60 research outputs found

    The ecology of herbivore-induced silicon defences in grasses

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    Silicon as a defence against herbivory in grasses has gained increasing recognition and has now been studied in a wide range of species, at scales from individual plants in pots to plant communities in the field. The impacts of these defences have been assessed on herbivores ranging from insects to rodents to ungulates. Here, we review current knowledge of silicon mediation of plant-herbivore interactions in an ecological context. The production of silicon defences by grasses is affected by both abiotic and biotic factors and by their interactions. Climate, soil type and water availability all influence levels of silicon uptake, as does plant phenology and previous herbivory. The type of defoliation matters and artificial clipping does not appear to have the same impact on silicon defence induction as herbivory which includes the presence of saliva. Induction of silicon defences has been demonstrated to require a threshold level of damage, both in the laboratory and in the field. In recent studies of vole-plant interactions, the patterns of induction were found to be quantitatively similar in glasshouse compared with field experiments, in terms of both the threshold required for induction and timing of the induction response. The impacts of silicon defences differ between different classes of herbivore, possibly reflecting differences in body size, feeding behaviour and digestive physiology. General patterns are hard to discern however, and a greater number of studies on wild mammalian herbivores are required to elucidate these, particularly with an inclusion of major groups for which there are currently no data, one such example being marsupials. We highlight new research areas to address what still remains unclear about the role of silicon as a plant defence, particularly in relation to plant-herbivore interactions in the field, where the effects of grazing on defence induction are harder to measure. We discuss the obstacles inherent in scaling up laboratory work to landscape-scale studies, the most ecologically relevant but most difficult to carry out, which is the next challenge in silicon ecology

    Homotopy on spatial graphs and generalized Sato-Levine invariants

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    Edge-homotopy and vertex-homotopy are equivalence relations on spatial graphs which are generalizations of Milnor's link-homotopy. Fleming and the author introduced some edge (resp. vertex)-homotopy invariants of spatial graphs by applying the Sato-Levine invariant for the constituent 2-component algebraically split links. In this paper, we construct some new edge (resp. vertex)-homotopy invariants of spatial graphs without any restriction of linking numbers of the constituent 2-component links by applying the generalized Sato-Levine invariant.Comment: 16 pages, 13 figure

    Cartilage-specific ablation of XBP1 signaling in mouse results in a chondrodysplasia characterized by reduced chondrocyte proliferation and delayed cartilage maturation and mineralization

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    SummaryObjectiveTo investigate the in vivo role of the IRE1/XBP1 unfolded protein response (UPR) signaling pathway in cartilage.DesignXbp1flox/flox.Col2a1-Cre mice (Xbp1CartΔEx2), in which XBP1 activity is ablated specifically from cartilage, were analyzed histomorphometrically by Alizarin red/Alcian blue skeletal preparations and X-rays to examine overall bone growth, histological stains to measure growth plate zone length, chondrocyte organization, and mineralization, and immunofluorescence for collagen II, collagen X, and IHH. Bromodeoxyuridine (BrdU) and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) analyses were used to measure chondrocyte proliferation and cell death, respectively. Chondrocyte cultures and microdissected growth plate zones were analyzed for expression profiling of chondrocyte proliferation or endoplasmic reticulum (ER) stress markers by Quantitative PCR (qPCR), and of Xbp1 mRNA splicing by RT-PCR to monitor IRE1 activation.ResultsXbp1CartΔEx2 displayed a chondrodysplasia involving dysregulated chondrocyte proliferation, growth plate hypertrophic zone shortening, and IRE1 hyperactivation in chondrocytes. Deposition of collagens II and X in the Xbp1CartΔEx2 growth plate cartilage indicated that XBP1 is not required for matrix protein deposition or chondrocyte hypertrophy. Analyses of mid-gestation long bones revealed delayed ossification in Xbp1CartΔEx2 embryos. The rate of chondrocyte cell death was not significantly altered, and only minimal alterations in the expression of key markers of chondrocyte proliferation were observed in the Xbp1CartΔEx2 growth plate. IRE1 hyperactivation occurred in Xbp1CartΔEx2 chondrocytes but was not sufficient to induce regulated IRE1-dependent decay (RIDD) or a classical UPR.ConclusionOur work suggests roles for XBP1 in regulating chondrocyte proliferation and the timing of mineralization during endochondral ossification, findings which have implications for both skeletal development and disease

    Shear Localization in Dynamic Deformation: Microstructural Evolution

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    Lung adenocarcinoma promotion by air pollutants

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    A complete understanding of how exposure to environmental substances promotes cancer formation is lacking. More than 70 years ago, tumorigenesis was proposed to occur in a two-step process: an initiating step that induces mutations in healthy cells, followed by a promoter step that triggers cancer development1. Here we propose that environmental particulate matter measuring ≤2.5 μm (PM2.5), known to be associated with lung cancer risk, promotes lung cancer by acting on cells that harbour pre-existing oncogenic mutations in healthy lung tissue. Focusing on EGFR-driven lung cancer, which is more common in never-smokers or light smokers, we found a significant association between PM2.5 levels and the incidence of lung cancer for 32,957 EGFR-driven lung cancer cases in four within-country cohorts. Functional mouse models revealed that air pollutants cause an influx of macrophages into the lung and release of interleukin-1β. This process results in a progenitor-like cell state within EGFR mutant lung alveolar type II epithelial cells that fuels tumorigenesis. Ultradeep mutational profiling of histologically normal lung tissue from 295 individuals across 3 clinical cohorts revealed oncogenic EGFR and KRAS driver mutations in 18% and 53% of healthy tissue samples, respectively. These findings collectively support a tumour-promoting role for PM2.5 air pollutants and provide impetus for public health policy initiatives to address air pollution to reduce disease burden

    Pulsed Doppler Signal Processing for Use in Mice: Applications

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