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Abstract

It has long been observed that toxic heavy metals at different concentrations can induce root hair development in plants. In oilseed rape we studied ethylene levels and root hair initiation under Cd2+ stress. Growth of the primary root was inhibited but close to root tips the development of subapical root hairs was significantly stimulated by Cd2+ at 30 μM. Versus the control, the distance between the root tip and the root hair zone and the length of the epidermal cell in the elongation zone were significantly reduced by Cd2+ at the same concentration. Exogenous application of Cd2+ and 1-aminocyclopropane-1-carboxylate (ACC) to roots had similar effects on subapical root hair development. Hair density increase and hair elongation in the presence of Cd2+ were reduced by the ethylene inhibitors CoCl2 at 15 μM and aminooxyacetic acid (AOA) at 10 μM. Exposing roots to Cd2+ caused a rapid increase in superoxide radical (O2 ·-) production in the root hair differentiation zone, and at the tips of emerging and newly formed root hairs. Cd2+-induced O2 ·- production at the growing hair tips was blocked in the presence of AOA. Our findings suggest that Cd2+-induced ethylene signaling may act upstream of O2 ·-. Cd2+ promotion of O2 ·- production may operate through an ethylene signaling pathway, and O2 ·- itself may stimulate root hair elongation.
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Abstract

Phosphorothioate CpG oligodeoxynucleotides (ODN) are reported to be recognized by the membrane-bound TLR9 and trigger the MyD88-dependent up-regulation of Type I interferons and pro-inflammatory cytokines. Whether plasmids containing multiple CpG motifs stimulate the same signaling pathway is yet to be determined. The present results show that the CpG motifs enrich plasmid pUC18-CpG stimulates RAW 264.7 in vitro, mainly through the TBK1-mediated signaling pathway, causing the up-regulation of IFN-β, and pro-inflammatory cytokines TNF-α and IL-6. When pUC18-CpG is co-administered with the recombinant Echinococcus granulosus antigen, the antigen-specific antibody titers are markedly increased compared to the Quil-A adju- vanted group. Antigen specific cytokine quantification shows that cytokine profiles from the pUC18-CpG adjuvanted-group are switched to a Th1-biased immune response.
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