Nickel is toxic and affects gene expression in sea urchin embryos (Paracentrotus lividus)

Heavy metals, such as Nickel (Ni), are naturally present in the seawater, but they become toxic beyond threshold concentrations, with adverse effects on marine organisms by interfering with many biological processes. Although many studies are available on Ni toxicity, the understanding of the mechanisms of its harmful effects on marine organisms is rather limited. It is known that Ni disrupts the dorso-ventral axis of sea urchin embryos, mainly affecting ectodermal differentiation and pattern formation of mesenchyme cells. Here, we used Paracentrotus lividus as a model to analyze the effects on the stress pathways in embryos continuously exposed to different Ni doses, ranging from 0.03 to 0.5mM. By an accurate analysis of the altered embryonic morphologies obtained at 24 and 48 h after Ni exposure, we found that embryos showed alterations not only at the expenses of the dorso-ventral axis, but also of the skeleton and/or the pigment cells. We studied the protein levels of stress markers, such as P-p38 MAPK, Mn-SOD, Grp78 at 24h after Ni-exposure. Furthermore, we analyzed the mRNA profiles of a pool of genes involved in stress response and development mechanisms, i.e. the transcription factors, Pl-NFkBand Pl-FOXO; a marker of DNA repair, Pl-XPB/ERCC3; a kinase, Pl-p38MAPK; a ER stress gene, Pl-grp78; an adapter protein, Pl-14-3-3e; two markers of pigment cells, Pl-PKS1 andPl-gcm. Our results indicated that Ni acts at several levels in P. lividussea urchin, by affecting embryo development and by activating the immune and stress response pathways, in order to cope with Ni injury and to promote embryos surviving.