitness, heritability and individuality. The volvocine green algae are a model system for the transition to multicellularity and for the evolution of cellular differentiation. Some of the developmental changes that collectively make up this transition have occurred more than once in the volvocine lineage; others have reverted from derived to ancestral states. The transition from cells to multicellular organisms began over 200 million years ago in this lineage, and the subsequent changes have been sporadic, with several important changes occurring early in the transition and some body plans remaining largely unchanged over long evolutionary time scales. Two suites of characters that differ among species within the genus Volvox have each evolved convergently or in parallel in lineages that diverged at least 175 million years ago. This complex history suggests that other origins of multicellularity may have involved important roles for cooperation, conflict and conflict mediation; parallel evolution of some traits; sporadic rather than constant change; and long-term coexistence of forms with different levels of complexity. Data from one species, Pleodorina starrii, support motility as a major selective pressure driving the the origins of cellular differentiation. Optimization of the proportion of soma in this species appears to be prevented by a constraint that prevents independent change in colonies with different numbers of cells. Finally, P. starrii presents an exceptionally high level of phenotypic variability, suggesting that the genotype-phenotype map has not completely shifted from the cell to the colony and that the transition to a new, higher-level individual in this species is incomplete.

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16

Hung, Hiu Wai. "Signal transduction mechanism in xenopus presynaptic differentiation /". View Abstract or Full-Text, 2003. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202003%20HUNG.

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17

Wang, Kepeng. "The involvement of JAK2/STAT2/STAT3 in myogenic differentiation /". View abstract or full-text, 2008. http://library.ust.hk/cgi/db/thesis.pl?BICH%202008%20WANGK.

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18

Rider, Beverley J. "Immunoregulatory and cellular differentiation activity of apolipoprotein E-derived self peptides". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq31117.pdf.

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19

Mohamed, Ahmed Safwat Mohamed. "Molecular modelling and synthesis of novel ligands related to cellular differentiation". Thesis, Cardiff University, 2009. http://orca.cf.ac.uk/54516/.

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Cancer is a leading cause of death all over the world. Retinoic acid and vitamin D3 play an important role in cellular proliferation and differentiation and as such have potential therapeutic value as differentiating agents in the treatment of cancer and hyperkeratinising diseases. The use of differentiating agents to suppress prostate and breast cancer proliferation is now one of the new therapeutic strategies. However, the use of all trans retinoic acid (ATRA) and vitamin D3 as differentiating agents is limited by their rapid metabolism through the self induction of the cytochrome P450 enzymes that are involved in their catabolism. The P450 enzymes responsible for the metabolism of ATRA and la,25-(OH)2-D3 (calcitriol) are cytochrome P450 26 (CYP26A1) and cytochrome P450 24 (CYP24A1) respectively. Therefore the use of potent and selective inhibitors of CYP26A1 and CYP24A1 with ATRA and la,25-(OH)2-D3 respectively may represent a new strategy for the treatment of cancer. The pharmacophore model of CYP26A1 inhibitors was constructed using MOE software. A database of 71 inhibitors with different conformations have been built and arranged according to activity. The resulting pharmacophore model has 8 features of which 5 features are essential to get the CYP26A1 inhibitory activity. The designed model was used to build new inhibitors, which have reasonable activity. Two series were synthesised for CYP26A1 inhibition. The first series was designed to investigate the effect of changing the structure of the lead compound on the inhibitory activity against CYP26A1 and was depending mainly on presence of imidazole moiety, and the second series was a result of the pharmacophore search and was mainly oxadiazole derivatives. These two series were biologically evaluated using a MCF-7 breast cancer cell assay previously described by our group and also some of the compounds were tested in the biochemical assay. Changing of the structure could be tolerated to a certain limit as long as the imidazole ring is included which is the main part responsible for the binding with the haem in CYP26A1 enzyme. Some of the resulting compounds has good activity, specially methyl w-3-(1-1-imidazolyl)-3-4-(phenylamino)phenyl-2-methylpropanoate which should IC50 of 26 nM in the biochemical CYP26A1 assay. The oxadiazole derivatives did not show very good activity against CYP26A1 cell based assay, may be owing to the decrease in the.

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20

Chaffee, Blake Richard. "Cell Cycle Regulation and Cellular Differentiation in the Developing Ocular Lens". Miami University / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=miami1437562575.

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21

Wu, George Tatung. "The role of anaphase-promoting complex in cellular differentiation and tumorigenesis /". Access full-text from WCMC, 2008. http://proquest.umi.com/pqdweb?did=1528351821&sid=7&Fmt=2&clientId=8424&RQT=309&VName=PQD.

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22

Duong, Khanh Linh. "Molecular and cellular basis of hematopoietic stem cells maintenance and differentiation". Diss., University of Iowa, 2014. https://ir.uiowa.edu/etd/1448.

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The blood system consists of two main lineages: myeloid and lymphoid. The myeloid system consists of cells that are part of the innate immune response while the lymphoid system consist of cells that are part of humoral response. These responses protect our bodies from foreign pathogens. Thus, malignancies in these systems often cause complications and mortality. Scientists world wide have been researching alternatives to treat hematologic disorders and have explored induced pluripotent stem cells (iPSCs) and the conversion of one cell type to another. First, iPS cells were generated by overexpression of four transcription factors: Oct4, Sox2, Klf4 an cMyc. These cells closely resemble embryonic stem cells (ESCs) at the molecular and cellular level. However, the efficiency of cell conversion is less than 0.1%. In addition, many iPS colonies can arise from the same culture, but each has a different molecular signature and potential. Identifying the appropriate iPS cell lines to use for patient specific therapy is crucial. Here we demonstrate that our system is highly efficient in generating iPS cell lines, and cell lines with silent transgenes are most efficient in differentiating to different cell types . Second, we are interested in generating hematopoietic stem cells (HSCs) from fibroblasts directly, without going through the pluripotent state, to increase efficiency and to avoid complications associated with a stem cell intermediate. However, a robust hematopoietic reporter system remains elusive. There are multiple hematopoietic reporter candidates, but we demonstrate that the CD45 gene was the most promising. CD45 is expressed early during hematopoiesis on the surface of HSCs; and as HSCs differentiate CD45 levels increase. Furthermore, the CD45 reporter is only active in hematopoietic cells. We were able to confirm the utility of the CD45 reporter using an in vitro and an in vivo murine model. In conclusion, The goal of this research was to expand the knowledge of stem cell reprogramming, specifically the reprogramming of iPS cells. Furthermore, it is our desire that the CD45 reporter system will undergo further validation and find utility in clinical and cell therapy environments.

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23

Mei, Hua. "The role of G[alpha]z during muscle differentiation /". View abstract or full-text, 2006. http://library.ust.hk/cgi/db/thesis.pl?BICH%202006%20MEI.

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24

Pitstick, Amy L. "Nuclear Reorganization and Gene Expression During Muscle Cell Differentiation". Wright State University / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=wright1309997417.

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25

Buensuceso, Charito Saradpon. "Cellular and molecular characterisation of vanadate-induced phenotypic change in PC12 cells". Thesis, King's College London (University of London), 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.336446.

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Newsome, Philip N. "Studies on cellular engraftment and hepatocytic differentiation in liver injury and repair". Thesis, University of Edinburgh, 2004. http://hdl.handle.net/1842/27118.

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Aim: In this thesis the factors which regulate the adhesion and survival of hepatocytes in the face of acute liver injury environment are examined. Also factors which regulate the differentiation of human stem cells towards hepatocytes are examined in vitro and in vivo. Materials and Methods: Human hepatoblastoma (HepG2) cells were used as a model of human hepatocytes to study the effect of serum from patients with acute liver failure. Various laboratory assays were used to determine effects on adhesion, cell necrosis/apoptosis, integrin expression (flow cytometry) and integrin activation. Human cord blood was used as a source of human stem cells for both in vitro experiments and the in vivo work with the NOD-SCID mice. Results: Paracetamol-induced liver injury results in the marked up regulation of collagen IV on hepatic sinusoids. Adhesion of HepG2 cells to Collagen IV after exposure to fulminant serum was reduced within only a few hours. Apoptosis occurred approximately 24-48 hours after incubation and is associated with caspase3 activation. Furthermore, fulminant serum reduces the adhesive capabilities of HepG2 cells by a rapid down-regulation of their β₁-integrin activity. Loss of cellular adhesion and subsequent apoptosis can be reversed by treatment of HepG2 cells with the stimulatory mAb TS2/16. Human cord blood could not be directed in vitro down the hepatocytic lineage under any of the different combinations of cytokines/matrix. In vivo however infused human cord blood cells are capable of engrafting into NOD-SCID mouse liver and differentiating down the hepatocytic lineage without fusion to host hepatocytes. Conclusion: In this thesis mechanisms regulating the engraftment and survival of HepG2 cells during exposure to fulminant serum were identified. Human stem cells were also demonstrated in vivo (but not in vitro) to differentiate into hepatocytes within the NOD-SCID mouse liver with no evidence of cellular fusion.

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27

Preston, Thomas John. "Studies on the regulation of adipocytic differentiation by cellular and viral oncogenes". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq22382.pdf.

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Gill, Robert James Montgomery. "Regulation and activity of cell cycle control factors in terminal cellular differentiation". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0024/NQ49922.pdf.

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Attias, Ortal. "The role of Rac1 in mouse podocyte cellular process formation and differentiation /". Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111588.

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The role of podocytes in glomerular permselectivity is tightly associated with their intricate morphology, featuring interdigitating foot processes from adjacent cells. The actin cytoskeleton is an integral component of podocyte foot processes and is regulated by a number of proteins expressed in podocytes. Rho-family of small GTPases are known key regulators of the actin cytoskeleton. This study, investigated the role of Rac1 in podocytes, using conditionally immortalized mouse podocytes (MPs). We studied Rho-GTPase activities and morphology/cytoskeleton of differentiating mouse podocytes stably expressing nephrin. We also studied the impact of transfection of various Rho-GTPase mutants and IQGAP1 mutants. We demonstrated that nephrin expression potentiates and sustains Rac1 activity during the differentiation process. We showed that Rac1 contributes to process formation in differentiating MPs and may have a similar role in vivo when podocytes are recovering from injuries.

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30

Patel, Imran Iqbal. "Vibrational spectroscopy for the interrogation of mechanisms for cellular transformation and differentiation". Thesis, Lancaster University, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.656331.

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Vibrational spectroscopy occurs through the interaction of specific frequencies of light with molecular chemical bonds. Both Raman and FTIR spectroscopy detect frequency change or absorbance respectively. Application to biological samples derives a vibrational spectrum of the biomolecular components present in the interrogated area. Subtle alterations in spectra can be determined through sophisticated multivariate approaches. In this PhD, a number of studies show the potential of vibrational spectroscopy in determining disease related biomolecular alterations prior to morphological manifestation, and its potential as a diagnostic tool. Raman microspectroscopy was employed to interrogate zones of the prostate with varying susceptibility to malignancy. Point spectra were acquired from glandular epithelial cells and stroma from central, peripheral and transitional zones. Exploratory analysis using principa component analysis (PCA) significantly discriminates spectra between all zones of the prostate. Wavenumber-intensity relationships primarily identified biomolecular alterations in DNA of epithelial cells between the peripheral zone (PZ) to less susceptible transitional zone (TZ) and central zone (CZ). These alterations may facilitate functional roles to the susceptibility of cancer. In addition to zone specific susceptibility to malignancy, incidence of prostate cancer varies worldwide amongst different demographical populations. A seven-fold difference incidence is present between UK and India populations. Multiple vibrational spectroscopy techniques were utilised to acquire spectra from prostate TZ glands and stroma between India and UK cohorts. Application of multivariate approaches PCA and principal component analysis-linear discriminant analysis (PCALDA) significantly discriminating spectra between both populations. Protein secondary structure alterations were present between cohorts with DNA alterations exclusively located in epithelial layers. These imply underlying alterations potentially contributing to differential incidence of prostate cancer worldwide. The application of vibrational spectroscopy as an in-vivo imaging technique is being established within the biomedical field. Contrast and resolution of tissue structures in images can be limited depending on the sophisticated computational analysis utilised to distinguish morphology. Such requirements are vital during surgical resections when a high degree of confidence is needed and to retain as much normal functioning tissue. We employed Raman microspectroscopy imaging of endometrial tissues and tested the applicability of a number of sophisticated computational approaches for biochemical image reconstruction. Comparison of results with histological images of tissue identified multivariate curve resolution-alternating least squares (MCR-ALS) as a superior computational analysis for image re-construction than PCA and Hierarchical Cluster Analysis (HCA). Cancer epidemiological studies suggest that cancers may arise decades after initial exposure to a carcinogen. The complexity for diagnosis of these latent cancers is due to the lack of biomarkers for identification. A by-product of chronic oxidative stress, 4-hydroxy-2-nonenal (4HNE) could provide a potential diagnostic biomarker. Synchrotron radiation-Fourier transform infrared spectroscopy (SR-FTIR) was employed to interrogate terminal ductal lobular units (TDLU) of breast identified as 4HNE positive or negative. Significant discrimination between TDLUs was achieved, with DNA (VsP02-) as tlie major biomolecular alteration present between epithelial cells of positive and negative TDLU. Such alterations were not present in inter or intra-lobular stroma. This suggests that DNA-damaging influences in early-life breast epiu~elium may confer alterations that may underlie subsequent later-life progression. Adult stem cells are vital for the maintenance, repair and regeneration of many tissues in the human body. Tracking of these stem cells has been limited to labelling techniques which has proven difficult as there is no definitive biomarker of adult stem cells. SR-FTIR microscopy was used to image map human inter-follicular epidermis as a non-labelling approach to stem cell identification in the epidermis. Focal plane array (FP A) imaging was also applied for sub-cellular spatial resolution and wider imaging areas. Primary exploratory analyses using peA was applied prior to application of linear discriminant analysis (LDA). Asymmetric and symmetric phosphate (P02) was identified as discriminating biomolecular markers between cells which are hypothesized to be stem, transit-amplifying (TA) and terminally differentiated (TD) cells. The basal layers of epidermal regions were identified to contain cells with signatures which are likely to represent stem cells approximately every 5 to 6 cells. Spectrally similar cells, likely to be adult stem cells were also identified in the dermis in close proximity to rete pegs possibly related to the region of the follicular bulge. This PhD utilises the potential of vibrational spectroscopy techniques coupled with computational analyses to determine biomolecular alterations that can assist in diagnosis and understanding the underlying mechanisms of a range of cancers. -

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31

Henderson, David John. "Studies on cellular differentiation in the dwarf tapeworm Hymenolepis nana (Cestoda: Cyclophyllidea)". Thesis, Queen's University Belfast, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.329352.

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32

Neems, Daniel. "The Formation and Function of Lineage Specific Nuclear Topologies during Cellular Differentiation". Thesis, Northwestern University, 2016. http://pqdtopen.proquest.com/#viewpdf?dispub=10044036.

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DNA is the physical medium for information storage inside of cells. Sub-regions of the DNA composed of linear stretches of nucleic acid sequences (DNA sequences), known as genes are the basic unit of storage in the human genome. Genes contain a myriad different types of information, of which a major class is protein coding genes. As the name suggests these genes hold the information required to make proteins, which then go on to perform cellular function and consequently dictate cellular activity and identity. Genes themselves are further grouped through the physical lineage of being contained on the same macromolecule known as chromosomes. The entire complement of chromosomes makes up the genome of the organism. In the case of humans, which are diploid, the genome is made up of 22 sets of autosomes and one set of sex chromosomes, a total of 46 discrete chromosomes. During interphase of the cell cycle all 46 of these chromosomes are found inside the nucleus in partially condensed, largely discrete regions known as chromosome territories.

The positioning of chromosome territories and the genes within them is non-random and has previously been demonstrated to be a function of gene expression. In order for a gene to be expressed, its sequence must be accessible to the RNA polymerases (RNAPs) that transcribe it, not tightly compacted around histones in an inaccessible form known as heterochromatin. As different types of cells need different types of proteins to function, and thus different genes to be expressed, the regions of the genome that are found in heterochromatin are cell type specific. The location of gene locus inside the nucleus relative to other sub-nuclear features such as RNAPII foci, known as transcription factories, also dictate expression. This relationship results in the interphase genome forming a cell type specific topology which is the result of the expressed genes. In spite of the persistent observation of cell type specific nuclear topologies, the factors that guide the formation and the function of observed topologies remains unclear.

Here, we test the relationship between linear and three-dimensional (3D) organization of gene regulation during myogenesis. Our analysis indicates that a subset of human chromosomes is significantly enriched for topologically associated domains (TADs) that contain muscle-specific genes. These lineage-enriched TADs demonstrate an expression dependent pattern of nuclear organization that also affects the positioning of non-enriched TADs. Therefore, lineage-enriched TADs affect cell-specific genome organization during myogenesis. The allelic spatial proximity of one of these domains, which encodes myogenin, reduces transcriptional variability. Moreover, this cell-specific nuclear topology is dependent on cell division. We propose that the linear and spatial organization of gene locus is functionally inter-dependent and that mitosis is critical in establishing this behavior during cellular differentiation.

We then extend this analysis into murine lymphocyte development. Specifically, we look at naturally occurring suppressive T-regulatory cells (T_regs) that dampen the strength/severity of the immune response and have been demonstrated to be clinically relevant in the emergence and pathogenesis of auto-immune disorders. T-regulatory cells are an interesting model for studying lineage specific nuclear topologies because during an active immune response they are a mixed population of natural T_regs and induced T_regs that phenocopy each other but have different developmental histories. There is also clinical interest in finding a reliable means to make a distinction between these two cell types for the potential treatment of auto-immune disease. By studying features of nuclear organization for two candidate genes, FoxP3 and Helios, and the chromosomes they reside on, X and one respectively, we were able to distinguish these two populations of cells on the basis of nuclear topologies. We propose this distinction is the result of differing nuclear topologies in the progenitor population in conjunction with only a sub-set of regions, such as LE-TADs, showing lineage specific localizations. This would lead to remnants of progenitor topologies in terminal lineages. We also make the interesting observation of unexpectedly high rates of coalescence between the active and inactive X chromosomes in cells that specifically express the X-linked gene FoxP3. This finding may lead to transvection based silencing of FoxP3 and the increase in autoimmunity observed in females.

Collectively, this body of work furthers the understanding of how lineage specific nuclear topologies emerge as a function of gene expression and greatly expands the current understanding of how these topologies exert influence over the expression of genes.

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33

Burr, Simon Jonathan. "The role of molecular oxygen in the epigenetic regulation of cellular differentiation". Thesis, King's College London (University of London), 2018. https://kclpure.kcl.ac.uk/portal/en/theses/the-role-of-molecular-oxygen-in-the-epigenetic-regulation-of-cellular-differentiation(4eae590b-fa8b-4d9e-862d-69ad3452734e).html.

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The developing mammalian embryo is subjected to low O2 tensions, which owing to the short diffusion distance of O2 may form a gradient within the early embryo, and thus may function as a developmental morphogen. It was observed that culture of mouse embryonic stem cells (mESCs) in 1% O2, compared to atmospheric [O2], acted to skew differentiation. The cause of this effect was studied with respect to alterations in chromatin structure, via regulation of epigenetic modifications. The ten-eleven translocation (Tet) demethylase enzymes, Tet1/2/3, oxidise methylated DNA to form 5-hydroxymethylcytosine (5-hmC); a stable epigenetic mark that is implicated in developmental events. The mechanism(s) which underlie the regulation of their function(s) are unknown. However, intriguingly the catalytic activity of these enzymes is mediated via a conserved O2-dependent hydroxylase domain. Therefore, it was hypothesised that the Tet enzymes may be differentially regulated by [O2] to influence cellular specification and thus contribute to asymmetry within the developing embryo. Here it was identified that Tet1 is the most likely isoform to be inhibited by O2 tensions deemed physiologically relevant during embryogenesis. Further, differentiating mESCs displayed a transient, Tet1-mediated, O2-dependent burst of hydroxylation. This hydroxylation was predominantly targeted to a CG rich region of a Tet3 promoter, driving expression of a truncated protein isoform that lacks a CXXC DNA binding domain. This promoter region was shown to associate with Tet1, and also both the repressive (H3K27me3) and activating (H3K4me3) histone marks, characteristic of a bivalent promoter. Here it was also confirmed that 2 distinct Tet3 protein isoforms are expressed in differentiated mESCs, which were found to have differential transcriptional regulation and are thus likely to serve distinct cellular functions. It is suggested that Tet1 activity, in part determined by [O2] within the early embryo, may regulate Tet3 expression spatially to control cell fate decisions.

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34

Pereira, Marie Antoinette Tanya. "Cellular differentiation and antibiotic production by Streptomyces nodosus immobilised in alginate capsules". View thesis, 2007. http://handle.uws.edu.au:8081/1959.7/20504.

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Thesis (PhD) -- University of Western Sydney, 2007.
A thesis submitted to the University of Western Sydney, College of Health and Science, School of Natural Sciences, as a requirement for the degree of Doctor of Philosophy. Includes bibliography.

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Wilczynska, Katarzyna Marta. "Inflammation-associated gene regulation in primary astrocytes, glial tumors and cellular differentiation". VCU Scholars Compass, 2008. http://hdl.handle.net/10156/1772.

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Choi, Olivia J. "Spag17 Deficiency Impairs Neuronal Cell Differentiation in Developing Brain". VCU Scholars Compass, 2019. https://scholarscompass.vcu.edu/etd/5877.

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The development of the nervous system is a multi-level, time-sensitive process that relies heavily on cell differentiation. However, the molecular mechanisms that control brain development remain poorly understood. We generated a knockout (KO) mouse for the cilia associated gene Spag17. These animals develop hydrocephalus and enlarged ventricles consistent with the role of Spag17 in the motility of ependymal cilia. However, other phenotypes that cannot be explained by this role were also present. Recently, a mutation in Spag17 has been associated with brain malformations and severe intellectual disability in humans. Therefore, we hypothesized that Spag17 plays a crucial role in nervous system development. To investigate this possibility, we first characterized the spatiotemporal expression of Spag17 in the developing brain by using Beta-galactosidase staining and immunohistochemistry. Results showed Spag17 expression in the spinal cord in embryonic E11. By E11.5-12.5 the expression extends to the rhombic lip from the developing hindbrain, as well as to the forebrain and midbrain regions. E14.5-15.5 embryos exhibit an intense expression in the developing ventricles as well as the cerebellum. From E17.5 to birth (P0), the gene is more broadly expressed. We then used a global Spag17 KO mouse model to characterize the function of Spag17 during brain development. Immunohistochemical studies performed in brain sections from E15.5 and P0 time points showed increased expression of the neural progenitor marker Nestin, and reduced expression of mature neuron marker NeuN, increasing positive trend with the young neuron marker Tuj1. Altogether, these findings reveal that Spag17 has a unique spatiotemporal distribution and may be critical for the maturation of neural progenitor cells.

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Jamie, Hajierah. "Possible crosstalk between signal transduction pathways in the induction of differentiation in HT-29 cells". Thesis, University of Port Elizabeth, 2000. http://hdl.handle.net/10948/d1019684.

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The investigation into the mechanisms by which compounds such as butyrate induce differentiation in HT-29 cells, is lacking. The colonic carcinoma cell line, HT-29, undergoes differentiation induction in the presence of butyrate and acetoacetate. The Caco-2 cell line spontaneously differentiates on contact inhibition. In this study, a signal transduction pathway involving ATP, cAMP, Ca2+ and the transcriptional factor CREB was investigated following suggestions that the energy state of the cell and diffferentiation are linked. The activity of the MAP kinase cascade, including possible crosstalk that may exist between these pathways was determined. The HT-29 cells were exposed to 5 mM acetoacetate, butyrate, DMSO and propionate. The results of this differentiation induction were compared to Caco-2 and HeLa cells, which are cervical carcinoma cells. It was found that ATP levels are decreased on differentiation induction in HT-29 cells, which, in turn affected the cAMP concentrations. Theoretically, the inducers do not have any effect on PDE 4 activity, and may facilitate the interaction between cAMP and PKA. Influx of Ca2+ into the cells was inhibited to a degree by the inducers, which was possibly overcome by crosstalk between the cAMP and Ca2+ pathways. CREB activation, lineage-specific gene expression, ERK activity and c-myc expression were all dependent on both the inducers used and the cell-type. PKA played a major role in CREB activation in acetoacetate- and butyrate -induced HT-29, Caco-2 and HeLa cells, while a2+/Calmodulin-dependent kinases I/IV may have a secondary role. Alkaline phosphatase expression in HeLa cells was independent of CREB. Evidence that crosstalk between the MAP kinase cascade and the REBactivation pathways exist, was illustrated by increased CREB activation on ERK inhibition in acetoacetate- and butyrate-induced HT-29 and HeLa cells. Also, the role that ERK played in the cells differed with inducer and cell-type. The dependence of cmyc expression on c-jun and c-fos, appeared to be differentiation induction- and celltype specific. Results from this study indicate the potential use of acetoacetate and butyrate as anti-cancer compounds.

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38

Barnett, David. "Activation antigens in the proliferation and differentiation of normal and malignant human leucocytes". Thesis, Open University, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.293382.

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Lautenschlaeger, Franziska. "Cell compliance : cytoskeletal origin and importance for cellular function". Thesis, University of Cambridge, 2011. https://www.repository.cam.ac.uk/handle/1810/239393.

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Mechanical properties of cells, mainly defined by their cytoskeleton, are closely related to cell function and can be measured with a dual-beam laser trap (optical stretcher). Functional changes, which go hand in hand with changes of the cytoskeleton, also occur during differentiation of stem cells. This suggests monitoring differentiation by the changing compliance of the cells. During the course of my PhD I measured the compliance of three different types of stem cells before and after differentiation and was able to detect differences in some of the cell types. In order to relate rheological experiments to cell migration as a further example of functional change I investigated the migration behavior of cells that showed different compliance and found differences in migration. I was additionally able to show an altered migration behavior after I actively changed the mechanical behavior of one cell type using cytoskeletal drugs. These migration experiments have been carried out in 2D and 3D migration assays. Furthermore, the influence of the stiffness of the surrounding material on the migration behavior has been investigated. After relating functional changes to changes in compliance, I studied which mechanisms can be used to actually influence cell compliance and investigated the effect of cytoskeletal stabilizers or destabilizers as well as drugs acting on molecular motors. The effect of the surrounding temperature has been considered as well. Finally, I developed a new version of the optical stretcher measurement tool, which enables cell sorting and drug screening using a monolithic glass chip. With the results presented in this thesis I relate mechanical compliance to the cytoskeleton and specific cellular functions. I deliver insights how mechanical changes in cells can be used to identify and follow functional changes and how this knowledge can help to interfere with such functions, specifically in pathologies correlated to these functions. My modified optical stretcher would be developed to screen the effects of drugs on cell compliance and to sort cells with different mechanical properties. Such drug screening and cell sorting will offer diagnostic treatment options for various pathologies.

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Biver, Galadrielle. "Identification and characterization of the control of murine MSC differentiation by the ADP receptors P2Y12 and P2Y13". Doctoral thesis, Universite Libre de Bruxelles, 2014. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209334.

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Extracellular nucleotides act as local intercellular messengers. In response to various stimuli, nucleotides can be released from the cytosol of damaged cells, exocytosis vesicles and efflux through membrane channel. In the extracellular fluids, nucleotides are rapidely degraded by ecto-nucleotidases, such as CD39,CD39L1 and CD73. Extracellular nucleotides activate the P2 receptor family .This family of receptors can be divided into 2 groups: P2X1-7R ( ionotropic receptors) and P2YR ( G protein-coupled receptors). Nowadays, there are eight accepted human P2Y receptors: P2Y1,2,4,6,11,12,13,14.

To determine the physiological roles of P2Y receptor family, our laboratory generated different strains of P2Y knockout mice (P2Y4 ,6 and 13). In collaboration with A. Gartland ,I. And Arnett TR Orriss ( Sheffield and London University) ,it has been observed that the P2Y13R-/- mice exhibit an impaired bone tissue metabolism that leads to a reduction in the volume of the femoral trabecular bone and the number of trabeculae. This phenotype is correlated with the decrease in the number of osteoblasts at the endo-cortical bone surface .

We therefore examined whether P2Y13 R activation was involved in the osteogenic differentiation of mesenchymal stem cells (MSCs). In the first part of our work we have shown that :

Induction of the MSCs differentiation is associated with the release of ATP and its conversion to ADP (agonist of the P2Y13R). ATP release probably involves the pannexine1 while the conversion of ATP into ADP is probably due to the activity of the ecto-nucleotidase CD39L1.

ADP stimulation of P2Y13 R+/+ (but not P2Y13 R-/-) adherent bone marrow stromal cells (BMSC) increased significantly the formation of alkaline phosphatase-colony forming units (CFU-ALP), as well as the expression of osteoblastic genes such as Osterix involved in the maturation of pre-osteoblasts into osteoblasts. The number of CFU-ALP obtained from P2Y13 R-/- BMSC and the level of osteoblastic gene expression after osteogenic stimulation were also strongly reduced compared to those obtained in wild-type cell cultures. In contrast, when P2Y13 R-/- BMSCs were incubated in an adipogenic medium, the number of adipocytes generated and the level of adipogenic gene expression (PPARγ2 and Adipsin) were higher than those obtained in P2Y13 R+/+ MSC. We also observed a significant increase of the number of bone marrow adipocytes in tibia of P2Y13 R-/- mice.

The P2ry12 gene deletion (also activated by ADP) also affects the ability of BMSCs to differentiate into osteoblasts but stimulates adipogenic differentiation.

In a second part of our work ,we have shown that the pro- osteogenic action of P2Y13R is indirect. Indeed ,this receptor is not expressed by MSCs but by adherent myeloid cells present in the bone marrow cell cultures (characterized by the expression of CD11b and CD45 markers) .In addition, we observed that following receptor activation by ADP ,these myeloid cells produce BMP2 factor.

We therefor propose that the stimulation of MSCs differentiation induces CD45- adherent cells to release ATP that is converted into ADP, most probably by the up-regulated CD39L1 ectonucleotidase. This ADP stimulates P2Y12R and P2Y13R expressed by CD45+/CD11b+ myeloid cells leading to the release of the osteogenic factor BMP2. This cytokine favours the maturation of pre-osteoblasts into osteoblasts and concomitantly inhibits the maturation of pre-adipocytes.

Doctorat en Sciences
info:eu-repo/semantics/nonPublished

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41

Yang, Liu, i 楊柳. "Genetic analyses of terminal differentiation of hypertrophic chondrocytes". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hdl.handle.net/10722/210320.

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Mudumba, Sreenivasu. "Characterization of polyamine-induced differentiation in PC12 cells". Scholarly Commons, 1997. https://scholarlycommons.pacific.edu/uop_etds/2609.

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The present investigation focused on three different aspects of polyamine involvement in induction of cell differentiation and neurite outgrowths: effects of polyamines on isolated bovine brain tubulin assembly, effects of polyamines on dopamine levels in PC12 cells, and influence of differentiating agents on polyamine and acetylpolyamine levels in PC12 cells. Among the polyamines, only spermine significantly induced tubulin assembly starting at 60 $\mu$M concentration (p $<$ 0.05). Colchicine at 100 $\mu$M concentration, and calcium chloride at 5 mM concentration inhibited spermine-induced polymerization (p $<$ 0.05). Spermine-induced polymerization was not stable in the presence of calcium or at 4$\sp\circ$C. NGF and dexamethasone increased the dopamine levels compared to that of control. Dopamine levels were increased up to 170% and 160% of control (p $<$ 0.05) with 10 $\mu$M N$\sp8$-acetylspermidine and 10 $\mu$M 7-(N-(3-aminopropyl)amino) heptan-2-one (APAH), respectively, after 48 hours. APAH is an inhibitor of N$\sp8$-acetylspermidine deacetylase. These effects of N$\sp8$-acetylspermidine and APAH appeared to be concentration dependent. Other polyamines did not have any significant effects on dopamine levels in PC12 cells. NGF and dexamethasone did not appear to have a significant effects on polyamine and acetylated polyamine levels in PC12 cells at the time periods studied. The amount of N$\sp8$-acetylspermidine detected after 24 hour treatment with 100 $\mu$M N$\sp8$-acetylspermidine was 18 $\pm$ 3 pmols/mg protein. The levels were increased up to 38 $\pm$ 6 and 52 $\pm$ 11 pmols/mg protein after days 3 and 7, respectively, with 100 $\mu$M N$\sp8$-acetylspermidine treatment. N$\sp8$-Acetylspermidine levels were detectable as early as day 1 with 100 $\mu$M APAH treatment and the levels detected after 1, 3, and 7 day treatments were 7.4 $\pm$ 0.9, 14 $\pm$ 1.2 and 21 $\pm$ 3 pmols/mg protein, respectively. The changes in the dopamine and N$\sp8$-acetylspermidine levels in PC12 cells starting at 10 $\mu$M APAH and N$\sp8$-acetylspermidine from day 1 onwards are well correlated with the morpholigical changes observed from day 3 onwards in an earlier study from our laboratory. The results from the present study suggest that polyamine-induced cell differentiation in PC12 cells is related to the formation of a metabolite N$\sp8$-acetylspermidine and NGF-induced cell differentiation does not appear to involve accumulation of N$\sp8$-acetylspermidine.

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Yang, Liu. "Genetic analyses of terminal differentiation of hypertrophic chondrocytes". Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B43223758.

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Sun, Qian. "Cellular and molecular mechanisms of dendritic cell differentiation from cells of leukaemic origin". Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/hkuto/record/B38885335.

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Carthy, Jonathon Morgan. "Cellular and molecular biology of Wnt signaling and versican expression in myofibroblast differentiation". Thesis, University of British Columbia, 2011. http://hdl.handle.net/2429/39838.

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Wound healing is a complex and dynamic process that restores tissue integrity after injury, but also contributes pathologically to the development of fibrosis. Growing evidence suggests a role for Wnt signaling during normal and aberrant wound healing. The proteoglycan versican is a target of Wnt signaling that is expressed following injury and accumulates pathologically in many chronic inflammatory conditions. In this dissertation, I hypothesized that Wnt signaling and its target versican are key regulators of mesenchymal cell phenotype. In Aim 1, I demonstrated that treatment of cultured fibroblasts with Wnt3a, a canonical Wnt ligand, stimulates the formation of a myofibroblast-like phenotype characterized by increased expression of smooth muscle α-actin. These changes appear to be mediated by Wnt3a upregulating the expression of TGF-β and its associated signaling through SMAD2 in a β-catenin-dependent mechanism. In Aim 2, I show that Wnt3a alters the phenotype of vascular smooth muscle cells and stimulates the formation of a contractile and secretory phenotype in these cells that is associated with increased gap junction communication. Again, these changes occurred through a mechanism that was dependent on canonical Wnt signaling. In Aim 3, I explored the functional roles of versican by examining its expression following injury to cultures of valve myofibroblasts. My data indicate that versican is secreted as extracellular matrix following injury to valve cells, and suggests a role for the membrane receptor CD44 in organizing this provisional versican matrix. In Aim 4, I delved further into the functional roles of versican by expressing this proteoglycan in murine fibroblasts. In this aim I showed that versican expression promotes myofibroblast differentiation, and these changes appear to be mediated by activation of TGF-β signaling. Lastly, in Aim 5, I explored potential intracellular functions for versican, and provide evidence to suggest versican localizes to the nucleus in mesenchymal cells where it regulates the organization of the mitotic spindle during cell division. Collectively, these data suggest Wnt signaling and versican are key regulators of mesenchymal cell phenotype, and as such, are important mediators of a wound healing response.

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46

Sun, Qian, i 孫倩. "Cellular and molecular mechanisms of dendritic cell differentiation from cells of leukaemic origin". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B38885335.

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Mello, Cintra L. Muller Thias. "The role of cohesin in regulating early steps of cellular differentiation and reprogramming". Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/18023.

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The cohesion protein complex is critical for sister chromatid cohesion and proper chromosome segregation in cycling cells and has additional roles in gene regulation and chromatin organisation. Particularly, cohesin has been implicated in regulating genes critical for maintaining pluripotency in embryonic stem (ES) cells. Here I ask whether cohesin regulates gene expression during early stages of ES cell differentiation and the reprogramming of somatic cells towards pluripotency. In order to dissociate the role of cohesin in gene expression from cohesin’s essential functions during the cell cycle I have established genetic approaches to conditionally delete cohesion in ES cells and in somatic cells. By depleting cohesin in ES cells my results reinforce the suggested role of cohesin in pluripotency maintenance, but also show that cohesin removal preferentially leads to mesoderm and neuroectoderm differentiation. In addition, data presented here suggest that cohesin is required for the silencing of X-inactivating genes that occurs during the differentiation of female ES cells. To explore the role of cohesin in reprogramming I used experimental heterokaryons generated by fusing ES cells and somatic cells. In this system, the re-expression of ES-specific genes in somatic cell nuclei occurs in the absence of cell division, thereby obviating the need for cohesin for cell division-related functions. Interestingly, by depleting cohesion in ES cells I found that cohesin is not required for the ability of ES cells to induce reprogramming of somatic cells. Instead, cohesin depletion enhanced their reprogramming ability to re-activate the expression of pluripotency markers in somatic cells, possibly by a mechanism that involves the up-regulation of the reprogramming factor c-Myc. In contrast, somatic cells require cohesin to be reprogrammed. Cohesin-depleted somatic cells were unable to re-activate pluripoency markers and failed to silence lineage-specific somatic genes after fusion. Finally, ongoing experiments to establish a rapid and reversible system for proteolytic cleavage of cohesion in mammalian cells, will contribute to understand the mechanisms by which cohesin regulates gene expression in cellular differentiation and reprogramming.

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Fong, Lai-ping Iris, i 方麗萍. "Modulation of dendritic cell differentiation, maturation by exogenous and endogenous "danger" signals". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B31971015.

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Strand, Laura Therese. "A Proteomic Analysis of Differentiation in the Mammary Epithelium". DigitalCommons@CalPoly, 2012. https://digitalcommons.calpoly.edu/theses/825.

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While a great deal is known about the changing hormonal environment and the structural development of the mammary gland from pregnancy to lactation, very little is known about the molecular mechanisms governing differentiation of the mammary epithelium into a milk-secreting phenotype. It is important to acknowledge the diversity among the mammary glands of different species in order to better understand applications in human health and the dairy industry. In this study, we examined global protein expression during two states of differentiation in mammary epithelial cells from two species: in vitro proliferating and differentiated MAC-T cells (a bovine immortal cell-line), and primary mammary epithelial cells isolated from pregnant and lactating mice. When comparing the lists of proteins that differed in abundance in the two experiments, we observed many similarities in proteins related to structural dynamics and mRNA processing within these two mammary epithelial cell types. Intriguingly, we observed several differences in the regulation of metabolic proteins, highlighting the distinct pathways by which different species probably metabolize energy and synthesize milk components.

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Roth, Ronelle. "Phenotypic characterization of maize bundle sheath defective mutants". Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.339349.

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