ArticleProtoplasma2005
Aluminium causes variable responses in actin filament cytoskeleton of the root tip cells of Triticum turgidum.
Article in Protoplasma, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 33 citations in OpenAlex.
- Identification and expression pattern of aluminium-responsive genes in roots of rice genotype with reference to Al-sensitivity.Scientific reports · 2023Article
- Nature and mechanisms of aluminium toxicity, tolerance and amelioration in symbiotic legumes and rhizobia.Biology and fertility of soils · 2018Review
- Root iTRAQ protein profile analysis of two Citrus species differing in aluminum-tolerance in response to long-term aluminum-toxicity.BMC genomics · 2015Article
- The nitrate reductase inhibitor, tungsten, disrupts actin microfilaments in Zea mays L.Protoplasma · 2014Article
- Structural changes in MSymbiosis (Philadelphia, Pa.) · 2012Article
- The role of the root apoplast in aluminium-induced inhibition of root elongation and in aluminium resistance of plants: a review.Annals of botany · 2010Review
- Article
- Actin is involved in early plant responses to heavy metal stress and associates with molecular chaperons in stress environments.Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sectionsArticle
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.