Al3+-Ca2+ interactions in aluminum rhizotoxicity

Several mineral rhizotoxicities, including those induced by Al³⁺, H⁺, and Na⁺, can be relieved by elevated Ca²⁺ in the rooting medium. This leads to the hypothesis that the toxic cations displace Ca²⁺ from transport channels or surface ligands that must be occupied by Ca²⁺ in order for root elongation to occur. In this study with wheat (Triticum aestivum L.) seedlings, we have determined, in the case of Al³⁺, that (i) Ca²⁺, Mg²⁺, and Sr²⁺ are equally ameliorative, (ii) that root elongation does not increase as Ca²⁺ replaces Mg²⁺ or Sr²⁺ in the rooting media, and (iii) that rhizotoxicity is a function solely of Al³⁺ activity at the root-cell membrane surface as computed by a Gouy-Chapman-Stern model. The rhizotoxicity was indifferent to the computed membrane-surface Ca²⁺ activity. The rhizotoxicity induced by high levels of tris(ethylenediamine)cobaltic ion (TEC³⁺), in contrast to Al³⁺, was specifically relieved by Ca²⁺ at the membrane surface. The rhizotoxicity induced by H⁺ exhibited a weak specific response to Ca²⁺ at the membrane surface. We conclude that the Ca²⁺-displacement hypothesis fails in the case of Al³⁺ rhizotoxicity and that amelioration by cations (including monovalent cations) occurs because of decreased membrane-surface negativity and the consequent decrease in the membrane-surface activity of Al³⁺. However, TEC³⁺, but not Al³⁺, may be toxic because it inhibits Ca²⁺ uptake. The nature of the specific H⁺-Ca²⁺ interaction is uncertain.Abbreviations {Al³⁺ }₀ chemical activity of Al³⁺ at the root-cell membrane surface - {Al³⁺ }_E chemical activity of Al³⁺ in the external rooting medium - E₀ electrical potential at the root-cell membrane surface - HXM²⁺ hexamethonium ion - TEC³⁺ tris(ethylenediamine)cobaltic ion     

Woody plant encroachment in granite barrens on the Frontenac Arch,eastern Ontario,Canada

Aims

Woody plant encroachment is a widespread phenomenon affecting treeless or sparsely treed habitats. We aimed to determine the extent and timing of tree and shrub encroachment into rock barrens of eastern Ontario over the last century, and to assess implications for their ongoing management.

Location

Queen's University Biological Station in the Frontenac Arch ecoregion.

Methods

We quantified the extent of change in woody vegetation in 290 rock barrens using aerial photography from 1925, 1965, and 2008. Composition and structure of woody plant communities in 10 barrens was subsequently quantified in the field using plot-based sampling. Cores or cross-sections were obtained from individuals >1.5 m height and dendrochronological techniques were used to determine their age and identify temporal patterns of any woody encroachment.

Results

Aerial photography indicated that the mean proportion of woody plant cover in barrens increased 22.5% from 1925 to 2008. Dendroecological analysis supported this. Few trees were present prior to 1900 and most established since 1960. Fraxinus americana, Juniperus virginiana, and Juniperus communis were the most common woody species colonizing the barrens. Remnants of large Pinus strobus stumps with extensive charring were found in 90% of the sampled barrens at a mean density of 22.6 stumps ha⁻¹.

Conclusions

Rock barrens on the Frontenac Arch have changed substantially over the past century; gradually being colonized by trees and shrubs and losing their distinctly open character. Active management — including prescribed fire and mechanical thinning — may be necessary if there is a desire to maintain these barrens and the rare species they support as components of the region's biodiversity. However, identification of a reference state for restoration is complicated by the fact that the structure and composition of these habitats were undoubtedly altered by European land clearance in the 19th century, and that some of these areas likely existed as pine woodlands before that.     

Loss of DNA repair mechanisms in cardiac myocytes induce dilated cardiomyopathy

Cardiomyopathy is a progressive disease of the myocardium leading to impaired contractility. Genotoxic cancer therapies are known to be potent drivers of cardiomyopathy, whereas causes of spontaneous disease remain unclear. To test the hypothesis that endogenous genotoxic stress contributes to cardiomyopathy, we deleted the DNA repair gene Ercc1 specifically in striated muscle using a floxed allele of Ercc1 and mice expressing Cre under control of the muscle-specific creatinine kinase (Ckmm) promoter or depleted systemically (Ercc1^−/D mice). Ckmm-Cre^+/−;Ercc1^−/fl mice expired suddenly of heart disease by 7 months of age. As young adults, the hearts of Ckmm-Cre^+/−;Ercc1^−/fl mice were structurally and functionally normal, but by 6-months-of-age, there was significant ventricular dilation, wall thinning, interstitial fibrosis, and systolic dysfunction indicative of dilated cardiomyopathy. Cardiac tissue from the tissue-specific or systemic model showed increased apoptosis and cardiac myocytes from Ckmm-Cre^+/-;Ercc1^−/fl mice were hypersensitive to genotoxins, resulting in apoptosis. p53 levels and target gene expression, including several antioxidants, were increased in cardiac tissue from Ckmm-Cre^+/−;Ercc1^−/fl and Ercc1^−/D mice. Despite this, cardiac tissue from older mutant mice showed evidence of increased oxidative stress. Genetic or pharmacologic inhibition of p53 attenuated apoptosis and improved disease markers. Similarly, overexpression of mitochondrial-targeted catalase improved disease markers. Together, these data support the conclusion that DNA damage produced endogenously can drive cardiac disease and does so mechanistically via chronic activation of p53 and increased oxidative stress, driving cardiac myocyte apoptosis, dilated cardiomyopathy, and sudden death.     

Isolation of signaling mutants of tomato (Lycopersicon esculentum)

As a first step towards developing a genetic system for investigating signaling processes in plants, we have developed a screen for signaling mutants deficient in a wound response. We have isolated two mutants of tomato that lack detectable production of proteinase inhibitors induced systemically in leaves by wounding. The mutants are deficient in the induction of both proteinase Inhibitor I and proteinase Inhibitor II but can be induced to respond at near wild-type levels by methyl jasmonate, a known elicitor of inhibitor production in tomato. While completely deficient in systemic production of proteinase inhibitors, both mutants produce some proteinase inhibitor in wounded leaves. This evidence suggests the existence of two signaling pathways, one local and one systemic, that regulate the induction of proteinase inhibitor snythesis in response to wounding.     

Chromosomal localization of uroplakin genes of cattle and mice

The asymmetric unit membrane (AUM) of the apical surface of mammalian urinary bladder epithelium contains several major integral membrane proteins, including uroplakins IA and IB (both 27 kDa), II (15 kDa), and III (47 kDa). These proteins are synthesized only in terminally differentiated bladder epithelial cells. They are encoded by separate genes and, except for uroplakins IA and IB, appear to be unrelated in their amino acid sequences. The genes encoding these uroplakins were mapped to chromosomes of cattle through their segregation in a panel of bovine x rodent somatic cell hybrids. Genes for uroplakins IA, IB, and II were mapped to bovine (BTA) Chromosomes (Chrs) 18 (UPK1A), 1 (UPK1B), and 15 (UPK2), respectively. Two bovine genomic DNA sequences reactive with a uroplakin III cDNA probe were identified and mapped to BTA 6 (UPK3A) and 5 (UPK3B). We have also mapped genes for uroplakins 1A and II in mice, to the proximal regions of mouse Chr 7 (Upk1a) and 9 (Upk2), respectively, by analyzing the inheritance of restriction fragment length variants in recombinant inbred mouse strains. These assignments are consistent with linkage relationships known to be conserved between cattle and mice. The mouse genes for uroplakins IB and III were not mapped because the mouse genomic DNA fragments reactive with each probe were invariant among the inbred strains tested. Although the stoichiometry of AUM proteins is nearly constant, the fact that the uroplakin genes are unlinked indicates that their expression must be independently regulated. Our results also suggest likely positions for two human uroplakin genes and should facilitate further analysis of their possible involvement in disease.     

Frequent nest relocation in the ant Aphaenogaster araneoides: resources, competition, and natural enemies

Sessile and vagile organisms differ from one another in some fundamental ways, including methods of resource acquisition and competition. Ant colonies are typically studied as sessile entities, even though a large fraction of ant species frequently relocate their nests in the course of their life history. Little is known about the causes and consequences of nest relocation, but it is likely that the costs and benefits of relocation are driven by nest quality, neighborhood competition, or resource availability. In this paper, we document several cycles of nest relocation in a population of the Central American ant Aphaenogaster araneoides . In our first experiment, we tracked the pattern of relocation, testing whether environmental characteristics and colony demography were associated with relocation behavior. In our second experiment, we manipulated resource availability by adding or subtracting leaf litter, which is known to predict colony growth. We found that colonies relocated their nests once per week on average and colonies often reoccupied nests from which they had once emigrated. Larger colonies relocated more frequently than smaller colonies, and quickly growing colonies utilized a greater number of nests within their home range compared to slowly growing colonies. Relocation events were most likely to occur in periods when vapor pressure deficits were greatest. Nearest neighbor distance and other measures of environmental conditions were not associated with relocation behavior and there was no significant effect of litter removal or supplementation. We found evidence that multiple natural enemies attacked A. araneoides colonies. Based on the demographic correlates of relocation and our rejection of other plausible hypotheses, we propose that nest relocation is driven by the escape from natural enemies.     

Inadequate rates are lower when FNAC samples are taken by cytopathologists

Inadequate rates (IR) in FNAC from different sources were compared. The rates were lowest when FNAC was performed by a cytopathologist (12%) and highest when done by a non-cytopathologist (32%). These differences were mirrored in high IRs in breast cancer cases. IR was not significantly improved when non-cytopathologist FNAC was attended by a cytotechnician.     

Identification of a Novel Cryptosporidium Genotype in Pigs

Over a 3-year period, a total of 646 fecal samples from pigs in 22 indoor and outdoor herds from Western Australia were screened for Cryptosporidium spp. by microscopy. Results revealed that 39 of 646 samples (6.03%) were positive for Cryptosporidium. Cryptosporidium was much more common in outdoor herds (17.2%) than in indoor herds (0.5%) and was more common in animals between the ages of 5 and 8 weeks (69.2%) than in younger animals (P < 0.0001). Molecular characterization of the positive samples at the 18S ribosomal DNA locus identified two distinct genotypes of Cryptosporidium: the previously identified pig genotype I and a novel pig genotype (pig genotype II), both of which warrant species status.     

IN VIVO EFFECTS OF CARDIOTROPHIN-1

Cardiotrophin-1 (CT-1) is a recently discovered cytokine that was isolated based on its ability to induce cardiac myocyte hypertrophy in vitro. In this study, the effects of chronic administration of CT-1 to mice (0.5 or 2 μg by intraperitoneal injection, twice a day for 14 days) were determined. A dose-dependent increase in both the heart weight and ventricular weight to body ratios was observed in the treated groups. The body weights of the animals were unaffected. These results indicate that CT-1 can induce cardiac hypertrophy in vivo. CT-1 was not specific for the heart, however. It stimulated the growth of the liver, kidney, and spleen, and caused atrophy of the thymus. CT-1 administration also increased the platelet counts by 70%, with no change in mean platelet volume. Red blood cell counts were increased in the treated animals, and there was a concomitant increase in haemoglobin concentration. Thus, CT-1 has a broad spectrum of biological activities in vivo. This observation is consistent with previous in-vitro findings showing that the mRNA for CT-1 is expressed in several tissues, and that CT-1 can function through binding to the leukaemia inhibitory factor (LIF) receptor and signalling through the gp130 pathway.