http://www.cnr.it/ontology/cnr/individuo/prodotto/ID279778
Cellular and molecular bases of biomineralization in sea urchin embryos (Articolo in rivista)
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- Cellular and molecular bases of biomineralization in sea urchin embryos (Articolo in rivista) (literal)
- Anno
- 2013-01-01T00:00:00+01:00 (literal)
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- Matranga V.; Pinsino A.; Bonaventura R.; Costa C.; Karakostis K.; Martino C.; Russo R.; Zito F. (literal)
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- http://www.scopus.com/inward/record.url?eid=2-s2.0-84888265360&partnerID=q2rCbXpz (literal)
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- Aistituto di Biomedicina e Immunologia Molecolare Alberto Monroy, Consiglio Nazionale Delle Ricerche, 90146 Palermo, Italy (literal)
- Titolo
- Cellular and molecular bases of biomineralization in sea urchin embryos (literal)
- Abstract
- Sea urchin embryos construct their skeleton following a precise gene-regulated time-and space-dependent programme, in concert with factors promoting cell adhesion and differentiation. The biomineral is deposited in a privileged extracellular space produced by the fused filopodia processes of the primary mesenchyme cells, the only cells producing a set of necessary matrix proteins. More than ten years ago we showed for the first time that signals from ectoderm cells promoted the expression of one of the major skeleton matrix genes by the primary mesenchyme cells. Since then, many of the crucial steps of this complex activation cascade, from ectoderm cells to embryonic spicules, have been elucidated. The experimental production of skeleton malformations, induced by the exposure to toxic metals or ionizing radiations, served as model to dissect the molecular mechanisms leading to biomineralization. With the aim of understanding the sea urchin skeleton physiology, we analysed the expression of well-known and newly-identified biomineral-related genes, including those coding for growth and transcription factors as well as for skeleton matrix proteins. This review summarizes our recent findings on sea urchin embryo skeletogenesis, with a particular attention to the role played by cellular and molecular signaling, approached by the use of experimentally induced skeleton malformations. (literal)
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