| Ectoderm | |
|---|---|
 Organs derived from ectoderm. | |
 Section through embryonic disk ofVespertilio murinus. | |
| Details | |
| Days | 16 |
| Identifiers | |
| MeSH | D004475 |
| FMA | 69070 |
| Anatomical terminology | |
Theectoderm is one of the three primarygerm layers formed in earlyembryonic development. It is the outermost layer, and is superficial to themesoderm (the middle layer) andendoderm (the innermost layer).[1] It emerges and originates from the outer layer of germ cells. The word ectoderm comes from theGreekektos meaning "outside", andderma meaning "skin".[2]
Generally speaking, the ectoderm differentiates to formepithelial andneural tissues (spinal cord,nerves andbrain). This includes theskin, linings of the mouth, anus, nostrils, sweat glands, hair and nails,[3] andtooth enamel. Other types of epithelium are derived from the endoderm.[3]
Invertebrate embryos, the ectoderm can be divided into two parts: the dorsalsurface ectoderm also known as the external ectoderm, and theneural plate, which invaginates to form theneural tube andneural crest.[4] The surface ectoderm gives rise to most epithelial tissues, and the neural plate gives rise to mostneural tissues. For this reason, the neural plate and neural crest are also referred to as theneuroectoderm.
Heinz Christian Pander, aBaltic German–Russianbiologist, has been credited for the discovery of the threegerm layers that form duringembryogenesis. Pander received his doctorate inzoology from theUniversity of Würzburg in 1817. He began his studies in embryology using chicken eggs, which allowed for his discovery of the ectoderm,mesoderm andendoderm. Due to his findings, Pander is sometimes referred to as the "founder of embryology".
Pander's work of the early embryo was continued by aPrussian–Estonian biologist namedKarl Ernst von Baer. Baer took Pander's concept of the germ layers and through extensive research of many different types of species, he was able to extend this principle to all vertebrates. Baer also received credit for the discovery of theblastula. Baer published his findings, including his germ layer theory, in a textbook which translates toOn the Development of Animals which he released in 1828.[5]
The ectoderm can first be observed inamphibians andfish during the later stages ofgastrulation. At the start of this process, the developing embryo has divided into many cells, forming a hollow ball called theblastula. The blastula ispolar, and its two halves are called theanimal hemisphere andvegetal hemisphere. It is the animal hemisphere will eventually become the ectoderm.[2]
Like the other two germ layers – i.e., the mesoderm and endoderm – the ectoderm forms shortly afterfertilization, after which rapidcell division begins. The position of the ectoderm relative to the other germ layers of theembryo is governed by "selective affinity", meaning that the inner surface of the ectoderm has a strong (positive) affinity for the mesoderm, and a weak (negative) affinity for the endoderm layer.[6] This selective affinity changes during different stages of development. The strength of the attraction between two surfaces of two germ layers is determined by the amount and type ofcadherin molecules present on the cells' surface. For example, the expression ofN-cadherin is crucial to maintaining separation of precursor neural cells from precursor epithelial cells.[2] Likewise, while thesurface ectoderm becomes theepidermis,[6] theneuroectoderm is induced along the neural pathway by thenotochord, which is typically positioned above it.[2][4]
During the process of gastrulation,bottle cells invaginate on the dorsal surface of the blastula to form theblastopore. The cells continue to extend inward and migrate along the inner wall of the blastula to form a fluid-filled cavity called theblastocoel. The once superficial cells of the animal pole are destined to become the cells of the middle germ layer called the mesoderm. Through the process of radial extension, cells of theanimal pole that were once several layers thick divide to form a thin layer. At the same time, when this thin layer of dividing cells reaches the dorsal lip of theblastopore, another process occurs termedconvergent extension. During convergent extension, cells that approach the lip intercalate mediolaterally, in such a way that cells are pulled over the lip and inside the embryo. These two processes allow for the prospective mesoderm cells to be placed between the ectoderm and the endoderm. Onceconvergent extension and radial intercalation are underway, the rest of thevegetal pole, which will become endoderm cells, is completely engulfed by the prospective ectoderm, as these top cells undergoepiboly, where the ectoderm cells divide in a way to form one layer. This creates a uniform embryo composed of the three germ layers in their respective positions.[2]
Once the three germ layers have been established,cellular differentiation can occur. The first major process here isneurulation, wherein the ectoderm differentiates to form theneural tube,neural crest cells and theepidermis. Each of these three components will give rise to a particular complement of cells. Theneural tube cells give rise to thecentral nervous system,neural crest cells give rise to the peripheral and enteric nervous system,melanocytes, and facialcartilage, and theepidermal region will give rise to theepidermis,hair,nails,sebaceous glands,olfactory and oral epithelium, andeyes.[2]
Neurulation occurs in two parts, primary and secondary neurulation. Both processes position neural crest cells between a superficial epidermal layer and the deep neural tube. During primary neurulation, the notochord cells of the mesoderm signal the adjacent, superficial ectoderm cells to reposition themselves into a columnar pattern to form cells of the ectodermalneural plate.[7] As the cells continue to elongate, a group of cells immediately above thenotochord change their shape, forming a wedge in the ectodermal region. These special cells are calledmedial hinge cells (MHPs). As the ectoderm continues to elongate, the ectodermal cells of the neural plate fold inward. The inward folding of the ectoderm by virtue of mainly cell division continues until another group of cells forms within the neural plate. These cells are termeddorsolateral hinge cells (DLHPs), and, once formed, the inward folding of the ectoderm stops. TheDLHP cells function in a similar fashion asMHP cells regarding their wedge like shape, however, the DLHP cells result in the ectoderm converging. This convergence is led by ectodermal cells above the DLHP cells known as the neural crest. The neural crest cells eventually pull the adjacent ectodermal cells together, which leaves neural crest cells between the prospectiveepidermis and hollow, neural tube.[2]
All of the organs that rise from the ectoderm such as the nervous system, teeth, hair and many exocrine glands, originate from two adjacent tissue layers: the epithelium and the mesenchyme.[8] Several signals mediate theorganogenesis of the ectoderm such as:FGF,TGFβ,Wnt, and regulators from thehedgehog family. The specific timing and manner that the ectodermal organs form is dependent on the invagination of the epithelial cells.[9] FGF-9 is an important factor during the initiation of tooth germ development. The rate of epithelial invagination in significantly increased by action of FGF-9, which is only expressed in the epithelium, and not in the mesenchyme. FGF-10 helps to stimulate epithelial cell proliferation, in order make larger tooth germs. Mammalian teeth develop from ectoderm derived from the mesenchyme: oral ectoderm and neural crest. The epithelial components of the stem cells for continuously growing teeth form from tissue layers called the stellate reticulum and the suprabasal layer of the surface ectoderm.[9]
Ectodermal dysplasia is a rare but severe condition where the tissue groups (specifically teeth, skin, hair, nails and sweat glands) derived from the ectoderm undergo abnormal development. This is a diffuse term, as there are over 170 subtypes of ectodermal dysplasia. It has been accepted that the disease is caused by a mutation or a combination of mutations in certain genes. Research of the disease is ongoing, as only a fraction of the mutations involved with an ectodermal dysplasia subtype have been identified.[10]
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Hypohidrotic ectodermal dysplasia (HED) is the most common subtype of the disease. Clinical cases of patients with this condition display a range of symptoms. The most relevant abnormality of HED ishypohidrosis, the inability to produce sufficient amounts of sweat, which is attributed to missing or dysfunctional sweat glands. This aspect represents a major handicap particularly in the summer, limits the patient's ability to participate in sports as well as his working capacity, and can be especially dangerous in warm climates where affected individuals are at risk of life-threateninghyperthermia. Facialmalformations are also related to HED, such as pointed or absent teeth, wrinkled skin around the eyes, a misshaped nose along with scarce and thin hair. Skin problems likeeczema are also observed in a number of cases.[11] Most patients carry variants of the X-chromosomalEDA gene.[12] This disease typically affects males more severely because they have only oneX chromosome, while in females the second, usually unaffected X chromosome may be sufficient to prevent most symptoms.
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