are produced by ectoderm cells and released into the blastocoel where they interact
with cognate receptor tyrosine kinases restricted to PMCs, which activate signaling cascades regulating the expression of biomineralization-related genes. We
demonstrated the implication of a TGF-beta family factor by a perturbation model
in which skeleton elongation was indirectly blocked by monoclonal antibodies to an
extracellular matrix (ECM) protein located on the apical surface of ectoderm. Thus,
it was inferred that interfering with the binding of the ECM ligand, a member of the
discoidin family, to its cell surface receptor, a bC integrin, disrupts the ectodermal
cell signaling cascade, resulting in reduced or aberrant skeletons. During the last few
years, we analyzed the expression of biomineralization-related genes in other
examples of experimentally induced skeleton malformations, produced by the
exposure to toxic metals, such as Cd and Mn or ionizing radiations, such as UV-B
and X-rays. Besides the obvious toxicological implication, since the mis-expression
of spicule matrix genes paralleled skeleton defects, we believe that by means of
these studies we can dissect the molecular steps taking place and possibly understand the physiological events regulating embryonic biomineralization.
8.1 The Basis of Biomineral Formation
Biomineralization refers to the biological processes employed by living organisms
to form minerals as a result of regulated processes. A biomineral represents a
complex material which incorporates both mineral and organic components
exhibiting advantageous properties compared to its inorganically formed counterpart. Compared to abiotic minerals, biominerals possess additional physical and
chemical characteristics which offer increased flexibility and duration. They vary in
morphology, shape, and size as well as in element composition. The structure of a
biomineral involves a mosaic of crystalline domains separated by occluded proteinaceous material forming a framework (Wilt 1999). The structure exhibits single
crystal diffraction properties as shown by X-ray diffraction studies (Simkiss 1986).
Classically, according to the degree of biological control over the precipitated
mineral, biomineralization processes can be categorized into two groups: the
“biologically induced” (Lowenstam 1981) and the “biologically controlled” mineralization (Mann 1983).
In biologically induced mineralization, cell surfaces may act as causative nucleation agents which lead to crystal growth. Mineral growth is indirectly affected, but
not controlled, by the biological system. The adopted mineral form is favored by
metabolic processes which define the chemical conditions of the microenvironment
(i.e., pH, pCO 2 , concentration of products resulting from secretion) (Frankel and
Bazylinski 2003). As environmental conditions play a potential role in the formation of the biologically induced minerals, these biominerals exhibit heterogeneity in
elemental composition, in water content, and in particle size, resulting in various
external morphologies.
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V. Matranga et al.
with cognate receptor tyrosine kinases restricted to PMCs, which activate signaling cascades regulating the expression of biomineralization-related genes. We
demonstrated the implication of a TGF-beta family factor by a perturbation model
in which skeleton elongation was indirectly blocked by monoclonal antibodies to an
extracellular matrix (ECM) protein located on the apical surface of ectoderm. Thus,
it was inferred that interfering with the binding of the ECM ligand, a member of the
discoidin family, to its cell surface receptor, a bC integrin, disrupts the ectodermal
cell signaling cascade, resulting in reduced or aberrant skeletons. During the last few
years, we analyzed the expression of biomineralization-related genes in other
examples of experimentally induced skeleton malformations, produced by the
exposure to toxic metals, such as Cd and Mn or ionizing radiations, such as UV-B
and X-rays. Besides the obvious toxicological implication, since the mis-expression
of spicule matrix genes paralleled skeleton defects, we believe that by means of
these studies we can dissect the molecular steps taking place and possibly understand the physiological events regulating embryonic biomineralization.
8.1 The Basis of Biomineral Formation
Biomineralization refers to the biological processes employed by living organisms
to form minerals as a result of regulated processes. A biomineral represents a
complex material which incorporates both mineral and organic components
exhibiting advantageous properties compared to its inorganically formed counterpart. Compared to abiotic minerals, biominerals possess additional physical and
chemical characteristics which offer increased flexibility and duration. They vary in
morphology, shape, and size as well as in element composition. The structure of a
biomineral involves a mosaic of crystalline domains separated by occluded proteinaceous material forming a framework (Wilt 1999). The structure exhibits single
crystal diffraction properties as shown by X-ray diffraction studies (Simkiss 1986).
Classically, according to the degree of biological control over the precipitated
mineral, biomineralization processes can be categorized into two groups: the
“biologically induced” (Lowenstam 1981) and the “biologically controlled” mineralization (Mann 1983).
In biologically induced mineralization, cell surfaces may act as causative nucleation agents which lead to crystal growth. Mineral growth is indirectly affected, but
not controlled, by the biological system. The adopted mineral form is favored by
metabolic processes which define the chemical conditions of the microenvironment
(i.e., pH, pCO 2 , concentration of products resulting from secretion) (Frankel and
Bazylinski 2003). As environmental conditions play a potential role in the formation of the biologically induced minerals, these biominerals exhibit heterogeneity in
elemental composition, in water content, and in particle size, resulting in various
external morphologies.
226
V. Matranga et al.