principal skeleton-forming cells also known as calcoblasts or odontoblast (M€ arkel
et al. 1986; Dubois and Ameye 2001).
Signals, activated in response to initial inflammatory events, trigger a series of
intracellular processes associated with survival, cell proliferation, migration,
attachment, differentiation, and eventually matrix deposition. All these steps are
required to accelerate tissue repair and reconstruction, including neural, muscular,
and skeletogenic tissues. Any regenerative process implies the existence of stem
cells present in the circulating fluids or in the tissues in the form of resident cells,
ready to be recruited after trauma (Pinsino et al. 2007). Scarce information is
available on the biomineralization process following regeneration. Pioneering
studies at the molecular level demonstrated the overexpression of three mRNA
specific of the primary mesenchyme cells (PMCs) in regenerating spines. By in situ
hybridization, it was shown that gene products were localized primarily in
calcoblasts that accumulated at the regeneration sites (Drager et al. 1989). More
studies are awaited in tissue calcification events, which are of fundamental importance, as they ensure that biomineralization proceeds normally in the proper sites,
while ectopic mineralization is prevented elsewhere.
8.4 Cellular Signaling and Biomineral Formation in the Sea
Urchin Embryo
Among echinoderms, the sea urchin embryo has been known for its versatility and
suitability since the end of the nineteenth century, when classical embryologists
performed the earliest studies on the basic mechanisms of embryo development,
facilitated by the optical transparency of the embryo, along with its simplicity in
shape and organization (H€ orstadius 1939). Since then, the sea urchin has been
utilized to a great extent for studies in several scientific fields, ranging from basic
developmental biology to ecotoxicology and applied research. In addition, the
ability to form a larval endoskeleton encourages the use of the sea urchin embryo
for detailed studies on the mechanisms underlying biomineralization, an extremely
interesting topic for nano(bio)technology. It is becoming increasingly clear that the
biomineralization process is genetically controlled and a great number of steps in
such biological control could exist.
Biomineralization in the sea urchin initiates from the early embryonic developmental stages and is mediated by the PMCs which express genes under a complex
signaling control of transcription and growth factors (for a review see Ettensohn
2009). Schematic drawings of the initial phases of embryonic skeleton deposition
and PMCs arrangement are presented in Fig. 8.2. Accumulating evidence
demonstrates that the PMCs express genes which control the formation and
remodeling of carbonate crystals. In sea urchin embryos, ACC is a transient
phase leading to the formation of calcitic spicules (Beniash et al. 1997; Weiss
et al. 2002). The formation of ACC results from a supersaturated solution produced
by ions and proteins (Raz et al. 2003).
8 Echinoderms as Blueprints for Biocalcification
231
et al. 1986; Dubois and Ameye 2001).
Signals, activated in response to initial inflammatory events, trigger a series of
intracellular processes associated with survival, cell proliferation, migration,
attachment, differentiation, and eventually matrix deposition. All these steps are
required to accelerate tissue repair and reconstruction, including neural, muscular,
and skeletogenic tissues. Any regenerative process implies the existence of stem
cells present in the circulating fluids or in the tissues in the form of resident cells,
ready to be recruited after trauma (Pinsino et al. 2007). Scarce information is
available on the biomineralization process following regeneration. Pioneering
studies at the molecular level demonstrated the overexpression of three mRNA
specific of the primary mesenchyme cells (PMCs) in regenerating spines. By in situ
hybridization, it was shown that gene products were localized primarily in
calcoblasts that accumulated at the regeneration sites (Drager et al. 1989). More
studies are awaited in tissue calcification events, which are of fundamental importance, as they ensure that biomineralization proceeds normally in the proper sites,
while ectopic mineralization is prevented elsewhere.
8.4 Cellular Signaling and Biomineral Formation in the Sea
Urchin Embryo
Among echinoderms, the sea urchin embryo has been known for its versatility and
suitability since the end of the nineteenth century, when classical embryologists
performed the earliest studies on the basic mechanisms of embryo development,
facilitated by the optical transparency of the embryo, along with its simplicity in
shape and organization (H€ orstadius 1939). Since then, the sea urchin has been
utilized to a great extent for studies in several scientific fields, ranging from basic
developmental biology to ecotoxicology and applied research. In addition, the
ability to form a larval endoskeleton encourages the use of the sea urchin embryo
for detailed studies on the mechanisms underlying biomineralization, an extremely
interesting topic for nano(bio)technology. It is becoming increasingly clear that the
biomineralization process is genetically controlled and a great number of steps in
such biological control could exist.
Biomineralization in the sea urchin initiates from the early embryonic developmental stages and is mediated by the PMCs which express genes under a complex
signaling control of transcription and growth factors (for a review see Ettensohn
2009). Schematic drawings of the initial phases of embryonic skeleton deposition
and PMCs arrangement are presented in Fig. 8.2. Accumulating evidence
demonstrates that the PMCs express genes which control the formation and
remodeling of carbonate crystals. In sea urchin embryos, ACC is a transient
phase leading to the formation of calcitic spicules (Beniash et al. 1997; Weiss
et al. 2002). The formation of ACC results from a supersaturated solution produced
by ions and proteins (Raz et al. 2003).
8 Echinoderms as Blueprints for Biocalcification
231