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Chapter 3 - Human embryology

from Section 1 - General principles

Published online by Cambridge University Press:  05 February 2013

Mark D. Kilby
Affiliation:
Department of Fetal Medicine, University of Birmingham
Anthony Johnson
Affiliation:
Baylor College of Medicine, Texas
Dick Oepkes
Affiliation:
Department of Obstetrics, Leiden University Medical Center
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Summary

How do embryos develop?

The early developing embryo is initially composed of three tissue layers, the ectoderm, endoderm, and mesoderm, that are generated during weeks two to three by gastrulation. The ectoderm, the most dorsal layer, gives rise to the skin whilst the neuroectoderm, which is induced within the ectoderm at the midline, rolls up to form the neural tube, and contains the progenitors of the brain and spinal cord (Figure 3.1). The endoderm, the most ventral layer, gives rise to the epithelial cells of the gastrointestinal tract and associated organs. Sandwiched between these layers is the mesoderm, which is subdivided. The paraxial mesoderm contributes to the musculoskeletal system and dermis in the trunk and head, the intermediate mesoderm contributes to the urogenital system, the somatic portion of lateral plate mesoderm forms the skeleton and connective tissue of the limbs together with the body wall whilst the splanchnic mesoderm portion of the lateral plate mesoderm forms the mesoethelial layers of the gastrointestinal tract. The cardiogenic mesoderm (not shown) contributes to the heart whilst the notochord (or axial mesoderm) gives rise to the nucleus pulposus of the intervertebral disks (Figure 3.1). In addition, a fourth tissue layer, the neural crest, arises at the interface of the ectoderm and neuroectoderm (Figure 3.1). Neural crest cells form by an epithelial-mesenchymal transformation, are pluripotent and migratory. In the trunk, the neural crest cells contribute to the peripheral nervous system whereas in the head, neural crest cells also give rise to the skeletal system and dermis of the face, odontoblasts, and connective tissues. Additionally, cranial neural crest cells contribute to the outflow tract and cushions of the heart. For further details of embryonic development, the reader is referred to Larsen’s Human Embryology [1].

Type
Chapter
Information
Fetal Therapy
Scientific Basis and Critical Appraisal of Clinical Benefits
, pp. 24 - 38
Publisher: Cambridge University Press
Print publication year: 2012

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References

Schoenwolf, G, Bleyl, S, Brauer, P, Francis-West, P. Larsen’s Human Embryology, 4th edn. Philadelphia, Elsevier, Churchill, Livingstone, 2009.
Shukla, V, Coumoul, X, Wang, RH, Kim, HS, Deng, CX. RNA interference and inhibition of MEK-ERK signaling prevent abnormal skeletal phenotypes in a mouse model of craniosynostosis. Nat Genet 2007;39(9):1145–50.Google Scholar
Mikkola, ML. Molecular aspects of hypohidrotic ectodermal dysplasia. Am J Med Genet A 2009;149A(9):2031–6.Google Scholar
Gaide, O, Schneider, P. Permanent correction of an inherited ectodermal dysplasia with recombinant EDA. Nat Med 2003;9(5):614–18.Google Scholar
Casal, ML, Lewis, JR, Mauldin, EA, et al. Significant correction of disease after postnatal administration of recombinant ectodysplasin A in canine X-linked ectodermal dysplasia. Am J Hum Genet 2007;81(5):1050–6.Google Scholar
Fernandez, F, Morishita, W, Zuniga, E, et al. Pharmacotherapy for cognitive impairment in a mouse model of Down syndrome. Nat Neurosci 2007;10(4):411–13.Google Scholar
Wilkie, AO, Bochukova, EG, Hansen, RM, et al. Clinical dividends from the molecular genetic diagnosis of craniosynostosis. Am J Med Genet A 2006;140(23):2631–9.Google Scholar
Chambers, SM, Studer, L. Cell fate plug and play: direct reprogramming and induced pluripotency. Cell 2011;145(6):827–30.Google Scholar
Wu, MY, Hill, CS. Tgf-beta superfamily signaling in embryonic development and homeostasis. Dev Cell 2009;16(3):329–43.Google Scholar
White, RJ, Schilling, TF. How degrading: Cyp26s in hindbrain development. Dev Dyn 2008;237(10):2775–90.Google Scholar
Zhou, Y, Liu, HX, Mistretta, CM. Bone morphogenetic proteins and noggin: inhibiting and inducing fungiform taste papilla development. Dev Biol 2006;297(1):198–213.Google Scholar
Varjosalo, M, Taipale, J. Hedgehog: functions and mechanisms. Genes Dev 2008;22(18):2454–72.Google Scholar
Chiang, C, Litingtung, Y, Lee, E, et al. Cyclopia and defective axial patterning in mice lacking Sonic hedgehog gene function. Nature 1996;383(6599):407–13.Google Scholar
Roessler, E, Muenke, M. The molecular genetics of holoprosencephaly. Am J Med Genet C Semin Med Genet 2010;154C(1):52–61.Google Scholar
Zeller, R, Lopez-Rios, J, Zuniga, A. Vertebrate limb bud development: moving towards integrative analysis of organogenesis. Nat Rev Genet 2009;10(12):845–58.Google Scholar
Teillet, M, Watanabe, Y, Jeffs, P, et al. Sonic hedgehog is required for survival of both myogenic and chondrogenic somitic lineages. Development 1998;125(11):2019–30.Google Scholar
Goetz, SC, Anderson, KV. The primary cilium: a signalling centre during vertebrate development. Nat Rev Genet 2010;11(5):331–44.Google Scholar
Ribes, V, Briscoe, J. Establishing and interpreting graded Sonic Hedgehog signaling during vertebrate neural tube patterning: the role of negative feedback. Cold Spring Harb Perspect Biol 2009;1(2):1–16.Google Scholar
Angers, S, Moon, RT. Proximal events in Wnt signal transduction. Nat Rev Mol Cell Biol 2009;10(7):468–77.Google Scholar
MacDonald, BT, Tamai, K, He, X. Wnt/beta-catenin signaling: components, mechanisms, and diseases. Dev Cell 2009;17(1):9–26.Google Scholar
Ulloa, F, Marti, E. Wnt won the war: antagonistic role of Wnt over Shh controls dorso-ventral patterning of the vertebrate neural tube. Dev Dyn 2008;239(1):69–76.Google Scholar
Cairns, DM, Sato, ME, Lee, PG, Lassar, AB, Zeng, L. A gradient of Shh establishes mutually repressing somitic cell fates induced by Nkx3.2 and Pax3. Dev Biol 2008;323(2):152–65.Google Scholar
Karner, C, Wharton, KA, Jr., Carroll, TJ. Planar cell polarity and vertebrate organogenesis. Semin Cell Dev Biol 2006;17(2):194–203.Google Scholar
Wallingford, JB. Planar cell polarity signaling, cilia and polarized ciliary beating. Curr Opin Cell Biol 2010;22(5):597–604.Google Scholar
Al-Qattan, MM. WNT pathways and upper limb anomalies. J Hand Surg Eur Vol 2010;36(1):9–22.Google Scholar
Kibar, Z, Salem, S, Bosoi, CM, et al. Contribution of VANGL2 mutations to isolated neural tube defects. Clin Genet 2008;80(1):76–82.Google Scholar
Kibar, Z, Torban, E, McDearmid, JR, et al. Mutations in VANGL1 associated with neural-tube defects. N Engl J Med 2007;356(14):1432–7.Google Scholar
Turner, N, Grose, R. Fibroblast growth factor signalling: from development to cancer. Nat Rev Cancer 2010;10(2):116–29.Google Scholar
Schier, AF. Nodal morphogens. Cold Spring Harb Perspect Biol 2009;1(5):a003459.Google Scholar
Thesleff, I, Vaahtokari, A, Partanen, AM. Regulation of organogenesis. Common molecular mechanisms regulating the development of teeth and other organs. Int J Dev Biol 1995;39(1):35–50.Google Scholar
Chappell, JC, Bautch, VL. Vascular development: genetic mechanisms and links to vascular disease. Curr Top Dev Biol 2010;90:43–72.Google Scholar
Stricker, S, Mundlos, S. Mechanisms of digit formation: human malformation syndromes tell the story. Dev Dyn 2011;240(5):990–1004.Google Scholar
Suzuki, S, Marazita, ML, Cooper, ME, et al. Mutations in BMP4 are associated with subepithelial, microform, and overt cleft lip. Am J Hum Genet 2009;84(3):406–11.Google Scholar
Josso, N, Belville, C, di Clemente, N, Picard, JY. AMH and AMH receptor defects in persistent Mullerian duct syndrome. Hum Reprod Update 2005;11(4):351–6.Google Scholar
Dorey, K, Amaya, E. FGF signalling: diverse roles during early vertebrate embryogenesis. Development 2010;137(22):3731–42.Google Scholar
Bhagavath, B, Layman, LC. The genetics of hypogonadotropic hypogonadism. Semin Reprod Med 2007;25(4):272–86.Google Scholar
Richette, P, Bardin, T, Stheneur, C. Achondroplasia: from genotype to phenotype. Joint Bone Spine 2008;75(2):125–30.Google Scholar
Andersson, ER, Sandberg, R, Lendahl, U. Notch signaling: simplicity in design, versatility in function. Development 2011;138(17):3593–612.Google Scholar
Fre, S, Bardin, A, Robine, S, Louvard, D. Notch signaling in intestinal homeostasis across species: the cases of Drosophila, Zebrafish and the mouse. Exp Cell Res 2005;317(19):2740–7.Google Scholar
Bray, SJ. Notch signalling: a simple pathway becomes complex. Nat Rev Mol Cell Biol 2006;7(9):678–89.Google Scholar
Daudet, N, Ariza-McNaughton, L, Lewis, J. Notch signalling is needed to maintain, but not to initiate, the formation of prosensory patches in the chick inner ear. Development 2007;134(12):2369–78.Google Scholar
Tossell, K, Kiecker, C, Wizenmann, A, Lang, E, Irving, C. Notch signalling stabilises boundary formation at the midbrain-hindbrain organiser. Development 2011;138(17):3745–57.Google Scholar
Louvi, A, Artavanis-Tsakonas, S. Notch signalling in vertebrate neural development. Nat Rev Neurosci 2006;7(2):93–102.Google Scholar
Dunwoodie, SL. The role of Notch in patterning the human vertebral column. Curr Opin Genet Dev 2009;19(4):329–37.Google Scholar
Teer, JK, Mullikin, JC. Exome sequencing: the sweet spot before whole genomes. Hum Mol Genet 2010;19(R2):R145–51.Google Scholar

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