11 research outputs found
Aluminium effects on microtubule organization in dividing root-tip cells of Triticum turgidum. I. Mitotic cells
The effects of aluminium (Al) on dividing root-tip cells of Triticum
turgidum were investigated with tubulin immunolabelling and electron
microscopy. Aluminium affects the mechanisms controlling the
organization of microtubule (MT) cytoskeleton, as well as tubulin
polymerization, and induces the following aberrations in mitotic cells.
(1) It delays the MT disassembly during mitosis, resulting in the
persistence of preprophase MT bands in the late prophase cells, the
presence of prophase spindles in prometaphase cells, and a disturbance
in the shortening of kinetochore MT bundles in anaphase cells. (2) It
interferes with the self-organization process of MTs into bipolar
systems, inhibiting the formation of prophase and metaphase spindles.
(3) Aluminium induces the formation of atypical MT arrays, which in the
immunofluorescent specimens appear as ring-like tubulin aggregations in
the cortical cytoplasm of the preprophase/prophase cells and as
endoplasmic tubulin bundles in prophase and metaphase/anaphase cells;
abnormal preprophase MT bands are assembled, consisting of atypical
cortical and endoplasmic MT bundles, the latter clearly lining the
nuclear envelope on the preprophase MT band plane. (4) It disorders the
chromosome movements carried out by the mitotic spindle. In addition,
after prolonged Al treatments chromatin condensation is inhibited. The
outcome is greatly disturbed organization and function of the mitotic
appartus, as well as inhibition of cells from entering mitosis. This
study shows that the MT cytoskeleton is a target site of Al toxicity in
mitotic root-tip cells of T. turgidum. The possible mechanisms by which
Al exerts its toxicity on MT organization and function are discussed
Aluminium causes variable responses in actin filament cytoskeleton of the root tip cells of Triticum turgidum
The effects of aluminium on the actin filament (AF) cytoskeleton of Triticum turgidum meristematic root tip cells were examined. In short treatments (up to 2 h) with 50-1000 μM AlCl3·6H2O, interphase cells displayed numerous AFs arrayed in thick bundles that lined the plasmalemma and traversed the endoplasm in different directions. Measurements using digital image analysis and assessment of the overall AF fluorescence revealed that, in short treatments, the affected cells possessed 25-30% more AFs than the untreated ones. The thick AF bundles were not formed in the Al-treated cells in the presence of the myosin inhibitors 2,3-butanedione monoxime (BDM) and 1-(5-iodonaphthalene-1-sulfonyl)-1H-hexahydro-1,4-diazepine (ML-7), a fact suggesting that myosins are involved in AF bundling. In longer Al treatments, the AF bundles were disorganised, forming granular actin accumulations, a process that was completed after 4 h of treatment. In the Al-treated cells, increased amounts of callose were uniformly deposited along the whole surface of the cell walls. In contrast, callose formed local deposits in the Al-treated cells in the presence of cytochalasin B, BDM, or ML-7. These results favour the hypothesis that the actomyosin system in the Al-treated cells, among other roles, participates in the mechanism controlling callose deposition. © Springer-Verlag 2005
Lethal and Sublethal Effects of Imidacloprid, After Chronic Exposure, On the Insect Model Drosophila melanogaster
International audienceNeonicotinoids are subjected to vigilance because of environmental contaminations and deleterious effects on bees. Imidacloprid (IMI) is one of the most representative insecticides of this family. At chronic exposure, concentration-effect relationships are non linear. An insect model should allow a better description of this toxicity. We compared the lethal concentration 50% (LC50) of IMI for a Drosophila-field strain, after acute and chronic exposure. Relative to the acute LC50, the chronic LC50 was lowered by a factor of 29 for males (1.3 mM/45 muM), 52 for larvae (157 muM/3 muM) and more than 172 for females (>3.1 mM/18 muM). Chronic exposure also revealed significant lethal and sublethal effects, at concentrations 3-5 orders of magnitude lower than the chronic LC50. Mean mortalities reached 28% (at 3.91 nM) and 27% (at 39.1 nM) for females and males, respectively. Fecundity decreased of 16% at 1.96 nM. Mating increased of 30% at 0.391 nM. The LOEC (lowest observed effect concentration: 0.391 nM) was 46 000 times lower than the chronic LC50 for males; it was 115 000 times lower than the chronic LC50 for females. This study illuminates effects that neonicotinoids can induce at very low concentrations. This is of particular interest for nontarget insects and for insect dependent species