Does aluminium affect root growth of maize through interaction with the cell wall – plasma membrane – cytoskeleton continuum?

The mechanism of aluminium-induced inhibition of root elongation is still not well understood. It is a matter of debate whether the primary lesions of Al toxicity are apoplastic or symplastic. The present paper summarises experimental evidence which offers new avenues in the understanding of Al toxicity and resistance in maize. Application of Al for 1 h to individual 1 mm sections of the root apex only inhibited root elongation if applied to the first 3 apical mm. The most Al-sensitive apical root zone appeared to be the 1–2 mm segment. Aluminium-induced prominent alterations in both the microtubular (disintegration) and the actin cytoskeleton (altered polymerisation patterns) were found especially in the apical 1–2 mm zone using monoclonal antibodies. Since accumulation of Al in the root apoplast is dependent on the properties of the pectic matrix, we investigated whether Al uptake and toxicity could be modulated by changing the pectin content of the cell walls through pre-treatment of intact maize plants with 150 mM NaCl for 5 days. NaCl-adapted plants with higher pectin content accumulated more Al in their root apices and they were more Al-sensitive as indicated by more severe inhibition of root elongation and enhanced callose induction by Al. This special role of the pectic matrix of the cell walls in the modulation of Al toxicity is also indicated by a close positive correlation between pectin, Al, and Al-induced callose contents of 1 mm root segments along the 5 mm root apex. On the basis of the presented data we suggest that the rapid disorganisation of the cytoskeleton leading to root growth inhibition may be mediated by interaction of Al with the apoplastic side of the cell wall – plasma membrane – cytoskeleton continuum. This revised version was published online in June 2006 with corrections to the Cover Date.     

Estrogen has rapid tissue-specific effects on rat bone.

The decrease in cancellous bone formation after estrogen treatment is generally thought to be coupled with a prior decrease in bone resorption. To test the possibility that estrogen has rapid tissue-specific actions on bone metabolism, we determined the time course (1-32 h) effects of diethylstilbestrol on steady-state mRNA levels for immediate-response genes, extracellular matrix proteins, and signaling peptides in the proximal tibial metaphysis and uterus by using Northern blot and RNase protection assays. The regulation of signaling peptides by estrogen, although tissue specific, followed a similar time course in bone and uterus. The observed rapid decreases in expression of insulin-like growth factor I, a growth factor associated with bone formation; decreases in mRNA levels for bone matrix proteins; evidence for reduced bone matrix synthesis; failure to detect rapid increases in mRNA levels for signaling peptides implicated in mediating the inhibitory effects of estrogen on bone resorption (interleukin-1 and -6) as well as other cytokines that can increase bone resorption; and the comparatively long duration of the bone remodeling cycle in rats indicate that estrogen can decrease bone formation by a mechanism that does not require a prior reduction in bone resorption.     

BCC-NER: bidirectional,contextual clues named entity tagger for gene/protein mention recognition

Tagging biomedical entities such as gene, protein, cell, and cell-line is the first step and an important pre-requisite in biomedical literature mining. In this paper, we describe our hybrid named entity tagging approach namely BCC-NER (bidirectional, contextual clues named entity tagger for gene/protein mention recognition). BCC-NER is deployed with three modules. The first module is for text processing which includes basic NLP pre-processing, feature extraction, and feature selection. The second module is for training and model building with bidirectional conditional random fields (CRF) to parse the text in both directions (forward and backward) and integrate the backward and forward trained models using margin-infused relaxed algorithm (MIRA). The third and final module is for post-processing to achieve a better performance, which includes surrounding text features, parenthesis mismatching, and two-tier abbreviation algorithm. The evaluation results on BioCreative II GM test corpus of BCC-NER achieve a precision of 89.95, recall of 84.15 and overall F-score of 86.95, which is higher than the other currently available open source taggers.     

On the Diversity of Environmental Signs: a Typological Approach

Environmental signs as physically manifested signs that we and other animals perceive and interpret in the natural environment are seldom focused on in contemporary semiotics. The aim of the present paper is to highlight the diversity of environmental signs and to propose a typology for analysing them. Combining ecosemiotics and the pragmatist semiotics of C. Peirce and C. Morris, the proposed typology draws its criteria from the properties of the object and the representamen of the sign, and of their relationships. The analysis distinguishes eight basic types of environmental signs and provides examples of these from the natural environment. The typology also integrates existing concepts of environmental affordances, ecofields, phonetic syntax, sign fields, ecological codes, meta-signs and others. In addition to basic types of environmental signs, compound environmental signs are discussed with three types of these distinguished: (1) environmental meta-signs; (2) ecological codes; and (3) environmental-cultural hybrid signs. Further study of compound environmental signs could lead to reconceptualising relations between linguistic and pre-linguistic semiosis.     

The autoimmune regulator PHD finger binds to non-methylated histone H3K4 to activate gene expression

Mutations in the gene autoimmune regulator (AIRE) cause autoimmune polyendocrinopathy candidiasis ectodermal dystrophy. AIRE is expressed in thymic medullary epithelial cells, where it promotes the expression of tissue-restricted antigens. By the combined use of biochemical and biophysical methods, we show that AIRE selectively interacts with histone H3 through its first plant homeodomain (PHD) finger (AIRE-PHD1) and preferentially binds to non-methylated H3K4 (H3K4me0). Accordingly, in vivo AIRE binds to and activates promoters containing low levels of H3K4me3 in human embryonic kidney 293 cells. We conclude that AIRE-PHD1 is an important member of a newly identified class of PHD fingers that specifically recognize H3K4me0, thus providing a new link between the status of histone modifications and the regulation of tissue-restricted antigen expression in thymus.     

An erythrocyte vesicle protein exported by the malaria parasite promotes tubovesicular lipid import from the host cell surface

Plasmodium falciparum is the protozoan parasite that causes the most virulent of human malarias. The blood stage parasites export several hundred proteins into their host erythrocyte that underlie modifications linked to major pathologies of the disease and parasite survival in the blood. Unfortunately, most are 'hypothetical' proteins of unknown function, and those that are essential for parasitization of the erythrocyte cannot be 'knocked out'. Here, we combined bioinformatics and genome-wide expression analyses with a new series of transgenic and cellular assays to show for the first time in malaria parasites that microarray read out from a chemical perturbation can have predictive value. We thereby identified and characterized an exported P. falciparum protein resident in a new vesicular compartment induced by the parasite in the erythrocyte. This protein, named Erythrocyte Vesicle Protein 1 (EVP1), shows novel dynamics of distribution in the parasite and intraerythrocytic membranes. Evidence is presented that its expression results in a change in TVN-mediated lipid import at the host membrane and that it is required for intracellular parasite growth, but not invasion. This exported protein appears to be needed for the maintenance of an essential tubovesicular nutrient import pathway induced by the pathogen in the host cell. Our approach may be generalized to the analysis of hundreds of 'hypothetical' P. falciparum proteins to understand their role in parasite entry and/or growth in erythrocytes as well as phenotypic contributions to either antigen export or tubovesicular import. By functionally validating these unknowns, one may identify new targets in host-microbial interactions for prophylaxis against this major human pathogen.     

Calreticulin mRNA and protein are localized to protein bodies in storage maize callus cells

Maize callus cells possess numerous protein bodies which develop as sub-compartments of the endoplasmic reticulum. We localized maize calreticulin mRNAs and protein in maize callus cells using in situ hybridization and immunocytochemistry. Calreticulin mRNAs were selectively targeted to the endoplasmic reticulum (ER) subdomains surrounding protein bodies. Profilin mRNAs, used as a positive control for in situ hybridization experiments, showed distinct and rather diffuse localization pattern. Using both, immunofluorescence and immunogold electron microscopy localization techniques, calreticulin was found to be enriched around and within protein bodies in maize callus storage cells. As a positive control for reticuloplasmins, HDEL antibody revealed labelling of protein bodies and of the nuclear envelope. The identity of protein bodies was confirmed by specific binding of an α zein antibody. These data suggest that calreticulin mRNA is targeted towards protein body forming subdomains of the ER, and that calreticulin is localized and enriched in these protein bodies. The possibility that calreticulin plays an important role in zein retention within the ER and/or its assembly and packaging into protein bodies during protein body biogenesis in maize callus is discussed.     

2-methoxyestradiol-induced cell death in osteosarcoma cells is preceded by cell cycle arrest

2-Methoxyestradiol (2-ME), a naturally occurring mammalian metabolite of 17beta-Estradiol (E2), induces cell death in osteosarcoma cells. To further understand the molecular mechanisms of action, we have investigated cell cycle progression in 2-ME-treated human osteosarcoma (MG63, SaOS-2 and LM7 [corrected]) cells. At 5 microM, 2-ME induced growth arrest by inducing a block in cell cycle; 2-ME-treatment resulted in 2-fold increases in G1 phase cells and a decrease in S phase cells in MG63 and SaOS-2 osteosarcoma cell lines, compared to the appropriate vehicle controls. 2-ME-treatment induced a threefold increase in the G2 phase in LM7 [corrected] osteosarcoma cells. The results demonstrated steroid specificity, as the tumorigenic metabolite, 16alpha-hydroxyestradiol (16-OHE), did not have any effect on cell cycle progression in osteosarcoma cells. The cell cycle arrest coincided with an increase in expression of the cell cycle markers p21, p27 and p53 proteins in 2-ME-treated osteosarcoma cells. Also, MG63 cells, transiently transfected with cDNA for a 'loss of function mutant' RNA-dependent protein kinase (PKR) protein, were resistant to 2-ME-induced cell cycle arrest. These results suggest that 2-ME works in concert with factors regulating cell cycle progression, and cell cycle arrest precedes cell death in 2-ME-treated osteosarcoma cells.