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 apparatus, 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.
The effects of aluminium (Al) on telophase/cytokinetic root-tip cells of Triticum tu@dum were examined, using tubulin immunolabeling and electron microscopy. In cells, which at the beginning of the treatment were at a transitional Wge between anaphase and telophase, the transformation of the interzonal microtubule (Mt) system into a phagmoplast was delayed. In cells treated at a telophasel cytokinetic stage, the lateral phragmoplast expansion towards the cell periphery was delayed or inhibited.Besides, in cells entering telophase through an abnormal mitosis, Al inhibited phragmoplast formation and induced the organization of atypical tubulin bundles. The latter formed a network around the reassembling polyploid nucleus. The Al-effects resulted in the disturbance of cytokinesis and the formation of binuclear or polyploid cells, which lacked typical Mts. Instead of them, the post-telophase cells displayed atypical tubulin aggregations. In addition, Al affects cell plate development. Dividing cells, encompassing early interphase daughter nuclei, contained incomplete, atypical cell plates. The latter were quite thick, wavy and perforated, showing large "islands", which contained electron transparent material. In some cells, the atypical cell plates gave rise to incomplete daughter walls, but in some others they were dismantled. The aberrant cell plates as well as the young daughter cell walls fluoresced intensely after aniline blue staining, an observation suggesting that they contain significant quantities of callose. The above findings combined with those derived from the study of the Al-effects on the mitotic spindle show that Mt cytoskeleton is a target site of Al toxicity in dividing cells.
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 microM 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.
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