skeletons of many organisms make them potentially susceptible to dissolution
in acidic waters (Orr et al. 2005). The pH shift consequent to CO 2 dissolution in
seawater changes the equilibrium between bicarbonate and carbonate, depleting
the available carbonate pool (Gattuso et al. 2010). It has been demonstrated that
CO 2 -induced seawater acidification alters skeletogenesis of different developing
sea urchin species: Hemicentrotus pulcherrimus and Echinometra mathaei
(Kurihara and Shirayama 2004), L. pictus (O’Donnell et al. 2010), P. lividus
(Dupon et al. 2010), and Tripneusteus gratilla (Sheppard-Brennand et al. 2010).
Embryos showed significant perturbation on both size and shape, which were
enhanced upon simultaneous seawater warming and acidification, suggesting that
although much emphasis has been placed on ocean acidification, embryos may
not reach the skeletogenic stage because of warm waters (Sheppard-Brennand
et al. 2010).
When looking at gene expression profiles using genome microarrays of
L. pictus, O’Donnell et al. (2010) showed that, among genes involved in energy
metabolism and biomineralization, only a few were downregulated, including
Suclg-1succinyl-CoA synthetase, SM30-like, osteonectin, whereas only the
Atp2a1-Ca
2+ ATPase, involved in ion regulation and acid–base balance pathways
was upregulated. All together, these results suggest that, although larvae are able
to form an endoskeleton, increased CO 2 levels have consequences on larval
transcriptome. Contrary to expectations, no visible differences in developmental
timing or obvious developmental skeleton abnormalities were associated with CO 2
treatments in S. purpuratus. However, the trascriptomic approach has evidenced the
downregulation of a few biomineralization genes, namely: cyclophylins, MSP130,
MSP130-related, collagens (COLP3a, COLP4a, etc.), P19, P16, P16-like,
osteonectin (Todgham and Hofmann 2009).
8.6 Concluding Remarks
The formation of the sea urchin skeleton offers a good model for the in vivo study of
biocalcification both in adults and embryos, the latter where most of the studies
were performed. In summary, to build the magnesian calcitic embryonic skeleton,
cellular, microenvironmental conditions and a biomolecular toolkit are needed.
PMCs, the only cells in the embryo controlling skeleton origin and growth, provide
a set of specific spicule matrix proteins and supersaturated calcium carbonate
niches. The process initiates with the formation of intermediate transient
aggregating nanoparticles of ACC, which then crystallizes into macroscopic single
rhombohedral crystals of calcite (Yang et al. 2011). Radial growth of the crystals
and its branching is probably dictated by more than 200 PMCs-specific proteins, the
most famous being SM30 and SM50, the first to be fully described (reviewed by
Wilt 1999), which take part in the above-mentioned mechanism, possessing different roles. Within the gene repertoire of PMCs, among a great number of annotated
242
V. Matranga et al.
in acidic waters (Orr et al. 2005). The pH shift consequent to CO 2 dissolution in
seawater changes the equilibrium between bicarbonate and carbonate, depleting
the available carbonate pool (Gattuso et al. 2010). It has been demonstrated that
CO 2 -induced seawater acidification alters skeletogenesis of different developing
sea urchin species: Hemicentrotus pulcherrimus and Echinometra mathaei
(Kurihara and Shirayama 2004), L. pictus (O’Donnell et al. 2010), P. lividus
(Dupon et al. 2010), and Tripneusteus gratilla (Sheppard-Brennand et al. 2010).
Embryos showed significant perturbation on both size and shape, which were
enhanced upon simultaneous seawater warming and acidification, suggesting that
although much emphasis has been placed on ocean acidification, embryos may
not reach the skeletogenic stage because of warm waters (Sheppard-Brennand
et al. 2010).
When looking at gene expression profiles using genome microarrays of
L. pictus, O’Donnell et al. (2010) showed that, among genes involved in energy
metabolism and biomineralization, only a few were downregulated, including
Suclg-1succinyl-CoA synthetase, SM30-like, osteonectin, whereas only the
Atp2a1-Ca
2+ ATPase, involved in ion regulation and acid–base balance pathways
was upregulated. All together, these results suggest that, although larvae are able
to form an endoskeleton, increased CO 2 levels have consequences on larval
transcriptome. Contrary to expectations, no visible differences in developmental
timing or obvious developmental skeleton abnormalities were associated with CO 2
treatments in S. purpuratus. However, the trascriptomic approach has evidenced the
downregulation of a few biomineralization genes, namely: cyclophylins, MSP130,
MSP130-related, collagens (COLP3a, COLP4a, etc.), P19, P16, P16-like,
osteonectin (Todgham and Hofmann 2009).
8.6 Concluding Remarks
The formation of the sea urchin skeleton offers a good model for the in vivo study of
biocalcification both in adults and embryos, the latter where most of the studies
were performed. In summary, to build the magnesian calcitic embryonic skeleton,
cellular, microenvironmental conditions and a biomolecular toolkit are needed.
PMCs, the only cells in the embryo controlling skeleton origin and growth, provide
a set of specific spicule matrix proteins and supersaturated calcium carbonate
niches. The process initiates with the formation of intermediate transient
aggregating nanoparticles of ACC, which then crystallizes into macroscopic single
rhombohedral crystals of calcite (Yang et al. 2011). Radial growth of the crystals
and its branching is probably dictated by more than 200 PMCs-specific proteins, the
most famous being SM30 and SM50, the first to be fully described (reviewed by
Wilt 1999), which take part in the above-mentioned mechanism, possessing different roles. Within the gene repertoire of PMCs, among a great number of annotated
242
V. Matranga et al.