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ECB-ART-40490
Dev Growth Differ 2007 Dec 01;499:731-41. doi: 10.1111/j.1440-169X.2007.00967.x.
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Skeletogenesis by transfated secondary mesenchyme cells is dependent on extracellular matrix-ectoderm interactions in Paracentrotus lividus sea urchin embryos.

Kiyomoto M , Zito F , Costa C , Poma V , Sciarrino S , Matranga V .


Abstract
In the sea urchin embryo, primary mesenchyme cells (PMCs) are committed early in development to direct skeletogenesis, provided that a permissive signal is conveyed from adjacent ectoderm cells. We showed that inhibition of extracellular matrix (ECM)-ectoderm cells interaction, by monoclonal antibodies (mAb) to Pl-nectin, causes an impairment of skeletogenesis and reduced expression of Pl-SM30, a spicule-specific matrix protein. When PMCs are experimentally removed, some secondary mesenchyme cells (SMCs) switch to skeletogenic fate. Here, for the first time we studied SMC transfating in PMC-less embryos of Paracentrotus lividus. We observed the appearance of skeletogenic cells within 10 h of PMCs removal, as shown by binding of wheat germ agglutinin (WGA) to cell surface molecules unique to PMCs. Interestingly, the number of WGA-positive cells, expressing also msp130, another PMC-specific marker, doubled with respect to that of PMCs present in normal embryos, though the number of SM30-expressing cells remained constant. In addition, we investigated the ability of SMCs to direct skeletogenesis in embryos exposed to mAbs to Pl-nectin after removal of PMCs. We found that, although phenotypic SMC transfating occurred, spicule development, as well as Pl-SM30-expression was strongly inhibited. These results demonstrate that ectoderm inductive signals are necessary for transfated SMCs to express genes needed for skeletogenesis.

PubMed ID: 17983367
Article link: Dev Growth Differ


Genes referenced: LOC100887844 LOC115919910 LOC115924199 LOC115924597 msp130
Antibodies: msp130 Ab2