From Bipotent Neuromesodermal Progenitors to Neural-Mesodermal Interactions During Embryonic Development
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3 Embryology and Development
BIOL 6505 − INTRODUCTION TO FETAL MEDICINE 3. EMBRYOLOGY AND DEVELOPMENT Arlet G. Kurkchubasche, M.D. INTRODUCTION Embryology – the field of study that pertains to the developing organism/human Basic embryology –usually taught in the chronologic sequence of events. These events are the basis for understanding the congenital anomalies that we encounter in the fetus, and help explain the relationships to other organ system concerns. Below is a synopsis of some of the critical steps in embryogenesis from the anatomic rather than molecular basis. These concepts will be more intuitive and evident in conjunction with diagrams and animated sequences. This text is a synopsis of material provided in Langman’s Medical Embryology, 9th ed. First week – ovulation to fertilization to implantation Fertilization restores 1) the diploid number of chromosomes, 2) determines the chromosomal sex and 3) initiates cleavage. Cleavage of the fertilized ovum results in mitotic divisions generating blastomeres that form a 16-cell morula. The dense morula develops a central cavity and now forms the blastocyst, which restructures into 2 components. The inner cell mass forms the embryoblast and outer cell mass the trophoblast. Consequences for fetal management: Variances in cleavage, i.e. splitting of the zygote at various stages/locations - leads to monozygotic twinning with various relationships of the fetal membranes. Cleavage at later weeks will lead to conjoined twinning. Second week: the week of twos – marked by bilaminar germ disc formation. Commences with blastocyst partially embedded in endometrial stroma Trophoblast forms – 1) cytotrophoblast – mitotic cells that coalesce to form 2) syncytiotrophoblast – erodes into maternal tissues, forms lacunae which are critical to development of the uteroplacental circulation. -
The Zebrafish Presomitic Mesoderm Elongates Through Compression-Extension
bioRxiv preprint doi: https://doi.org/10.1101/2021.03.11.434927; this version posted March 11, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. The zebrafish presomitic mesoderm elongates through compression-extension Lewis Thomson1, Leila Muresan2 and Benjamin Steventon1* 1) Department of Genetics, University of Cambridge, Cambridge, UK, CB2 3EH 2) Cambridge Advanced Imaging Centre, University of Cambridge, Cambridge, UK *[email protected] Abstract In vertebrate embryos the presomitic mesoderm become progressively segmented into somites at the anterior end while extending along the anterior- posterior axis. A commonly adopted model to explain how this tissue elongates is that of posterior growth, driven in part by the addition of new cells from uncommitted progenitor populations in the tailbud. However, in zebrafish, much of somitogenesis is associated with an absence of overall volume increase and posterior progenitors do not contribute new cells until the final stages of somitogenesis. Here, we perform a comprehensive 3D morphometric analysis of the paraxial mesoderm and reveal that extension is linked to a volumetric decrease, compression in both dorsal-ventral and medio-lateral axes, and an increase in cell density. We also find that individual cells decrease in their cell volume over successive somite stages. Live cell tracking confirms that much of this tissue deformation occurs within the presomitic mesoderm progenitor zone and is associated with non-directional rearrangement. Furthermore, unlike the trunk somites that are laid down during gastrulation, tail somites develop from a tissue that can continue to elongate in the absence of functional PCP signalling. -
Vocabulario De Morfoloxía, Anatomía E Citoloxía Veterinaria
Vocabulario de Morfoloxía, anatomía e citoloxía veterinaria (galego-español-inglés) Servizo de Normalización Lingüística Universidade de Santiago de Compostela COLECCIÓN VOCABULARIOS TEMÁTICOS N.º 4 SERVIZO DE NORMALIZACIÓN LINGÜÍSTICA Vocabulario de Morfoloxía, anatomía e citoloxía veterinaria (galego-español-inglés) 2008 UNIVERSIDADE DE SANTIAGO DE COMPOSTELA VOCABULARIO de morfoloxía, anatomía e citoloxía veterinaria : (galego-español- inglés) / coordinador Xusto A. Rodríguez Río, Servizo de Normalización Lingüística ; autores Matilde Lombardero Fernández ... [et al.]. – Santiago de Compostela : Universidade de Santiago de Compostela, Servizo de Publicacións e Intercambio Científico, 2008. – 369 p. ; 21 cm. – (Vocabularios temáticos ; 4). - D.L. C 2458-2008. – ISBN 978-84-9887-018-3 1.Medicina �������������������������������������������������������������������������veterinaria-Diccionarios�������������������������������������������������. 2.Galego (Lingua)-Glosarios, vocabularios, etc. políglotas. I.Lombardero Fernández, Matilde. II.Rodríguez Rio, Xusto A. coord. III. Universidade de Santiago de Compostela. Servizo de Normalización Lingüística, coord. IV.Universidade de Santiago de Compostela. Servizo de Publicacións e Intercambio Científico, ed. V.Serie. 591.4(038)=699=60=20 Coordinador Xusto A. Rodríguez Río (Área de Terminoloxía. Servizo de Normalización Lingüística. Universidade de Santiago de Compostela) Autoras/res Matilde Lombardero Fernández (doutora en Veterinaria e profesora do Departamento de Anatomía e Produción Animal. -
Slit1 and Slit2 Cooperate to Prevent Premature Midline Crossing of Retinal Axons in the Mouse Visual System
Neuron, Vol. 33, 219–232, January 17, 2002, Copyright 2002 by Cell Press Slit1 and Slit2 Cooperate to Prevent Premature Midline Crossing of Retinal Axons in the Mouse Visual System Andrew S. Plump,1,2,6 Lynda Erskine,3,6,7 midbrain. Some axons do not cross, projecting to the Christelle Sabatier,1 Katja Brose,1 same targets but ipsilaterally. As with many other brain Charles J. Epstein,2 Corey S. Goodman,4 commissures, formation of the optic chiasm occurs at Carol A. Mason,3 and Marc Tessier-Lavigne1,5,8 an invariant position along the antero-posterior axis of 1 Departments of Anatomy and the developing forebrain. Mechanisms must therefore of Biochemistry and Biophysics exist not only to direct divergence at the midline but also Howard Hughes Medical Institute to prevent retinal axons from crossing at inappropriate 2 Division of Medical Genetics locations. University of California, San Francisco While significant progress in recent years has led to San Francisco, California 94143 a greater understanding of the factors that help establish 3 Departments of Pathology, Anatomy, a topographic map within the retina and its targets and Cell Biology (O’Leary et al., 1999), less progress has been made in Center for Neurobiology and Behavior identifying the rudimentary axon guidance cues that es- Columbia University College of Physicians tablish the basic trajectories within the vertebrate visual and Surgeons system, particularly those that function at the midline New York, New York 10032 to regulate the positioning and decussation of retinal 4 Department of Molecular and Cell Biology axons. In mammals, chondroitin sulfate proteoglycans Howard Hughes Medical Institute (CSPGs), L1, netrin-1, and specific EphB ligands are University of California, Berkeley important for guidance within the retina (Birgbauer et Berkeley, California 94720 al., 2000; Brittis et al., 1992, 1995; Deiner et al., 1997; Snow et al., 1991). -
The Genetic Basis of Mammalian Neurulation
REVIEWS THE GENETIC BASIS OF MAMMALIAN NEURULATION Andrew J. Copp*, Nicholas D. E. Greene* and Jennifer N. Murdoch‡ More than 80 mutant mouse genes disrupt neurulation and allow an in-depth analysis of the underlying developmental mechanisms. Although many of the genetic mutants have been studied in only rudimentary detail, several molecular pathways can already be identified as crucial for normal neurulation. These include the planar cell-polarity pathway, which is required for the initiation of neural tube closure, and the sonic hedgehog signalling pathway that regulates neural plate bending. Mutant mice also offer an opportunity to unravel the mechanisms by which folic acid prevents neural tube defects, and to develop new therapies for folate-resistant defects. 6 ECTODERM Neurulation is a fundamental event of embryogenesis distinct locations in the brain and spinal cord .By The outer of the three that culminates in the formation of the neural tube, contrast, the mechanisms that underlie the forma- embryonic (germ) layers that which is the precursor of the brain and spinal cord. A tion, elevation and fusion of the neural folds have gives rise to the entire central region of specialized dorsal ECTODERM, the neural plate, remained elusive. nervous system, plus other organs and embryonic develops bilateral neural folds at its junction with sur- An opportunity has now arisen for an incisive analy- structures. face (non-neural) ectoderm. These folds elevate, come sis of neurulation mechanisms using the growing battery into contact (appose) in the midline and fuse to create of genetically targeted and other mutant mouse strains NEURAL CREST the neural tube, which, thereafter, becomes covered by in which NTDs form part of the mutant phenotype7.At A migratory cell population that future epidermal ectoderm. -
The GATA2 Transcription Factor Negatively Regulates the Proliferation of Neuronal Progenitors
RESEARCH ARTICLE 2155 Development 133, 2155-2165 (2006) doi:10.1242/dev.02377 The GATA2 transcription factor negatively regulates the proliferation of neuronal progenitors Abeer El Wakil*, Cédric Francius*,†, Annie Wolff, Jocelyne Pleau-Varet† and Jeannette Nardelli†,§ Postmitotic neurons are produced from a pool of cycling progenitors in an orderly fashion that requires proper spatial and temporal coordination of proliferation, fate determination, differentiation and morphogenesis. This probably relies on complex interplay between mechanisms that control cell cycle, specification and differentiation. In this respect, we have studied the possible implication of GATA2, a transcription factor that is involved in several neuronal specification pathways, in the control of the proliferation of neural progenitors in the embryonic spinal cord. Using gain- and loss-of-function manipulations, we have shown that Gata2 can drive neural progenitors out of the cycle and, to some extent, into differentiation. This correlates with the control of cyclin D1 transcription and of the expression of the p27/Kip1 protein. Interestingly, this functional aspect is not only associated with silencing of the Notch pathway but also appears to be independent of proneural function. Consistently, GATA2 also controls the proliferation capacity of mouse embryonic neuroepithelial cells in culture. Indeed, Gata2 inactivation enhances the proliferation rate in these cells. By contrast, GATA2 overexpression is sufficient to force such cells and neuroblastoma cells to stop dividing but not to drive either type of cell into differentiation. Furthermore, a non-cell autonomous effect of Gata2 expression was observed in vivo as well as in vitro. Hence, our data have provided evidence for the ability of Gata2 to inhibit the proliferation of neural progenitors, and they further suggest that, in this regard, Gata2 can operate independently of neuronal differentiation. -
Supplementary Table 1: Adhesion Genes Data Set
Supplementary Table 1: Adhesion genes data set PROBE Entrez Gene ID Celera Gene ID Gene_Symbol Gene_Name 160832 1 hCG201364.3 A1BG alpha-1-B glycoprotein 223658 1 hCG201364.3 A1BG alpha-1-B glycoprotein 212988 102 hCG40040.3 ADAM10 ADAM metallopeptidase domain 10 133411 4185 hCG28232.2 ADAM11 ADAM metallopeptidase domain 11 110695 8038 hCG40937.4 ADAM12 ADAM metallopeptidase domain 12 (meltrin alpha) 195222 8038 hCG40937.4 ADAM12 ADAM metallopeptidase domain 12 (meltrin alpha) 165344 8751 hCG20021.3 ADAM15 ADAM metallopeptidase domain 15 (metargidin) 189065 6868 null ADAM17 ADAM metallopeptidase domain 17 (tumor necrosis factor, alpha, converting enzyme) 108119 8728 hCG15398.4 ADAM19 ADAM metallopeptidase domain 19 (meltrin beta) 117763 8748 hCG20675.3 ADAM20 ADAM metallopeptidase domain 20 126448 8747 hCG1785634.2 ADAM21 ADAM metallopeptidase domain 21 208981 8747 hCG1785634.2|hCG2042897 ADAM21 ADAM metallopeptidase domain 21 180903 53616 hCG17212.4 ADAM22 ADAM metallopeptidase domain 22 177272 8745 hCG1811623.1 ADAM23 ADAM metallopeptidase domain 23 102384 10863 hCG1818505.1 ADAM28 ADAM metallopeptidase domain 28 119968 11086 hCG1786734.2 ADAM29 ADAM metallopeptidase domain 29 205542 11085 hCG1997196.1 ADAM30 ADAM metallopeptidase domain 30 148417 80332 hCG39255.4 ADAM33 ADAM metallopeptidase domain 33 140492 8756 hCG1789002.2 ADAM7 ADAM metallopeptidase domain 7 122603 101 hCG1816947.1 ADAM8 ADAM metallopeptidase domain 8 183965 8754 hCG1996391 ADAM9 ADAM metallopeptidase domain 9 (meltrin gamma) 129974 27299 hCG15447.3 ADAMDEC1 ADAM-like, -
Mouse Slit1 Conditional Knockout Project (CRISPR/Cas9)
https://www.alphaknockout.com Mouse Slit1 Conditional Knockout Project (CRISPR/Cas9) Objective: To create a Slit1 conditional knockout Mouse model (C57BL/6J) by CRISPR/Cas-mediated genome engineering. Strategy summary: The Slit1 gene (NCBI Reference Sequence: NM_015748 ; Ensembl: ENSMUSG00000025020 ) is located on Mouse chromosome 19. 37 exons are identified, with the ATG start codon in exon 1 and the TAA stop codon in exon 37 (Transcript: ENSMUST00000025993). Exon 6~8 will be selected as conditional knockout region (cKO region). Deletion of this region should result in the loss of function of the Mouse Slit1 gene. To engineer the targeting vector, homologous arms and cKO region will be generated by PCR using BAC clone RP23-332I24 as template. Cas9, gRNA and targeting vector will be co-injected into fertilized eggs for cKO Mouse production. The pups will be genotyped by PCR followed by sequencing analysis. Note: Mice homozygous for a reporter allele exhibit normal interneuron numbers and morphology. Exon 6 starts from about 10.58% of the coding region. The knockout of Exon 6~8 will result in frameshift of the gene. The size of intron 5 for 5'-loxP site insertion: 992 bp, and the size of intron 8 for 3'-loxP site insertion: 1117 bp. The size of effective cKO region: ~1526 bp. The cKO region does not have any other known gene. Page 1 of 7 https://www.alphaknockout.com Overview of the Targeting Strategy Wildtype allele 5' gRNA region gRNA region 3' 1 5 6 7 8 9 10 11 37 Targeting vector Targeted allele Constitutive KO allele (After Cre recombination) Legends Exon of mouse Slit1 Homology arm cKO region loxP site Page 2 of 7 https://www.alphaknockout.com Overview of the Dot Plot Window size: 10 bp Forward Reverse Complement Sequence 12 Note: The sequence of homologous arms and cKO region is aligned with itself to determine if there are tandem repeats. -
Understanding Paraxial Mesoderm Development and Sclerotome Specification for Skeletal Repair Shoichiro Tani 1,2, Ung-Il Chung2,3, Shinsuke Ohba4 and Hironori Hojo2,3
Tani et al. Experimental & Molecular Medicine (2020) 52:1166–1177 https://doi.org/10.1038/s12276-020-0482-1 Experimental & Molecular Medicine REVIEW ARTICLE Open Access Understanding paraxial mesoderm development and sclerotome specification for skeletal repair Shoichiro Tani 1,2, Ung-il Chung2,3, Shinsuke Ohba4 and Hironori Hojo2,3 Abstract Pluripotent stem cells (PSCs) are attractive regenerative therapy tools for skeletal tissues. However, a deep understanding of skeletal development is required in order to model this development with PSCs, and for the application of PSCs in clinical settings. Skeletal tissues originate from three types of cell populations: the paraxial mesoderm, lateral plate mesoderm, and neural crest. The paraxial mesoderm gives rise to the sclerotome mainly through somitogenesis. In this process, key developmental processes, including initiation of the segmentation clock, formation of the determination front, and the mesenchymal–epithelial transition, are sequentially coordinated. The sclerotome further forms vertebral columns and contributes to various other tissues, such as tendons, vessels (including the dorsal aorta), and even meninges. To understand the molecular mechanisms underlying these developmental processes, extensive studies have been conducted. These studies have demonstrated that a gradient of activities involving multiple signaling pathways specify the embryonic axis and induce cell-type-specific master transcription factors in a spatiotemporal manner. Moreover, applying the knowledge of mesoderm development, researchers have attempted to recapitulate the in vivo development processes in in vitro settings, using mouse and human PSCs. In this review, we summarize the state-of-the-art understanding of mesoderm development and in vitro modeling of mesoderm development using PSCs. We also discuss future perspectives on the use of PSCs to generate skeletal tissues for basic research and clinical applications. -
Slit Proteins: Molecular Guidance Cues for Cells Ranging from Neurons to Leukocytes Kit Wong, Hwan Tae Park*, Jane Y Wu* and Yi Rao†
583 Slit proteins: molecular guidance cues for cells ranging from neurons to leukocytes Kit Wong, Hwan Tae Park*, Jane Y Wu* and Yi Rao† Recent studies of molecular guidance cues including the Slit midline glial cells was thought to be abnormal [2,3]. family of secreted proteins have provided new insights into the Projection of the commissural axons was also abnormal: mechanisms of cell migration. Initially discovered in the nervous instead of crossing the midline once before projecting system, Slit functions through its receptor, Roundabout, and an longitudinally, the commissural axons from two sides of the intracellular signal transduction pathway that includes the nerve cord are fused at the midline in slit mutants [2,3]. Abelson kinase, the Enabled protein, GTPase activating proteins Because the midline glial cells are known to be important and the Rho family of small GTPases. Interestingly, Slit also in axon guidance, the commissural axon phenotype in slit appears to use Roundabout to control leukocyte chemotaxis, mutants was initially thought to be secondary to the cell- which occurs in contexts different from neuronal migration, differentiation phenotype [3]. suggesting a fundamental conservation of mechanisms guiding the migration of distinct types of somatic cells. In early 1999, results from three groups demonstrated independently that Slit functioned as an extracellular cue Addresses to guide axon pathfinding [4–6], to promote axon branching Department of Anatomy and Neurobiology, and *Departments of [7], and to control neuronal migration [8]. The functional Pediatrics and Molecular Biology and Pharmacology, Box 8108, roles of Slit in axon guidance and neuronal migration were Washington University School of Medicine, 660 S Euclid Avenue St Louis, soon supported by other studies in Drosophila [9] and in Missouri 63110, USA *e-mail: [email protected] vertebrates [10–14]. -
Six3 Repression of Wnt Signaling in the Anterior Neuroectoderm Is Essential for Vertebrate Forebrain Development
Downloaded from genesdev.cshlp.org on September 24, 2021 - Published by Cold Spring Harbor Laboratory Press Six3 repression of Wnt signaling in the anterior neuroectoderm is essential for vertebrate forebrain development Oleg V. Lagutin,1 Changqi C. Zhu,1 Daisuke Kobayashi,2 Jacek Topczewski,3 Kenji Shimamura,2 Luis Puelles,4 Helen R.C. Russell,1 Peter J. McKinnon,1 Lilianna Solnica-Krezel,3 and Guillermo Oliver1,5 1Department of Genetics, St. Jude Children’s Research Hospital, Memphis, Tennessee 38105-2794, USA; 2Department of Neurobiology, Graduate School of Medicine, University of Tokyo, Bunkyo-ku, Tokyo 113-0033, Japan; 3 Department of Biological Sciences, Vanderbilt University, Nashville, Tennessee 37232, USA; 4Department of Morphological Sciences, Faculty of Medicine, University of Murcia, E-30100 Murcia, Spain In vertebrate embryos, formation of anterior neural structures requires suppression of Wnt signals emanating from the paraxial mesoderm and midbrain territory. In Six3−/− mice, the prosencephalon was severely truncated, and the expression of Wnt1 was rostrally expanded, a finding that indicates that the mutant head was posteriorized. Ectopic expression of Six3 in chick and fish embryos, together with the use of in vivo and in vitro DNA-binding assays, allowed us to determine that Six3 is a direct negative regulator of Wnt1 expression. These results, together with those of phenotypic rescue of headless/tcf3 zebrafish mutants by mouse Six3, demonstrate that regionalization of the vertebrate forebrain involves repression of Wnt1 expression by Six3 within the anterior neuroectoderm. Furthermore, these results support the hypothesis that a Wnt signal gradient specifies posterior fates in the anterior neural plate. [Keywords: Six3; forebrain; mouse; homeobox; Wnt; zebrafish] Received November 15, 2002; revised version accepted December 9, 2002. -
Genes for Extracellular Matrix-Degrading Metalloproteinases and Their Inhibitor, TIMP, Are Expressed During Early Mammalian Development
Downloaded from genesdev.cshlp.org on September 23, 2021 - Published by Cold Spring Harbor Laboratory Press Genes for extracellular matrix-degrading metalloproteinases and their inhibitor, TIMP, are expressed during early mammalian development Carol A. Brenner, 1 Richard R. Adler, 2 Daniel A. Rappolee, Roger A. Pedersen, and Zena Werb 3 Laboratory of Radiobiology and Environmental Health, and Department of Anatomy, University of California, San Francisco, California 94143-0750 USA Extracellular matrix (ECM) remodeling accompanies cell migration, cell--cell interactions, embryo expansion, uterine implantation, and tissue invasion during mammalian embryogenesis. We have found that mouse embryos secrete functional ECM-degrading metalloproteinases, including collagenase and stromelysin, that are inhibitable by the tissue inhibitor of metalloproteinases (TIMP) and that are regulated during peri-implantation development and endoderm differentiation, mRNA transcripts for collagenase, stromelysin, and TIMP were detected as maternal transcripts in the unfertilized egg, were present at the zygote and cleavage stages, and increased at the blastocyst stage and with endoderm differentiation. These data suggest that metalloproteinases function in cell-ECM interactions during growth, development, and implantation of mammalian embryos. [Key Words: Collagenase; stromelysin; polymerase chain reaction; tissue inhibitor of metalloproteinases; maternal mRNA; endoderm differentiation] January 31, 1989; revised version accepted March 15, 1989. The extracellular matrix (ECM) forms a substrate for cell 1988}. The activity of these proteinases is regulated by attachment and migration and directs cell form and the tissue inhibitor of metalloproteinases {TIMPI function through cell-ECM interactions. ECM macro- (Murphy et al. 1985; Herron et al. 1986a, b; Gavrilovic et molecules first appear in the mammalian embryo in the al.