Development and Control of Tissue Separation at Gastrulation in Xenopus
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Gastrulation
Embryology of the spine and spinal cord Andrea Rossi, MD Neuroradiology Unit Istituto Giannina Gaslini Hospital Genoa, Italy [email protected] LEARNING OBJECTIVES: LEARNING OBJECTIVES: 1) To understand the basics of spinal 1) To understand the basics of spinal cord development cord development 2) To understand the general rules of the 2) To understand the general rules of the development of the spine development of the spine 3) To understand the peculiar variations 3) To understand the peculiar variations to the normal spine plan that occur at to the normal spine plan that occur at the CVJ the CVJ Summary of week 1 Week 2-3 GASTRULATION "It is not birth, marriage, or death, but gastrulation, which is truly the most important time in your life." Lewis Wolpert (1986) Gastrulation Conversion of the embryonic disk from a bilaminar to a trilaminar arrangement and establishment of the notochord The three primary germ layers are established The basic body plan is established, including the physical construction of the rudimentary primary body axes As a result of the movements of gastrulation, cells are brought into new positions, allowing them to interact with cells that were initially not near them. This paves the way for inductive interactions, which are the hallmark of neurulation and organogenesis Day 16 H E Day 15 Dorsal view of a 0.4 mm embryo BILAMINAR DISK CRANIAL Epiblast faces the amniotic sac node Hypoblast Primitive pit (primitive endoderm) faces the yolk sac Primitive streak CAUDAL Prospective notochordal cells Dias Dias During -
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. -
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. -
Floral Ontogeny and Histogenesis in Leguminosae. Kittie Sue Derstine Louisiana State University and Agricultural & Mechanical College
Louisiana State University LSU Digital Commons LSU Historical Dissertations and Theses Graduate School 1988 Floral Ontogeny and Histogenesis in Leguminosae. Kittie Sue Derstine Louisiana State University and Agricultural & Mechanical College Follow this and additional works at: https://digitalcommons.lsu.edu/gradschool_disstheses Recommended Citation Derstine, Kittie Sue, "Floral Ontogeny and Histogenesis in Leguminosae." (1988). LSU Historical Dissertations and Theses. 4493. https://digitalcommons.lsu.edu/gradschool_disstheses/4493 This Dissertation is brought to you for free and open access by the Graduate School at LSU Digital Commons. It has been accepted for inclusion in LSU Historical Dissertations and Theses by an authorized administrator of LSU Digital Commons. For more information, please contact [email protected]. INFORMATION TO USERS The most advanced technology has been used to photo graph and reproduce this manuscript from the microfilm master. UMI films the original text directly from the copy submitted. Thus, some dissertation copies are in typewriter face, while others may be from a computer printer. In the unlikely event that the author did not send UMI a complete manuscript and there are missing pages, these will be noted. Also, if unauthorized copyrighted material had to be removed, a note will indicate the deletion. Oversize materials (e.g., maps, drawings, charts) are re produced by sectioning the original, beginning at the upper left-hand corner and continuing from left to right in equal sections with small overlaps. Each oversize page is available as one exposure on a standard 35 mm slide or as a 17" x 23" black and white photographic print for an additional charge. Photographs included in the original manuscript have been reproduced xerographically in this copy. -
THE HISTOGENESIS of BONE by C
THE HISTOGENESIS OF BONE By C. WITHERINGTON STUMP, M.D. From the Laboratory of the Royal College of Physicians, Edinburgh INTRODUCTION FEW processes in histogenesis have been the subject of so much controversy, as that of the development of bone. On reading over the literature, even incompletely, the conviction came with considerable force, that the chief cause of the inability of observers, to find agreement, lay in technical difficulties in obtaining satisfactory preparations for cytological study. The divergent opinions are accounted for by the singular absence of detailed work-a fact which has fostered and sustained a controversy into which there is no need to enter. Microscopic evidence of cell growth and change is yielded by slight morpho- logical variations in different individual cells. Slight differences in structure, and staining reaction, are the only factors by means of which variations can be determined. It is essential, with cells examined in a dead state, to have a standard of fixation which registers detailed and minute structure. Further, it is constantly to be borne in mind, that merely a phase of life is represented, through which the cell was passing at the time of its death. Especially is this so in actively growing, developing tissue, where many structural tendencies are manifested by the act of growth. Thus, in fixed primitive tissue, the ontogeny of any given cell is a matter of conjecture, and it can only be defined with any degree of certainty by an experienced observer. It would be redundant to attempt an historical survey of the contributions to the problem of osteogenesis. -
(Pro)Insulin Correlates with Prevention of Apoptosis
Proc. Natl. Acad. Sci. USA Vol. 95, pp. 9950–9955, August 1998 Developmental Biology Modulation of the chaperone heat shock cognate 70 by embryonic (pro)insulin correlates with prevention of apoptosis ENRIQUE J. DE LA ROSA*, ELENA VEGA-NU´NEZ˜ *, AIXA V. MORALES*†,JOSE´ SERNA,EVA RUBIO, AND FLORA DE PABLO‡ Department of Cell and Developmental Biology, Centro de Investigaciones Biolo´gicas, Consejo Superior de Investigaciones Cientı´ficas, Vela´zquez144, E-28006 Madrid, Spain Communicated by William H. Daughaday, University of California, Irvine, CA, June 25, 1998 (received for review February 18, 1998) ABSTRACT Insights have emerged concerning insulin (13, 14), the physiological survival effect of (pro)insulin has function during development, from the finding that apoptosis received less attention. during chicken embryo neurulation is prevented by prepan- Molecular chaperones assist folding, translocation, and as- creatic (pro)insulin. While characterizing the molecules in- sembly of newly synthesized proteins (reviewed in refs. 15 and volved in this survival effect of insulin, we found insulin- 16) and also protect the cell from heat shock and other dependent regulation of the molecular chaperone heat shock physiological or environmental stresses, increasing cell sur- cognate 70 kDa (Hsc70), whose cloning in chicken is reported vival after stress (17, 18). The specific mechanisms involved in here. This chaperone, generally considered constitutively ex- the cell survival effect of some chaperones have nonetheless pressed, showed regulation of its mRNA and protein levels in been approached only recently (19–21). How extracellular unstressed embryos during early development. More impor- survival factors might modulate these chaperones and whether tant, Hsc70 levels were found to depend on endogenous these molecules mediate the factors’ antiapoptotic function (pro)insulin, as shown by using antisense oligodeoxynucleoti- have not been elucidated. -
Human Anatomy Bio 11 Embryology “Chapter 3”
Human Anatomy Bio 11 Embryology “chapter 3” Stages of development 1. “Pre-” really early embryonic period: fertilization (egg + sperm) forms the zygote gastrulation [~ first 3 weeks] 2. Embryonic period: neurulation organ formation [~ weeks 3-8] 3. Fetal period: growth and maturation [week 8 – birth ~ 40 weeks] Human life cycle MEIOSIS • compare to mitosis • disjunction & non-disjunction – aneuploidy e.g. Down syndrome = trisomy 21 • visit http://www.ivc.edu/faculty/kschmeidler/Pages /sc-mitosis-meiosis.pdf • and/or http://www.ivc.edu/faculty/kschmeidler/Pages /HumGen/mit-meiosis.pdf GAMETOGENESIS We will discuss, a bit, at the end of the semester. For now, suffice to say that mature males produce sperm and mature females produce ova (ovum; egg) all of which are gametes Gametes are haploid which means that each gamete contains half the full portion of DNA, compared to somatic cells = all the rest of our cells Fertilization restores the diploid state. Early embryonic stages blastocyst (blastula) 6 days of human embryo development http://www.sisuhospital.org/FET.php human early embryo development https://opentextbc.ca/anatomyandphysiology/chapter/28- 2-embryonic-development/ https://embryology.med.unsw.edu.au/embryology/images/thumb/d/dd/Model_human_blastocyst_development.jpg/600px-Model_human_blastocyst_development.jpg Good Sites To Visit • Schmeidler: http://www.ivc.edu/faculty/kschmeidler/Pages /sc_EMBRY-DEV.pdf • https://embryology.med.unsw.edu.au/embryol ogy/index.php/Week_1 • https://opentextbc.ca/anatomyandphysiology/c hapter/28-2-embryonic-development/ -
Histogenesis of Ovarian Malignant Mixed Mesodermal Tumours J Clin Pathol: First Published As 10.1136/Jcp.43.4.287 on 1 April 1990
J Clin Pathol 1990;43:287-290 287 Histogenesis of ovarian malignant mixed mesodermal tumours J Clin Pathol: first published as 10.1136/jcp.43.4.287 on 1 April 1990. Downloaded from T J Clarke Abstract embedded tumour tissue were cut at 4 im and The histogenesis of ovarian malignant stained with haematoxylin and eosin, periodic mixed mesodermal tumours, which acid Schiff (PAS) before and after diastase includes the concept of metaplastic car- treatment, Caldwell and Rannie's reticulin cinoma, is controversial. Four such stain, and phosphotungstic acid haematoxylin tumours were examined for evidence of (PTAH). Sequential sections were stained by metaplastic transition from carcinoma to the indirect immunoperoxidase technique sarcoma using morphology and reticulin using monoclonal antibodies directed against stains. Consecutive sections were stained cytokeratin (PKK1 which reacts with low immunohistochemically using cyto- molecular weight cytokeratins of44, 46, 52 and keratin and vimentin to determine 54 kilodaltons), vimentin, a-l-antitrypsin and whether cells at the interface between myoglobin. Appropriate positive and negative carcinoma and sarcoma expressed both controls, with omission of specific antisera in cytokeratin and vimentin. There was no the latter, were performed. Haematoxylin and evidence ofmorphological, architectural, eosin stained sections were examined for or immunohistochemical transitions secondary fluorescence using a Leitz Dialux from carcinoma to sarcoma in the four 20ES microscope and mercury vapour light tumours studied. This suggests that source epifluorescence. ovarian malignant mixed mesodermal Four patients, aged 68, 71, 72 and 73 presen- tumours are not metaplastic carcinomas ted with abdominal distension and discomfort but are composed of histogenetically dif- and were found to have an ovarian malignant ferent elements. -
Wnt-3A Regulates Somite and Tailbud Formation in the Mouse Embryo
Downloaded from genesdev.cshlp.org on October 2, 2021 - Published by Cold Spring Harbor Laboratory Press Wnt-3a regulates somite and tailbud formation in the mouse embryo Shinji Takada/ Kevin L. Stark,^ Martin J. Shea,^ Galya Vassileva, Jill A. McMahon/ and Andrew P. McMahon* Roche Institute of Molecular Biology, Roche Research Center, Nutley, New Jersey 07110 USA Amphibian studies have implicated Wnt signaling in the regulation of mesoderm formation, although direct evidence is lacking. We have characterized the expression of 12 mammalian Wnt-genes, identifying three that are expressed during gastrulation. Only one of these, Wnt-3a, is expressed extensively in cells fated to give rise to embryonic mesoderm, at egg cylinder stages. A likely null allele of Wnt-3a was generated by gene targeting. All Wiit-3fl~/Wnt-3a~ embryos lack caudal somites, have a disrupted notochord, and fail to form a tailbud. Thus, Wnt-Sa may regulate dorsal (somitic) mesoderm fate and is required, by late primitive steak stages, for generation of all new embryonic mesoderm. Wnt-3a is also expressed in the dorsal CNS. Mutant embryos show CNS dysmorphology and ectopic expression of a dorsal CNS marker. We suggest that dysmorphology is secondary to the mesodermal and axial defects and that dorsal patterning of the CNS may be regulated by inductive signals arising from surface ectoderm. [Key Words: Wnt; gastrulation; mesoderm formation; somite; tailbud; gene targeting] Received November 9, 1993; revised version accepted December 8, 1993. Cell-cell interaction plays an important role in the de ton 1992) receptors. Interestingly, mesoderm induction velopment of all organisms. In the vertebrate, consider by FGFs and TGF-p-related factors is qualitatively differ able progress has been made in recent years in identify ent. -
Programmed Cell Death During Xenopus Development
DEVELOPMENTAL BIOLOGY 203, 36–48 (1998) ARTICLE NO. DB989028 View metadata, citation and similar papers at core.ac.uk brought to you by CORE Programmed Cell Death during Xenopus provided by Elsevier - Publisher Connector Development: A Spatio-temporal Analysis Carmel Hensey and Jean Gautier1 Department of Genetics and Development and Department of Dermatology, College of Physicians and Surgeons of Columbia University, 630 West 168th Street, New York, New York 10032 Programmed cell death (PCD) is an integral part of many developmental processes. In vertebrates little is yet known on the patterns of PCD and its role during the early phases of development, when embryonic tissue layers migrate and pattern formation takes place. We describe the spatio-temporal patterns of cell death during early Xenopus development, from fertilization to the tadpole stage (stage 35/36). Cell death was analyzed by a whole-mount in situ DNA end-labeling technique (the TUNEL protocol), as well as by serial sections of paraffin-embedded TUNEL-stained embryos. The first cell death was detected during gastrulation, and as development progressed followed highly dynamic and reproducible patterns, strongly suggesting it is an important component of development at these stages. The detection of PCD during neural induction, neural plate patterning, and later during the development of the nervous system highlights the role of PCD throughout neurogenesis. Additionally, high levels of cell death were detected in the developing tail and sensory organs. This is the first detailed description of PCD throughout early development of a vertebrate, and provides the basis for further studies on its role in the patterning and morphogenesis of the embryo. -
Early Embryonic Development Till Gastrulation (Humans)
Gargi College Subject: Comparative Anatomy and Developmental Biology Class: Life Sciences 2 SEM Teacher: Dr Swati Bajaj Date: 17/3/2020 Time: 2:00 pm to 3:00 pm EARLY EMBRYONIC DEVELOPMENT TILL GASTRULATION (HUMANS) CLEAVAGE: Cleavage in mammalian eggs are among the slowest in the animal kingdom, taking place some 12-24 hours apart. The first cleavage occurs along the journey of the embryo from oviduct toward the uterus. Several features distinguish mammalian cleavage: 1. Rotational cleavage: the first cleavage is normal meridional division; however, in the second cleavage, one of the two blastomeres divides meridionally and the other divides equatorially. 2. Mammalian blastomeres do not all divide at the same time. Thus the embryo frequently contains odd numbers of cells. 3. The mammalian genome is activated during early cleavage and zygotically transcribed proteins are necessary for cleavage and development. (In humans, the zygotic genes are activated around 8 cell stage) 4. Compaction: Until the eight-cell stage, they form a loosely arranged clump. Following the third cleavage, cell adhesion proteins such as E-cadherin become expressed, and the blastomeres huddle together and form a compact ball of cells. Blatocyst: The descendents of the large group of external cells of Morula become trophoblast (trophoblast produce no embryonic structure but rather form tissues of chorion, extraembryonic membrane and portion of placenta) whereas the small group internal cells give rise to Inner Cell mass (ICM), (which will give rise to embryo proper). During the process of cavitation, the trophoblast cells secrete fluid into the Morula to create blastocoel. As the blastocoel expands, the inner cell mass become positioned on one side of the ring of trophoblast cells, resulting in the distinctive mammalian blastocyst. -
Cell Death in the Avian Blastoderm: Resistance to Stress- Induced Apoptosis and Expression of Anti-Apoptotic Genes
Cell Death and Differentiation (1998) 5, 529 ± 538 1998 Stockton Press All rights reserved 13509047/98 $12.00 http://www.stockton-press.co.uk/cdd Cell death in the avian blastoderm: resistance to stress- induced apoptosis and expression of anti-apoptotic genes Stephen E. Bloom1,2, Donna E. Muscarella1, Mitchell Y. Lee1 in cleavage stages and subsequent extensive cell migration in and Melissa Rachlinski1 the formation of the initial and primitive streaks (Romanoff, 1960; Eyal-Giladi and Kochav, 1976). Cell death has been 1 Department of Microbiology and Immunology, Cornell University, Ithaca, New shown to occur in regions of gastrulating embryos (Jacobson, York 14853, USA 1938; Glucksmann, 1951; Sanders et al., 1997a,b). However, 2 corresponding author: tel: 607-253-4041; fax: 607-253-3384; it is unclear whether programmed cell death (PCD) occurs, or email: [email protected] is required, at stages preceding gastrulation. In fact, classical reviews of early development in the avian embryo do not mention cell deaths in connection with cleavage division Received 13.11.97; revised 21.1.98; accepted 4.3.98 stages, in the formation of epiblast and hypoblast layers of the Edited by C.J. Thiele blastoderm, or in the establishment of polarity in embryos (Romanoff, 1960, 1972; Eyal-Giladi and Kochav, 1976). Abstract An early suggestion of cell death by an apoptotic mode in the blastoderm was provided in the ultrastructural study We investigated the expression of an apoptotic cell death of unincubated and grastrulating chick embryos (Bellairs, program in blastodermal cells prior to gastrulation and the 1961). This work revealed `chromatic patches' near the susceptibility of these cells to stress-induced cell death.