9 research outputs found

    Photosynthesis and conductance of spring-wheat leaves: field response to continuous free-air atmospheric CO2 enrichment

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    Spring wheat was grown from emergence to grain maturity in two partial pressures of CO2 (pCO2): ambient air of nominally 37 Pa and air enriched with CO2 to 55 Pa using a free-air CO2 enrichment (FACE) apparatus. This experiment was the first of its kind to be conducted within a cereal field without the modifications or disturbance of microclimate and rooting environment that accompanied previous studies. It provided a unique opportunity to examine the hypothesis that continuous exposure of wheat to elevated pCO2 will lead to acclimatory loss of photosynthetic capacity. The diurnal courses of photosynthesis and conductance for upper canopy leaves were followed throughout the development of the crop and compared to model-predicted rates of photosynthesis. The seasonal average of midday photosynthesis rates was 28% greater in plants exposed to elevated pCO2 than in contols and the seasonal average of the daily integrals of photosynthesis was 21% greater in elevated pCO2 than in ambient air. The mean conductance at midday was reduced by 36%. The observed enhancement of photosynthesis in elevated pCO2 agreed closely with that predicted from a mechanistic biochemical model that assumed no acclimation of photosynthetic capacity. Measured values fell below predicted only in the flag leaves in the mid afternoon before the onset of grain-filling and over the whole diurnal course at the end of grain-filling. The loss of enhancement at this final stage was attributed to the earlier senescence of flag leaves in elevated pCO2. In contrast to some controlled-environment and field-enclosure studies, this field-scale study of wheat using free-air CO2 enrichment found little evidence of acclimatory loss of photosynthetic capacity with growth in elevated pCO2 and a significant and substantial increase in leaf photosynthesis throughout the life of the crop

    Crk Adapter Proteins Promote an Epithelial–Mesenchymal-like Transition and Are Required for HGF-mediated Cell Spreading and Breakdown of Epithelial Adherens Junctions

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    Activation of the Met receptor tyrosine kinase through its ligand, hepatocyte growth factor (HGF), promotes an epithelial–mesenchymal transition and cell dispersal. However, little is known about the HGF-dependent signals that regulate these events. HGF stimulation of epithelial cell colonies leads to the enhanced recruitment of the CrkII and CrkL adapter proteins to Met-dependent signaling complexes. We provide evidence that signals involving CrkII and CrkL are required for the breakdown of adherens junctions, the spreading of epithelial colonies, and the formation of lamellipodia in response to HGF. The overexpression of a CrkI SH3 domain mutant blocks these HGF-dependent events. In addition, the overexpression of CrkII or CrkL promotes lamellipodia formation, loss of adherens junctions, cell spreading, and dispersal of colonies of breast cancer epithelial cells in the absence of HGF. Stable lines of epithelial cells overexpressing CrkII show enhanced activation of Rac1 and Rap1. The Crk-dependent breakdown of adherens junctions and cell spreading is inhibited by the expression of a dominant negative mutant of Rac1 but not Rap1. These findings provide evidence that Crk adapter proteins play a critical role in the breakdown of adherens junctions and the spreading of sheets of epithelial cells

    Surgical Treatment of Nonruptured Infrarenal Abdominal Aortic Aneurysms

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    Cellular Signaling Mechanisms for Muscarinic Acetylcholine Receptors

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