title: Echinoderms as blueprints for biocalcification: regulation of skeletogenic genes and matrices.
abstract: Echinoderms have an extensive endoskeleton composed of magnesian calcite, a form of calcium carbonate that contains small amounts of magnesium carbonate and occluded matrix proteins. Adult sea urchins have several calcified structures, including test, teeth, and spines, composed of numerous ossicles which form a three-dimensional meshwork of mineral trabeculae, the stereom. The biomineral development begins in 24-hour-old embryos within the primary mesenchyme cells (PMCs), the only cells producing a set of necessary matrix proteins. The deposition of the biomineral occurs in a privileged extracellular space produced by the fused filopodial processes of the PMCs. We showed for the first time that signals from ectoderm cells overlying PMCs play an important role in the regulation of biomineralization-related genes. It is believed that growth factors 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 βC 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.
authors.affiliation: Consiglio Nazionale delle Ricerche, Istituto di Biomedicina e Immunologia Molecolare "Alberto Monroy", Via Ugo La Malfa 153, 90146, Palermo, Italy, matranga@ibim.cnr.it.
authors.forename: Valeria
authors.initials: V
authors.lastname: Matranga
authors.forename: Rosa
authors.initials: R
authors.lastname: Bonaventura
authors.forename: Caterina
authors.initials: C
authors.lastname: Costa
authors.forename: Konstantinos
authors.initials: K
authors.lastname: Karakostis
authors.forename: Annalisa
authors.initials: A
authors.lastname: Pinsino
authors.forename: Roberta
authors.initials: R
authors.lastname: Russo
authors.forename: Francesca
authors.initials: F
authors.lastname: Zito
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000235:genetics; D002119:Calcium Carbonate / Q000378:metabolism; D004475:Ectoderm / Q000166:cytology; D005109:Extracellular Matrix / Q000378:metabolism; D016326:Extracellular Matrix Proteins / Q000235:genetics; D018507:Gene Expression Regulation, Developmental; D008648:Mesoderm / Q000166:cytology; D012617:Sea Urchins / Q000196:embryology; D016212:Transforming Growth Factor beta / Q000235:genetics
chemical_list: D000911:Antibodies, Monoclonal; D016326:Extracellular Matrix Proteins; D016212:Transforming Growth Factor beta; D002119:Calcium Carbonate