996 resultados para Weed competition


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Cell competition is a conserved mechanism where slow proliferating cells (so called losers) are eliminated by faster proliferating neighbors (so called winners) through apoptosis.(1) It is an important process which prevents developmental malformations and maintains tissue fitness in aging adults.(2) Recently, we have shown that the probability of elimination of loser cells correlates with the surface of contact between losers and winners in Myc-induced competition.(3) Moreover, we have characterized an active mechanism that increases the surface of contact between losers and winners, hence accelerating the elimination of loser cells. This is the first indication that cell shape and mechanics can influence cell competition. Here, we will discuss the consequence of the relationship between shape and competition, as well as the relevance of this model for other modes of competition.

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Regulation of tissue size requires fine tuning at the single-cell level of proliferation rate, cell volume, and cell death. Whereas the adjustment of proliferation and growth has been widely studied [1, 2, 3, 4 and 5], the contribution of cell death and its adjustment to tissue-scale parameters have been so far much less explored. Recently, it was shown that epithelial cells could be eliminated by live-cell delamination in response to an increase of cell density [6]. Cell delamination was supposed to occur independently of caspase activation and was suggested to be based on a gradual and spontaneous disappearance of junctions in the delaminating cells [6]. Studying the elimination of cells in the midline region of the Drosophila pupal notum, we found that, contrary to what was suggested before, Caspase 3 activation precedes and is required for cell delamination. Yet, using particle image velocimetry, genetics, and laser-induced perturbations, we confirmed [ 6] that local tissue crowding is necessary and sufficient to drive cell elimination and that cell elimination is independent of known fitness-dependent competition pathways [ 7, 8 and 9]. Accordingly, activation of the oncogene Ras in clones was sufficient to compress the neighboring tissue and eliminate cells up to several cell diameters away from the clones. Mechanical stress has been previously proposed to contribute to cell competition [ 10 and 11]. These results provide the first experimental evidences that crowding-induced death could be an alternative mode of super-competition, namely mechanical super-competition, independent of known fitness markers [ 7, 8 and 9], that could promote tumor growth.

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Tissue growth and regeneration are autonomous, stem-cell-mediated processes in which stem cells within the organ self-renew and differentiate to create new cells, leading to new tissue. The processes of growth and regeneration require communication and interplay between neighboring cells. In particular, cell competition, which is a process in which viable cells are actively eliminated by more competitive cells, has been increasingly implicated to play an important role. Here, we discuss the existing literature regarding the current landscape of cell competition, including classical pathways and models, fitness fingerprint mechanisms, and immune system mechanisms of cell competition. We further discuss the clinical relevance of cell competition in the physiological processes of tissue growth and regeneration, highlighting studies in clinically important disease models, including oncological, neurological, and cardiovascular diseases.

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Cell competition is a process by which the slow dividing cells (losers) are recognized and eliminated from growing tissues. Loser cells are extruded from the epithelium and engulfed by the haemocytes, the Drosophila macrophages. However, how macrophages identify the dying loser cells is unclear. Here we show that apoptotic loser cells secrete Tyrosyl-tRNA synthetase (TyrRS), which is best known as a core component of the translational machinery. Secreted TyrRS is cleaved by matrix metalloproteinases generating MiniTyr and EMAP fragments. EMAP acts as a guiding cue for macrophage migration in the Drosophila larvae, as it attracts the haemocytes to the apoptotic loser cells. JNK signalling and Kish, a component of the secretory pathway, are autonomously required for the active secretion of TyrRS by the loser cells. Altogether, this mechanism guarantees effective removal of unfit cells from the growing tissue.

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The transistor was an American invention, and American firms led the world in semiconductor production and innovation for the first three decades of that industry's existence. In the 1980s, however, Japanese producers began to challenge American dominance. Shrill cries arose from the literature of public policy, warning that the American semiconductor industry would soon share the fate of the lamented American consumer electronics business. Few dissented from the implications: the only hope for salvation would be to adopt Japanese-style public policies and imitate the kinds of capabilities Japanese firms possessed. But the predicted extinction never occurred. Instead, American firms surged back during the 1990s, and it now seems the Japanese who are embattled. This striking American turnaround has gone largely unremarked upon in the public policy literature. And even scholarship in strategic management, which thrives on stories of success instead of stories of failure, has been comparatively silent. Drawing on a more thorough economic history of the worldwide semiconductor industry (Langlois and Steinmueller 1999), this essay attempts to collect some of the lessons for strategy research of the American resurgence. We argue that, although some of the American response did consist in changing or augmenting capabilities, most of the renewed American success is in fact the result not of imitating superior Japanese capabilities but rather of taking good advantage of a set of capabilities developed in the heyday of American dominance. Serendipity played at least as important a role as did strategy.

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While many tend to think of memory systems in the brain as a single process, in reality several experiments have supported multiple dissociations of different forms of learning, such as spatial learning and response learning. In both humans and rats, the hippocampus has long been shown to be specialized in the storage of spatial and contextual memory whereas the striatum is associated with motor responses and habitual behaviors. Previous studies have examined how damage to hippocampus or striatum has affected the acquisition of either a spatial or response navigation task. However even in a very familiar environment organisms must continuously switch between place and response strategies depending upon circumstances. The current research investigates how these two brain systems interact under normal conditions to produce navigational behavior. Rats were tested using a task developed by Jacobson and colleagues (2006) in which the two types of navigation could be controlled and studied simultaneously. Rats were trained to solve a plus maze using both a spatial and a response strategy. A cue (flashing light) was employed to indicate the correct strategy on a given trial. When no light was present, the animals were rewarded for making a 90º right turn (motor response). When the light was on, the animals were rewarded for going to a specific goal location (place strategy). After learning the task, animals had a sham surgery or dorsal striatum or hippocampus damaged. In order to investigate the individual role of each brain system and evaluate whether these brain regions compete or cooperate for control over strategy, we utilized a within-animal comparisons. The configuration of the maze allowed for the comparison of behavior in individual animals before and after specific brain areas were damaged. Animals with hippocampal lesions showed selective deficits on place trials after surgery and learned the reversal of the motor response more rapidly than striatal lesioned or sham rats. Unlike previous findings regarding maze learning, animals with striatal lesions showed deficits in both place and response trials and had difficulty learning the reversal of motor response. Therefore, the effects of lesions on the ability to switch back and forth between strategies were more complex than previously suggested. This work may reveal important new insight on the integration of hippocampal and striatal learning systems, and facilitate a better understanding of the brain dynamics underlying similar navigational processes in humans.

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Signatur des Originals: S 36/F10234

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Signatur des Originals: S 36/F10412

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The purpose of this study was to evaluate various herbicides for corn injury and weed control when applied preemergence and postemergence.

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The purpose of this study was to evaluate various herbicides for corn injury and weed control when applied preemergence and postemergence.

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The purpose of this study was to evaluate various herbicides and application timings in soybean for crop injury and weed control.

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Since pre-industrial times, uptake of anthropogenic CO2 by surface ocean waters has caused a documented change of 0.1 pH units. Calcifying organisms are sensitive to elevated CO2 concentrations due to their calcium carbonate skeletons. In temperate rocky intertidal environments, calcifying and noncalcifying macroalgae make up diverse benthic photoautotrophic communities. These communities may change as calcifiers and noncalcifiers respond differently to rising CO2 concentrations. In order to test this hypothesis, we conducted an 86?d mesocosm experiment to investigate the physiological and competitive responses of calcifying and noncalcifying temperate marine macroalgae to 385, 665, and 1486 µatm CO2. We focused on comparing 2 abundant red algae in the Northeast Atlantic: Corallina officinalis (calcifying) and Chondrus crispus (noncalcifying). We found an interactive effect of CO2 concentration and exposure time on growth rates of C. officinalis, and total protein and carbohydrate concentrations in both species. Photosynthetic rates did not show a strong response. Calcification in C. officinalis showed a parabolic response, while skeletal inorganic carbon decreased with increasing CO2. Community structure changed, as Chondrus crispus cover increased in all treatments, while C. officinalis cover decreased in both elevated-CO2 treatments. Photochemical parameters of other species are also presented. Our results suggest that CO2 will alter the competitive strengths of calcifying and noncalcifying temperate benthic macroalgae, resulting in different community structures, unless these species are able to adapt at a rate similar to or faster than the current rate of increasing sea-surface CO2 concentrations.

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