Desulfovibrio magneticus RS-1 contains an iron- and phosphorus-rich organelle distinct from its bullet-shaped magnetosomes.

Intracellular magnetite crystal formation by magnetotactic bacteria has emerged as a powerful model for investigating the cellular and molecular mechanisms of biomineralization, a process common to all branches of life. Although magnetotactic bacteria are phylogenetically diverse and their crystals morphologically diverse, studies to date have focused on a few, closely related species with similar crystal habits. Here, we investigate the process of magnetite biomineralization in Desulfovibrio magneticus sp. RS-1, the only reported species of cultured magnetotactic bacteria that is outside of the alpha-Proteobacteria and that forms bullet-shaped crystals. Using a variety of high-resolution imaging and analytical tools, we show that RS-1 cells form amorphous, noncrystalline granules containing iron and phosphorus before forming magnetite crystals. Using NanoSIMS (dynamic secondary ion mass spectroscopy), we show that the iron-phosphorus granules and the magnetite crystals are likely formed through separate cellular processes. Analysis of the cellular ultrastructure of RS-1 using cryo-ultramicrotomy, cryo-electron tomography, and tomography of ultrathin sections reveals that the magnetite crystals are not surrounded by membranes but that the iron-phosphorus granules are surrounded by membranous compartments. The varied cellular paths for the formation of these two minerals lead us to suggest that the iron-phosphorus granules constitute a distinct bacterial organelle.

Zinc deficiency reduces paclitaxel efficacy in LNCaP prostate cancer cells.

Chemotherapeutics used to treat prostate cancer are often from a class of drugs that target microtubule networks, such as paclitaxel. A previous report indicated that supplemental zinc sensitized prostate cancer cells to paclitaxel-induced apoptosis, suggesting that increased zinc levels might enhance paclitaxel efficacy. The effect of zinc deficiency on paclitaxel activity is not known though, so we tested this in two prostate cancer cell lines maintained under moderately zinc-deficient conditions. LNCaP and PC3 cell lines were used as models of early and late-stage prostate cancer, respectively. Cells cultured in reduced zinc levels did not demonstrate altered cell viability, growth rates, or intracellular zinc content. Additionally, zinc deficiency alone had no apparent effect on cell cycle kinetics or apoptosis levels. However, the IC(50) for paclitaxel-induced cell cycle arrest increased in LNCaP cells from zinc-deficient compared to zinc-replete conditions. Consequently, paclitaxel-induced apoptosis was reduced in LNCaP cells from zinc-deficient compared to zinc-replete conditions. In PC3 cells, the effects of paclitaxel were independent of zinc status. Reduced extracellular zinc levels were shown to affect paclitaxel activity in a prostate cancer cell line. Given the prevalence of zinc deficiency, determining how chemotherapeutic action is modulated by zinc adequacy may have clinical importance.