Programmed Cell Death in the Developing Somites Is Promoted By
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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. -
Notch Signaling Regulates the Differentiation of Neural Crest From
ß 2014. Published by The Company of Biologists Ltd | Journal of Cell Science (2014) 127, 2083–2094 doi:10.1242/jcs.145755 RESEARCH ARTICLE Notch signaling regulates the differentiation of neural crest from human pluripotent stem cells Parinya Noisa1,2, Carina Lund2, Kartiek Kanduri3, Riikka Lund3, Harri La¨hdesma¨ki3, Riitta Lahesmaa3, Karolina Lundin2, Hataiwan Chokechuwattanalert2, Timo Otonkoski4,5, Timo Tuuri5,6,* and Taneli Raivio2,4,*,` ABSTRACT Kokta et al., 2013). Neural crest cells originate from neuroectoderm at the border between the neural plate and the Neural crest cells are specified at the border between the neural epiderm (Meulemans and Bronner-Fraser, 2004), and they are plate and the epiderm. They are capable of differentiating into marked by the expression of genes that are specific for the neural- various somatic cell types, including craniofacial and peripheral plate border, such as DLX5, MSX1, MSX2 and ZIC1. Later, during nerve tissues. Notch signaling plays important roles during the neural-tube folding process, neural crest cells remain within neurogenesis; however, its function during human neural crest the neural folds and subsequently localize inside the dorsal development is poorly understood. Here, we generated self- portion of the neural tube. These premigratory neural crest cells renewing premigratory neural-crest-like cells (pNCCs) from human express specifier genes, such as SNAIL (also known as SNAI1), pluripotent stem cells (hPSCs) and investigated the roles of Notch SLUG (also known as SNAI2), SOX10 and TWIST1 (LaBonne and signaling during neural crest differentiation. pNCCs expressed Bronner-Fraser, 2000; Mancilla and Mayor, 1996). Following the various neural-crest-specifier genes, including SLUG (also known formation of the neural tube, premigratory neural crest cells as SNAI2), SOX10 and TWIST1, and were able to differentiate into undergo an epithelial-to-mesenchymal transition (EMT) and most neural crest derivatives. -
The Migration of Neural Crest Cells and the Growth of Motor Axons Through the Rostral Half of the Chick Somite
/. Embryol. exp. Morph. 90, 437-455 (1985) 437 Printed in Great Britain © The Company of Biologists Limited 1985 The migration of neural crest cells and the growth of motor axons through the rostral half of the chick somite M. RICKMANN, J. W. FAWCETT The Salk Institute and The Clayton Foundation for Research, California division, P.O. Box 85800, San Diego, CA 92138, U.S.A. AND R. J. KEYNES Department of Anatomy, University of Cambridge, Downing St, Cambridge, CB2 3DY, U.K. SUMMARY We have studied the pathway of migration of neural crest cells through the somites of the developing chick embryo, using the monoclonal antibodies NC-1 and HNK-1 to stain them. Crest cells, as they migrate ventrally from the dorsal aspect of the neural tube, pass through the lateral part of the sclerotome, but only through that part of the sclerotome which lies in the rostral half of each somite. This migration pathway is almost identical to the path which pre- sumptive motor axons take when they grow out from the neural tube shortly after the onset of neural crest migration. In order to see whether the ventral root axons are guided along this pathway by neural crest cells, we surgically excised the neural crest from a series of embryos, and examined the pattern of axon outgrowth approximately 24 h later. In somites which contained no neural crest cells, ventral root axons were still found only in the rostral half of the somite, although axonal growth was slightly delayed. These axons were surrounded by sheath cells, which had presumably migrated out of the neural tube, to a point about 50 jan proximal to the growth cones. -
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 Nature of Programmed Cell Death
Biological Theory https://doi.org/10.1007/s13752-018-0311-0 ORIGINAL ARTICLE The Nature of Programmed Cell Death Pierre M. Durand1 · Grant Ramsey2 Received: 14 March 2018 / Accepted: 10 October 2018 © Konrad Lorenz Institute for Evolution and Cognition Research 2018 Abstract In multicellular organisms, cells are frequently programmed to die. This makes good sense: cells that fail to, or are no longer playing important roles are eliminated. From the cell’s perspective, this also makes sense, since somatic cells in multicel- lular organisms require the cooperation of clonal relatives. In unicellular organisms, however, programmed cell death (PCD) poses a difficult and unresolved evolutionary problem. The empirical evidence for PCD in diverse microbial taxa has spurred debates about what precisely PCD means in the case of unicellular organisms (how it should be defined). In this article, we survey the concepts of PCD in the literature and the selective pressures associated with its evolution. We show that defini- tions of PCD have been almost entirely mechanistic and fail to separate questions concerning what PCD fundamentally is from questions about the kinds of mechanisms that realize PCD. We conclude that an evolutionary definition is best able to distinguish PCD from closely related phenomena. Specifically, we define “true” PCD as an adaptation for death triggered by abiotic or biotic environmental stresses. True PCD is thus not only an evolutionary product but must also have been a target of selection. Apparent PCD resulting from pleiotropy, genetic drift, or trade-offs is not true PCD. We call this “ersatz PCD.” Keywords Adaptation · Aging · Apoptosis · Price equation · Programmed cell death · Selection · Unicellular organisms Introduction in animal ontogeny, was made explicit several decades later (Glücksmann 1951; Lockshin and Williams 1964). -
Segmentation and Specification of the Drosophila Mesoderm
Downloaded from genesdev.cshlp.org on September 25, 2021 - Published by Cold Spring Harbor Laboratory Press Segmentation and specification of the Drosophila mesoderm Natalia Azpiazu, 1,3 Peter A. Lawrence, 2 Jean-Paul Vincent, 2 and Manfred Frasch 1'4 1Brookdale Center for Molecular Biology, Mount Sinai School of Medicine, New York, New York 10029 USA; 2Medical Research Council Laboratory of Molecular Biology, Cambridge CB2 2QH, UK Patterning of the developing mesoderm establishes primordia of the visceral, somatic, and cardiac tissues at defined anteroposterior and dorsoventral positions in each segment. Here we examine the mechanisms that locate and determine these primordia. We focus on the regulation of two mesodermal genes: bagpipe (hap), which defines the anlagen of the visceral musculature of the midgut, and serpent (srp), which marks the anlagen of the fat body. These two genes are activated in specific groups of mesodermal cells in the anterior portions of each parasegment. Other genes mark the anlagen of the cardiac and somatic mesoderm and these are expressed mainly in cells derived from posterior portions of each parasegment. Thus the parasegments appear to be subdivided, at least with respect to these genes, a subdivision that depends on pair-rule genes such as even-skipped (eve). We show with genetic mosaics that eve acts autonomously within the mesoderm. We also show that hedgehog (hh) and wingless (wg) mediate pair-rule gene functions in the mesoderm, probably partly by acting within the mesoderm and partly by inductive signaling from the ectoderm, hh is required for the normal activation of hap and srp in anterior portions of each parasegment, whereas wg is required to suppress bap and srp expression in posterior portions. -
Mesoderm Induction and the Control of Gastrulation in Xenopus Laevis:The
Development 108, 229-238 (1990) 229 Printed in Great Britain ©The Company of Biologists Limited 1990 Mesoderm induction and the control of gastrulation in Xenopus laevis: the roles of fibronectin and integrins J. C. SMITH1, K. SYMESH, R. O. HYNES2'3 and D. DeSIMONE3* ' Laboratory of Embryogenesis, National Institute for Medical Research, The Ridgeway, Mill Hill, London NW71AA, UK ^Howard Hughes Medical Institute and ^Center for Cancer Research, Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA * Present address: University of Virginia, Health Sciences Center, Department of Anatomy and Cell Biology, Box 439, School of Medicine, Charlottesville, VA 22908, USA t Present address: Department of Cell and Molecular Biology, 385 LSA, University of California, Berkeley, CA 94720, USA Summary Exposure of isolated Xenopus animal pole ectoderm to diated cell migration is not required for convergent the XTC mesoderm-inducing factor (XTC-MIF) causes extension. the tissue to undergo gastrulation-like movements. In We have investigated the molecular basis of XTC- this paper, we take advantage of this observation to MIF-induced gastrulation-like movements by measuring investigate the control of various aspects of gastrulation rates of synthesis of fibronectin and of the integrin f}y in Xenopus. chain in induced and control explants. No significant Blastomcres derived from induced animal pole regions differences were observed, and this suggests that gastru- are able, like marginal zone cells, but unlike control lation is not initiated simply by control of synthesis of animal pole blastomeres, to spread and migrate on a these molecules. In future work, we intend to investigate fibronectin-coated surface. -
Fate of the Mammalian Cardiac Neural Crest
Development 127, 1607-1616 (2000) 1607 Printed in Great Britain © The Company of Biologists Limited 2000 DEV4300 Fate of the mammalian cardiac neural crest Xiaobing Jiang1,3, David H. Rowitch4,*, Philippe Soriano5, Andrew P. McMahon4 and Henry M. Sucov2,3,‡ Departments of 1Biological Sciences and 2Cell & Neurobiology, 3Institute for Genetic Medicine, Keck School of Medicine, University of Southern California, 2250 Alcazar St., IGM 240, Los Angeles, CA 90033, USA 4Department of Molecular and Cell Biology, Harvard University, 16 Divinity Ave., Cambridge, MA 02138, USA 5Program in Developmental Biology, Division of Basic Sciences, A2-025, Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue North, PO Box 19024, Seattle, WA 98109, USA *Present address: Department of Pediatric Oncology, Dana Farber Cancer Institute, 44 Binney St., Boston, MA 02115, USA ‡Author for correspondence (e-mail: [email protected]) Accepted 26 January; published on WWW 21 March 2000 SUMMARY A subpopulation of neural crest termed the cardiac neural of these vessels. Labeled cells populate the crest is required in avian embryos to initiate reorganization aorticopulmonary septum and conotruncal cushions prior of the outflow tract of the developing cardiovascular to and during overt septation of the outflow tract, and system. In mammalian embryos, it has not been previously surround the thymus and thyroid as these organs form. experimentally possible to study the long-term fate of this Neural-crest-derived mesenchymal cells are abundantly population, although there is strong inference that a similar distributed in midgestation (E9.5-12.5), and adult population exists and is perturbed in a number of genetic derivatives of the third, fourth and sixth pharyngeal arch and teratogenic contexts. -
Stages of Embryonic Development of the Zebrafish
DEVELOPMENTAL DYNAMICS 2032553’10 (1995) Stages of Embryonic Development of the Zebrafish CHARLES B. KIMMEL, WILLIAM W. BALLARD, SETH R. KIMMEL, BONNIE ULLMANN, AND THOMAS F. SCHILLING Institute of Neuroscience, University of Oregon, Eugene, Oregon 97403-1254 (C.B.K., S.R.K., B.U., T.F.S.); Department of Biology, Dartmouth College, Hanover, NH 03755 (W.W.B.) ABSTRACT We describe a series of stages for Segmentation Period (10-24 h) 274 development of the embryo of the zebrafish, Danio (Brachydanio) rerio. We define seven broad peri- Pharyngula Period (24-48 h) 285 ods of embryogenesis-the zygote, cleavage, blas- Hatching Period (48-72 h) 298 tula, gastrula, segmentation, pharyngula, and hatching periods. These divisions highlight the Early Larval Period 303 changing spectrum of major developmental pro- Acknowledgments 303 cesses that occur during the first 3 days after fer- tilization, and we review some of what is known Glossary 303 about morphogenesis and other significant events that occur during each of the periods. Stages sub- References 309 divide the periods. Stages are named, not num- INTRODUCTION bered as in most other series, providing for flexi- A staging series is a tool that provides accuracy in bility and continued evolution of the staging series developmental studies. This is because different em- as we learn more about development in this spe- bryos, even together within a single clutch, develop at cies. The stages, and their names, are based on slightly different rates. We have seen asynchrony ap- morphological features, generally readily identi- pearing in the development of zebrafish, Danio fied by examination of the live embryo with the (Brachydanio) rerio, embryos fertilized simultaneously dissecting stereomicroscope. -
Snapshot: BCL-2 Proteins J
SnapShot: BCL-2 Proteins J. Marie Hardwick and Richard J. Youle Johns Hopkins, Baltimore, MD 21205, USA and NIH/NINDS, Bethesda, MD 20892, USA 404 Cell 138, July 24, 2009 ©2009 Elsevier Inc. DOI 10.1016/j.cell.2009.07.003 See online version for legend and references. SnapShot: BCL-2 Proteins J. Marie Hardwick and Richard J. Youle Johns Hopkins, Baltimore, MD 21205, USA and NIH/NINDS, Bethesda, MD 20892, USA BCL-2 family proteins regulate apoptotic cell death. BCL-2 proteins localize to intracellular membranes such as endoplasmic reticulum and mitochondria, and some fam- ily members translocate from the cytoplasm to mitochondria following a cell death stimulus. The prototypical family member Bcl-2 was originally identified at chromo- some translocation breakpoints in human follicular lymphoma and was subsequently shown to promote tumorigenesis by inhibiting cell death rather than by promoting cell-cycle progression. BCL-2 family proteins have traditionally been classified according to their function and their BCL-2 homology (BH) motifs. The general categories include multidomain antiapoptotic proteins (BH1-BH4), multidomain proapoptotic proteins (BH1-BH3), and proapoptotic BH3-only proteins (see Table 1). In the traditional view, anti-death BCL-2 family members in healthy cells hold pro-death BCL-2 family members in check. Upon receiving a death stimulus, BH3-only proteins inactivate the protective BCL-2 proteins, forcing them to release their pro-death partners. These pro-death BCL-2 family proteins homo-oligomerize to create pores in the mitochondrial outer membrane, resulting in cytochrome c release into the cytoplasm, which leads to caspase activation and cell death. -
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. -
Sonic Hedgehog a Neural Tube Anti-Apoptotic Factor 4013 Other Side of the Neural Plate, Remaining in Contact with Midline Cells, RESULTS Was Used As a Control
Development 128, 4011-4020 (2001) 4011 Printed in Great Britain © The Company of Biologists Limited 2001 DEV2740 Anti-apoptotic role of Sonic hedgehog protein at the early stages of nervous system organogenesis Jean-Baptiste Charrier, Françoise Lapointe, Nicole M. Le Douarin and Marie-Aimée Teillet* Institut d’Embryologie Cellulaire et Moléculaire, CNRS FRE2160, 49bis Avenue de la Belle Gabrielle, 94736 Nogent-sur-Marne Cedex, France *Author for correspondence (e-mail: [email protected]) Accepted 19 July 2001 SUMMARY In vertebrates the neural tube, like most of the embryonic notochord or a floor plate fragment in its vicinity. The organs, shows discreet areas of programmed cell death at neural tube can also be recovered by transplanting it into several stages during development. In the chick embryo, a stage-matched chick embryo having one of these cell death is dramatically increased in the developing structures. In addition, cells engineered to produce Sonic nervous system and other tissues when the midline cells, hedgehog protein (SHH) can mimic the effect of the notochord and floor plate, are prevented from forming by notochord and floor plate cells in in situ grafts and excision of the axial-paraxial hinge (APH), i.e. caudal transplantation experiments. SHH can thus counteract a Hensen’s node and rostral primitive streak, at the 6-somite built-in cell death program and thereby contribute to organ stage (Charrier, J. B., Teillet, M.-A., Lapointe, F. and Le morphogenesis, in particular in the central nervous system. Douarin, N. M. (1999). Development 126, 4771-4783). In this paper we demonstrate that one day after APH excision, Key words: Apoptosis, Avian embryo, Cell death, Cell survival, when dramatic apoptosis is already present in the neural Floor plate, Notochord, Quail/chick, Shh, Somite, Neural tube, tube, the latter can be rescued from death by grafting a Spinal cord INTRODUCTION generally induces an inflammatory response.