Soil-to-plant transfer of naphthalene and its effects on seedlings pea (Pisum sativum L.) grown on contaminated soil.

The aim of this work was to determinate effect of naphthalene at different concentrations on morphological, physiological and some metabolic responses of pea seedlings. The quantification of naphthalene and its by-products were also recorded by Gas Chromatography/ Mass Spectrometry (GC / MS) in soil and in the different plant parts (roots, stems, leaves and fruit). In our controlled laboratory studies, plants exposed to naphthalene were able to efficiently grow and maintain their content of chlorophyll and carotenoids comparatively to the control plants. However, the pollutant slightly increased the amounts of fatty acid peroxides and strongly those of malonyldialdehyde, the product of lipid peroxidation. The glutathione S transferase activity was also increased for all concentrations used especially in leaves. Chromatograms showed that naphthalene has fallen sharply in the soil or even disappeared for the highest concentration from the second to third week. Furthermore, the removal ratio of 67% of the pollutant from the soil was distributed between two metabolites (ion 47 and ion 59) in the leaves for this same concentration in only three weeks of cultivation. In parallel, the amount of pollutant remained higher in unvegetated control soil. These results suggest that seedlings of pea (Pisum sativum L.) can remove naphthalene from contaminated soil and consequently have a high potential to be used as a promising candidate for the phytoremediation of naphthalene-contaminated soil.

Complex regulation of LCoR signaling in breast cancer cells.

Ligand-dependent corepressor (LCoR) is a transcriptional repressor of ligand-activated estrogen receptors (ERs) and other transcription factors that acts both by recruiting histone deacetylases and C-terminal binding proteins. Here, we first studied LCOR gene expression in breast cancer cell lines and tissues. We detected two mRNAs variants, LCoR and LCoR2 (which encodes a truncated LCoR protein). Their expression was highly correlated and localized in discrete nuclear foci. LCoR and LCoR2 strongly repressed transcription, inhibited estrogen-induced target gene expression and decreased breast cancer cell proliferation. By mutagenesis analysis, we showed that the helix-turn-helix domain of LCoR is required for these effects. Using in vitro interaction, coimmunoprecipitation, proximity ligation assay and confocal microscopy experiments, we found that receptor-interacting protein of 140 kDa (RIP140) is a LCoR and LCoR2 partner and that this interaction requires the HTH domain of LCoR and RIP140 N- and C-terminal regions. By increasing or silencing LCoR and RIP140 expression in human breast cancer cells, we then showed that RIP140 is necessary for LCoR inhibition of gene expression and cell proliferation. Moreover, LCoR and RIP140 mRNA levels were strongly correlated in breast cancer cell lines and biopsies. In addition, RIP140 positively regulated LCoR expression in human breast cancer cells and in transgenic mouse models. Finally, their expression correlated with overall survival of patients with breast cancer. Taken together, our results provide new insights into the mechanism of action of LCoR and RIP140 and highlight their strong interplay for the control of gene expression and cell proliferation in breast cancer cells.