Дисертації з теми "Tbx16"
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Muyskens, Jonathan B. "Tbx16 and Wnt11 coordinately regulate prechordal plate morphogenesis /." view abstract or download file of text, 2005. http://www.lib.umi.com/cr/uoregon/fullcit?p3201693.
Повний текст джерелаTypescript. Includes vita and abstract. Includes bibliographical references (leaves 55-58). Also available for download via the World Wide Web; free to University of Oregon users.
Burbridge, Sarah. "The role of Tbx18 in axial mesoderm development." Thesis, University of Sheffield, 2012. http://etheses.whiterose.ac.uk/3312/.
Повний текст джерелаArribas, Arranz Jéssica. "Los factores de transcripción TBX15 e YY1 en cáncer. Función y regulación de TBX15. Expresión de YY1 en cáncer de tiroides." Doctoral thesis, Universitat Autònoma de Barcelona, 2015. http://hdl.handle.net/10803/323905.
Повний текст джерелаTBX15 and YY1 are transcription factors; these molecules are able to transduction signals, being essential in the regulation of many basic cellular processes including cell proliferation and apoptosis. Therefore, the anomalous expression and function of these transcription factors is crucial in the beginning and in the development of cancer. Transcription factors act as oncogenes or tumor suppressor genes and their expression is found altered in multiple types of cancer. Specific transcription factors of the thyroid gland have been reported to be associated with thyroid cancer; however there is no information about the implication of general transcription factors, such as TBX15 or YY1. The involvement of YY1 in cancer is well documented; whereas there are scarcely any studies describing the possible implication of TBX15 in cancer. In this context, the present thesis provides knowledge about the role of transcription factor TBX15 in the development of cancer; moreover, it also analyzes the expression of transcription factor YY1 in differentiated thyroid cancer. Our study reveals a novel function of transcription factor TBX15 as an inhibitor of cellular apoptosis, which can contribute to the proliferative potential of cancer cells, and may suggest TBX15 as a potential therapeutic target in cancer treatment. Furthermore, we have also proven that NFkB activates the transcription of TBX15 by binding to the 5’-flanking regulatory region of the gene TBX15. Thus, the interaction between TBX15 and NFkB could prove to be important to understand the function of TBX15 in cancer. Without any previous information regarding the expression of transcription factor YY1 in thyroid cancer, our results represent the first study about the implication of YY1 in this type of cancer. We demonstrate how YY1 is overexpressed in differentiated thyroid cancer, and what’s more, its positive expression has been found to be more frequent in the papillary type rather than in the follicular type. Therefore these results evidence the possible implication of transcription factor YY1 in thyroid cancer.
Cinzia, Caprio. "Tbx1 functions in pharyngeal arch and cardiovascular development." Thesis, Open University, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.663223.
Повний текст джерелаMartin, Jody Carl. "TBx18 and the epicardium in cardiac development and regenerative medicine." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2008. http://wwwlib.umi.com/cr/ucsd/fullcit?p3336705.
Повний текст джерелаTitle from first page of PDF file (viewed January 6, 2009). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (p. 128-139).
De, Mesmaeker Julie Anne Laurence Nathalie. "Molecular mechanisms connecting genotype and phenotype in Tbx1 deficiency." Thesis, University of Oxford, 2012. http://ora.ox.ac.uk/objects/uuid:56013dc6-50af-454c-b036-284e5449aa8f.
Повний текст джерелаGiménez, Esteban Mariano. "Expresión y regulación De los genes WDR3 y TBX15 en cáncer." Doctoral thesis, Universitat Autònoma de Barcelona, 2012. http://hdl.handle.net/10803/121601.
Повний текст джерелаThere are numerous studies dedicated to find out the causes of cancer and its progression and the application of this knowledge to improving the prevention, diagnosis and treatment. In this context our group contributes to these objectives, providing new insights into the processes involved in tumor development of thyroid cancer in particular and carcinogenesis in general. The main objective of this thesis is to study the involvement of the genes WDR3 and TBX15 in cancer. The study of these genes arises from studies conducted in our laboratory that identified two polymorphisms markers of thyroid cancer susceptibility in the chromosomal region 1p12, where these genes have been mapped. Additionally, this chromosomal region has often been associated with many types of cancer. One of the polymorphisms identified is located in WDR3 (intron 24) gene and the other in a region located at 460 Kb from TBX15 gene. The function of these genes has not been completely known, however, it has been proposed that WDR3 is involved in the proliferation of the cell cycle through the disruption of the ribosome biogenesis. In addition, several studies have shown an irregular expression of WD repeat proteins in certain types of cancer. Moreover, the TBX15 gene, like other members of the T-box family, has been related to developmental processes and several evidences suggest a relationship between the T-box genes and tumorigenesis, with effects on cell proliferation, invasion and metastasis. That is why we hypothesize that genes WDR3 and TBX15 may be related to cancer. Numerous studies are conducted in our laboratory to elucidate the role of these genes in the etiology of thyroid cancer in particular and also in cancer in general. In this thesis was performed an association study of genes WDR3 and TBX15 with thyroid cancer susceptibility, and their expression and regulation were analyzed in thyroid cancer, colon cancer and brain tumors. The gene association study of WDR3 with thyroid cancer indicates that this gene is a susceptibility factor for this cancer. The expression analysis shows that the WDR3 is over-expressed in thyroid cancer and colon cancer. The methylation analysis of the promoter region of WDR3 indicates that this epigenetic modification is not involved in the regulation of WDR3 expression at transcriptional level, however, analysis of transcription factors binding to the promoter shows that the c-Myc and CTCF factors could act as regulators of the WDR3 expression. Moreover, the association study of TBX15 gene with thyroid cancer indicates that this gene is not a susceptibility factor for this cancer. The expression analysis of TBX15 shows decreased expression of this gene in thyroid cancer. The methylation analysis of the promoter region of TBX15 in thyroid tissues and brain tissues, indicates that this epigenetic modification is involved in the regulation of TBX15 expression at transcriptional level. This thesis highlights the role of genes WDR3 and TBX15 in the etiology of thyroid cancer and suggests their involvement in carcinogenesis in general.
Briones, Leon Jose Alberto. "Investigating a Tbx1 and Pax9 genetic interaction during cardiovascular development." Thesis, University of Newcastle upon Tyne, 2015. http://hdl.handle.net/10443/2839.
Повний текст джерелаBussen, Markus. "Die funktionelle Analyse des T-box-Transkriptionsfaktors Tbx18 in der Somitogenese der Maus." [S.l.] : [s.n.], 2005. http://deposit.ddb.de/cgi-bin/dokserv?idn=976695405.
Повний текст джерелаMarco, Viviani de. "Estudos dos genes Tbx19 e Crhr1 em cães da raça poodle com hipercortisolismo ACTH-dependente." Universidade de São Paulo, 2010. http://www.teses.usp.br/teses/disponiveis/5/5135/tde-28052010-113552/.
Повний текст джерелаThe ACTH-dependent hypercortisolism (ADH), also called Cushing\'s disease, is one of the most commonly diagnosed endocrine diseases in dogs. The symptoms occur due to glucocorticoids excess leading to gluconeogenic, catabolic, anti-inflammatory and immunosuppressive effects in multiple organs and systems. There is a high incidence of Cushing\'s disease in Poodles and familial disease has been identified suggesting a genetic involvement. The molecular changes that lead to the development of ACTH-dependent hypercortisolism in dogs remain undefined. Among genes implicated in corticotroph development and in corticotropic axis regulation, we would like to point out Tbx19 and Crhr1, respectively. Tbx19 gene is a transcription factor required for transcription of the proopiomelanocortin gene and for terminal differentiation of the corticotroph. Inactivating mutations in that gene are associated with human isolated ACTH deficiency. Since Tbx19 is present exclusively in normal and adenomatous corticotroph cells, its involvement in the secretion of ACTH in Cushing\'s disease was proposed. The presence of CRHR1 in corticotrophinomas in humans and dogs raised the possibility of its involvement in pituitary tumorigenesis, promoting prolonged cell stimulation, even in the absence of hypothalamic hormones. An increased expression of the CRHR1 mRNA was demonstrated in human and canine ACTH-secreting pituitary adenomas, despite the autonomous ACTH secretion and the low portal levels of CRH. The aim of this study was to investigate Tbx19 and Crhr1 coding region mutations in Poodle dogs with ACTH-dependent hypercortisolism. We studied 50 Poodle dogs with ADH (33 females and 17 males) with a mean age of 8.71 years and 50 control dogs of the same breed (32 females and 18 males) older than 6 years (mean 9.38 years) and without endocrinopathies. Genomic DNA was extracted from peripheral blood, amplified by the polymerase chain reaction (PCR) using specific intronic primers and submitted to automatic sequence. We identified a new allelic variant in the Tbx19 and Crhr1 coding regions. The allelic variant p. S343G in the Tbx19 gene was found in two unrelated dogs, but also in two normal controls, suggesting that this is a new polymorphism. The Crhr1 allelic variant p. V97M was found in heterozygosity in one animal with ACTH-dependent hypercortisolism, but was not observed in one hundred normal alleles. The codon 97 is located in the extracellular amino terminal domain of the Crhr1 and is extremely important for high affinity ligand binding. The molecular analysis of the quaternary structure of normal and mutated proteins, followed by evaluation of the binding energy of the contact surface between the hormone and the receptor showed a structural rearrangement of the mutated protein by changing the contact surface between the CRH and its receptor CRHR1, resulting in a binding energy 17% higher than the wild type. In conclusion, this study did not identify Tbx19 mutations associated with canine ACTH-dependent hypercortisolism, but on the other hand, we first identified a Crhr1 gain-of-function mutation probably responsible for ACTH-dependent hypercortisolism in a Poodle dog of our cohort.
Radosevic, Marija. "Spatial control of inner ear neurogenesis by retinoic acid, Tbx1 and her genes." Doctoral thesis, Universitat Pompeu Fabra, 2011. http://hdl.handle.net/10803/38436.
Повний текст джерелаLes neurones sensorials de l’oïda interna són mediadores claus en la transducció dels estímuls externs des de l’oïda interna al cervell. Entendre a on, quan i com el sistema nerviós sensorial s’organitza durant el desenvolupament embrionari pot ajudar en l’estudi de les malalties neurosensorials. En el present treball, mostro en peix zebra que el factor de transcripció Her9 és un element clau en el control de la neurogènesi òtica i que Her9 es troba sota el control directe del factor Tbx1. A més, ambdos factors estan regulats de manera positva per la via de senyalització de l’àcid retinoic i negativament per la vía de hedgehog. En resum, la tesis demostra un paper de l’àcid retinoic en la regionalització axial del primordi òtic en l’eix anteroposterior i l’establiment d’un domini neurogènic a través de Tbx1 i Her9. En estadis tardans, l’àcid retinoic regula la diferenciació neuronal en el gangli estato-acústic.
Schmidt, Martina Karin [Verfasser]. "Untersuchungen zur Funktion der Transkriptionsfaktoren Tbx18 and Uncx4.1 in der Somitogenese der Maus / Martina Karin Schmidt." Hannover : Technische Informationsbibliothek und Universitätsbibliothek Hannover (TIB), 2012. http://d-nb.info/1031334092/34.
Повний текст джерелаBettenhausen, Eva [Verfasser]. "Functional analysis of the T-box transcription factor Tbx18 in murine urogenital system development / Eva Bettenhausen." Hannover : Technische Informationsbibliothek (TIB), 2017. http://d-nb.info/1170362583/34.
Повний текст джерелаGiuliani, Giuliano. "The role of TBX1 and OTX1 in the development of the zebrafish inner ear." Thesis, University of Sheffield, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.548543.
Повний текст джерелаPapangeli, I. "Tbx1 : potential targets and interactors relevant to development of structures affected in DiGeorge Syndrome." Thesis, University College London (University of London), 2010. http://discovery.ucl.ac.uk/794443/.
Повний текст джерелаJackson, Abigail. "The regulation of pharyngeal pouch morphogenesis by TBX1 and FGF signalling in the endoderm." Thesis, King's College London (University of London), 2013. https://kclpure.kcl.ac.uk/portal/en/theses/the-regulation-of-pharyngeal-pouch-morphogenesis-by-tbx1-and-fgf-signalling-in-the-endoderm(fbd54a00-52cc-4fcc-ae8e-70662a660a4c).html.
Повний текст джерелаMehmet, Mugayer Boral. "Etablierung molekulargenetischer Methoden zur Mutationsanalyse des TBX1-Gens unter Verwendung der denaturierenden Hochdruck-Flüssigkeits-chromatographie (DHPLC)." Doctoral thesis, Universitätsbibliothek Leipzig, 2012. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-88720.
Повний текст джерелаRoberts, C. "The role of putative Tbx1 traget genes in the pathogenesis of the 22q11 deletion syndrome phenotype." Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1390696/.
Повний текст джерелаMoraes, Filipa Pontes. "Tbx1 and Bmp2 in the development of the ear, neural crest and pharyngeal system in mice." Doctoral thesis, Universidade Nova de Lisboa. Instituto de Tecnologia Química e Biológica, 2010. http://hdl.handle.net/10362/11895.
Повний текст джерелаDevelopment of the vertebrate head involves complex interactions between tissues derived from the three germ layers. Significantly, alterations in the development of this region of the embryo are often associated with a wide variety of human congenital birth defects. Some of them are inherited disorders such as Treacher Collins, Branchio-oto-renal and DiGeorge syndromes. During embryonic development, morphogenesis of the craniofacial area occurs sequentially with the formation of a variety of transient structures, which then undergo complex sequential reorganization to form the adult structures.(...)
Choudhury, Moinuddin Hasan. "Biopacemaking : new targets and new mechanisms." Thesis, University of Manchester, 2016. https://www.research.manchester.ac.uk/portal/en/theses/biopacemaking-new-targets-and-new-mechanisms(b35ec222-29eb-432f-9b6d-238f3cbcd72d).html.
Повний текст джерелаLefevre, Beyer Sabrina. "Développement d'un nouvel outil génétique pour l'étude du développement du tissu conducteur ventriculaire et application à l'analyse phénotypique du mutant Tbx1, un modèle du syndrome de DiGeorge." Thesis, Aix-Marseille, 2013. http://www.theses.fr/2013AIXM4102.
Повний текст джерелаThe ventricular conduction system (VCS) is responsible for the rapid propagation of electrical activity in the heart. The VCS is composed of the His bundle, the left and right bundle branches, and the peripheral Purkinje fibers. 1) The development of the VCS has been studied by using transgenic mice expressing the inducible Cre recombinase, introduced by homologous recombination at the locus of gene of connexin-40 (Cx40). Cx40 encodes for a protein expressing in the ventricular trabeculae and the VCS. The recombination is observed in the cells expressing Cx40 and in their descendants. My results suggest a progressive restriction of the fate of Cx40-positive trabeculae in conductive cardiomyocytes. Cx40-positive progenitors give rise to the formation of the compact myocardium and of the VCS when they are induced between E10.5-E14.5; while they participate only in the cardiomyocytes of VCS after E16.5. 2) The analysis of the VCS has been studied in a model of congenital heart malformation. The mutant Tbx1-/-, model of the DiGeorge syndrome, present a ventricular septal defect. Morphological defects of the VCS are found in Tbx1-/- hearts: an absence of right bundle branch and a non-compacted His bundle; which are correlated with functional defect. The phenotype observed in these mutants does not result from a defect of the activation in the genetic program being at the origin of the establishment in the VCS, but seems to be explain by the presence of a large ventricular septal defect, because it could block the progression of the progenitors of the VCS along the crest of the inter-ventricular septum
Jullian, Estelle. "Myogenic fate choice in the cardiopharyngeal mesoderm." Thesis, Aix-Marseille, 2019. http://www.theses.fr/2019AIXM0363.
Повний текст джерелаCardiopharyngeal mesoderm is localized at the cranial level of the mouse embryo, and contributes to head and neck muscles, derived from pharyngeal arches, and cardiac muscle. Study cardiopharyngeal mesoderm allows to understand some congenital abnormalities, which have cardiac and craniofacial defects, like DiGeorge syndrome. In mouse, retrospective clonal analysis allows to determinate a relationship between second heart field and specific branchiomeric muscles. Each pharyngeal arch gives rise to a specific branchiomeric muscles group which is linked to a part of the heart. Indeed, it has been showed in Chordates, a progenitor cell which is able to contribute to the heart and head muscles. My thesis objective is to investigate heart versus head muscles fate in cardiopharyngeal mesoderm. I wanted to understand the mechanism underlying heart and head muscles specification. The first part of the thesis will undercover the localization and the timeline of the potential bipotent myogenic progenitor cells present in cardiopharyngeal mesoderm and how they are regulated. The results showed that the conserved components are present but the regulation between each component seemed to be different in the mouse compared to Ciona. The second part and the three part of the thesis will undercover the heterogeneity intra- and inter-pharyngeal arches. Domains through the core of the arches could be observed and the fate of each domain needs to be explored
Francou, Alexandre. "Epithelial properties of Second Heart Field cardiac progenitor cells." Thesis, Aix-Marseille, 2015. http://www.theses.fr/2015AIXM4062.
Повний текст джерелаA major part of the heart is formed by progenitor cells called the second heart field, that contribute to rapid elongation of the heart tube. Defects in second heart field development leads to congenital heart malformations. Second heart field cells are localised in pharyngeal mesoderm in the dorsal pericardial wall. This study focuses on the epithelial properties of second heart field cells and first shows that these progenitors in the dorsal pericardial wall are epithelial and polarised, and form dynamic basal filopodia. Deletion of the transcription factor Tbx1 perturbs epithelial polarity and filopodia formation and upregulates the apical determinant aPKCζ. Treatment with an activator of aPKCζ reveals that epithelial integrity, polarity and basal filopodia are coupled to the progenitor status of second heart field cells. Next we evaluated planar polarity of second heart field cells in the dorsal pericardial wall. Cells are anisotropic, being stretched and elongated on an axis directed towards the arterial pole. This stretch results in oriented epithelial tension revealed by polarised actomyosin accumulation through a negative feedback loop. In the absence of cell addition to the cardiac poles oriented tension is absent. We identified a posterior region in the epithelium with high tension, elevated proliferation and a high level of active YAP/TAZ that may act as relay between tension and proliferation. Oriented tension orients the axis of cell division and the growth of the tissue on an axis toward the arterial pole, further promoting addition of the tissue to the pole. Biomechanical feedback may thus be an important driver of heart tube elongation
Rammah, Mayyasa. "Characterization of cardiopharyngeal progenitor cells and transcriptional regionalisation in the cardiac outflow tract." Thesis, Aix-Marseille, 2016. http://www.theses.fr/2016AIXM4061.
Повний текст джерелаThe vertebrate heart develops from the heart tube and the contribution of mesodermal progenitors termed second heart field (SHF). Perturbation in SHF addition leads to congenital heart defects (CHD). The outflow tract (OFT) myocardium is entirely derived from the SHF. Distinct regions of the embryonic OFT have been shown to give rise to subaortic and subpulmonary myocardium of the heart. The work described here focuses on SHF progenitor subpopulations in mouse giving rise to distinct OFT domains and characterizes the regional transcriptional identity and regulation of future subaortic and subpulmonary myocardium. We identified Notch-dependent subaortic myocardial SHF progenitors in anterior pharyngeal mesoderm. We demonstrated that Notch/Hes1 and Tbx1/Pparg cross regulatory cascades are important to establish functionally important OFT regional domains. Explant and embryo culture experiments revealed that Pparg is required for both the deployment of SHF cells and transcriptional regulation of the future subpulmonary myocardial domain. We also found that Dlk1, a negative regulator of Pparg, is expressed in the complementary subaortic domain upstream of Notch receptor activation and potentially participates in the establishment of OFT regional identity. We also report an overlapping transcriptional profile between future subaortic myocardium and subpopulation of epicardial cells at fetal stages. Finally, we provide evidence for the existence of conserved bipotential myogenic progenitors in cardiopharyngeal mesoderm coexpressing Nkx2-5 and Tbx1. Overall this work identifies novel pathways and genes in cardiopharyngeal mesoderm that may contribute to clinically relevant CHD
Rivera, Reyes Reginaldo [Verfasser], Andreas [Akademischer Betreuer] Kispert, Thomas [Akademischer Betreuer] Thum, and Ina [Akademischer Betreuer] Gruh. "Two complementary proteomic analyses uncover new regulators of TBX18 transcriptional function / Reginaldo Rivera Reyes ; Akademische Betreuer: Andreas Kispert, Thomas Thum, Ina Gruh ; Hannover Biomedical Research School, Institut für Molekularbiologie." Hannover : Bibliothek der Medizinischen Hochschule Hannover, 2020. http://d-nb.info/1212872134/34.
Повний текст джерелаTheriault, Mylene A. "Development and Validation of Quantitative PCR Assays for DNA-Based Newborn Screening of 22q11.2 Deletion Syndrome, Spinal Muscular Atrophy, Severe Combined Immunodeficiency and Congenital Cytomegalovirus Infection." Thesis, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/30318.
Повний текст джерелаWells, Simon J. "An investigation into the development and patterning of dorsal longitudinal ascending interneurons in Danio rerio." Thesis, 2011. http://hdl.handle.net/2440/71720.
Повний текст джерелаThesis (Ph.D.) -- University of Adelaide, School of Molecular and Biomedical Science, 2011
Farin, Henner [Verfasser]. "Function and regulation of the murine T-box genes Tbx15 and Tbx18 / von Henner Farin." 2009. http://d-nb.info/998929948/34.
Повний текст джерелаNguyen, Thi Hoang Lan. "Essays on the Economics of Education and Market Design." Thesis, 2020. https://doi.org/10.7916/d8-gtxr-tb16.
Повний текст джерела"Tbx18 and the epicardium in cardiac development and regenerative medicine." UNIVERSITY OF CALIFORNIA, SAN DIEGO, 2009. http://pqdtopen.proquest.com/#viewpdf?dispub=3336705.
Повний текст джерелаBussen, Markus [Verfasser]. "Die funktionelle Analyse des T-box-Transkriptionsfaktors Tbx18 in der Somitogenese der Maus / von Markus Bussen." 2005. http://d-nb.info/976695405/34.
Повний текст джерелаLiu, Li Yang. "Association of Tissue Promoter Methylation Levels of APC, RASSF1A, CYP26A1, and TBX15 with Prostate Cancer Progression." Thesis, 2012. http://hdl.handle.net/1807/33724.
Повний текст джерелаConcepcion, Daniel. "The roles of T and Tbx6 during gastrulation and determination of left/right asymmetry." Thesis, 2013. https://doi.org/10.7916/D8S75FPT.
Повний текст джерелаCamboa, Nuno Miguel Guimarães de Sá. "A role for the Tbx18 transcription factor in the development of mesenchymal lineages through embryogenesis and adulthood." Doctoral thesis, 2013. https://repositorio-aberto.up.pt/handle/10216/75027.
Повний текст джерелаCamboa, Nuno Miguel Guimarães de Sá. "A role for the Tbx18 transcription factor in the development of mesenchymal lineages through embryogenesis and adulthood." Tese, 2013. https://repositorio-aberto.up.pt/handle/10216/75027.
Повний текст джерелаMehmet, Mugayer Boral. "Etablierung molekulargenetischer Methoden zur Mutationsanalyse des TBX1-Gens unter Verwendung der denaturierenden Hochdruck-Flüssigkeits-chromatographie (DHPLC)." Doctoral thesis, 2011. https://ul.qucosa.de/id/qucosa%3A11425.
Повний текст джерелаHami, Danyal. "Zebrafish Cardiac Development Requires a Conserved Secondary Heart Field." Diss., 2011. http://hdl.handle.net/10161/5707.
Повний текст джерелаDespite its lack of septation, the tissue patterning of the arterial pole of the zebrafish is remarkably similar to the patterning of pulmonary and aortic arterial poles observed in mouse and chick. The secondary heart field (SHF) is a conserved developmental domain in avian and mammalian embryos that contributes myocardium and smooth muscle to the cardiac arterial pole. This field is part of the overall heart field, and its myocardial component has been fate mapped from the mesoderm to the heart in both mammals and birds. In this study I demonstrate that the population that gives rise to the arterial pole of the zebrafish can be traced from the epiblast, is a discrete part of the mesodermal heart field. This zebrafish SHF contributes myocardium after initial heart tube formation, giving rise to both smooth muscle and myocardium. I show that this field expresses Isl1, a transcription factor associated with the SHF in other species. I further show that differentiation, induced by Bmp signaling, occurs in this progenitor population as cells are added to the heart tube. Some molecular pathways required for SHF development in birds and mammals are conserved in teleosts, as Nkx2.5 and Nkx2.7 as well as Fgf8 regulate Bmp signaling in the zebrafish heart fields. Additionally, the transcription factor Tbx1 and the Sonic hedgehog pathway are necessary for normal development of the zebrafish arterial pole.
Dissertation