Introduction
The «gene architecture» of its chromosomes is responsible for the control of embryonic development. Since for obvious ethical reasons experiments cannot be performed on humans, the results that have been obtained up till now are derived from the study of a few model organisms such as caenorhabditis elegans (C. elegans, nematodes), drosophila (fruit flies) and laboratory mice.
Embryonic development depends on genetic as well as environmental influences that are temporally and locationally adjusted to one another. The factors that, for example, determine the interactions between the tissues, the migration and differentiation of the cells, the proliferation of the cell colonies, as well as the apoptosis (programmed death of cells) are numerous.
Embryonic development is a process of growth and differentiation in which the embryo becomes increasingly complex and is more and more enhanced with structures and functions.
The growth depends on the somatic multiplication of the cells through mitosis. In order to control the growth, certain restriction mechanisms are needed which are able to stop cell divisions at the right moment. The complexity of the structures is connected with morphogenesis and differentiation.
One of the most fascinating aspects of embryonic development is the fact that out of a simple zygote (fertilized oocyte) an organism arises that consists of billions of cells. In the following chapter only a few of the many important factors for prenatal development are discussed.
Control factors of embryonic and fetal origin
Numerous molecules (hormones, growth factors and enzymes) play a role in the growth and differentiation of the embryo. Only a few are mentioned here since a complete study lies outside the bounds of this module.
The IGF's (insulin-like growth factors) are mitogenic, stimulating the fetal metabolism and coordinating the feto-placental metabolism. IGF-II regulates early embryonic development while IGF-I is responsible for the growth of the newborn.
Fetal insulin plays an indirect role in the regulation of fetal growth. It modulates the expression of the fetal IGF. On the other hand, it has direct effects on the adipose tissue and the proliferation of the cells within the fetus. Its effects, though, on the differentiation of the tissue and thus on prenatal maturation are small.
Fetal glucocorticoid affects tissue differentiation and prenatal development of the organs such as, for example, lungs (maturation of the surfactant), liver (control of glycemia), as well as the intestines (maturation of the expression of digestive enzymes and proliferation of the villi).
In addition glucocorticoid, together with thyroid gland hormones, affects the maturation of the lungs and the nervous system .
The fetal growth hormone GH has no effects on prenatal growth. This explains the absence of growth deficiencies in congenital hypopituitarism.
Further growth factors exist that affect the proliferation, differentiation and maturation of the cells. They play an important role in embryogenesis.
- EGF (epidermal growth factor)are strongly mitogenic and form a group of molecules that bind to the same receptors (tyrosine kinase).
- TGF (tranforming growth factor) form a super-family that numbers more than 30 members (TGFb, activin, BMP [bone morphogenetic proteins], compare with GDNF [glial- derived neurotropic factor]).
- FGF (fibroblast growth factor) of which around 20 are known.
Embryonic cholinesterase (ChE) is an enzyme that is active in morphogenesis. Depending on their developmental stage embryonic cells express muscarinic receptors on their surfaces for acetylcholine and synthesize cholinesterase, which is able to inactivate neurotransmitters.
The interleukins 1 form a family that belongs to the cytokines. They play an important role during implantation.
Sexual hormones with embryonic origin. Sexual differentiation occurs between the 3rd and 12th week. Responsible are genetic and also hormonal factors.
Since 1950 it is known that the secondary sexual differentiation (phenotypical gender) in contrast to primary sexual differentiation (gonadal gender) mainly depends on hormonal factors.
After the 6th week Leydig's cells in the embryonic testes secrete testosterone, which is responsible for male differentiation and so leads to the genesis of the male sexual apparatus.
At around the 7th week the anti-Müllerian hormone (AMH), which belongs to the TGF-β family and is secreted by Sertoli's cells, induces the atrophy of the paramesonephric ducts (Müller).
The female sexual apparatus develops spontaneously when the hormonal influence mentioned above is absent.
Control factors of maternal origin
The maternal hormone and growth factors normally do not pass through the placenta. If it nevertheless happens, an altered placenta metabolism is present.
If the mother has consumed drugs (alcohol, tobacco) or is herself diseased (e.g., diabetes), this can influence embryonic and fetal growth.