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John W Patrick - One of the best experts on this subject based on the ideXlab platform.
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Turgor dependent unloading of photosynthates from coats of developing seed of phaseolus vulgaris and vicia faba Turgor homeostasis and set points
Physiologia Plantarum, 1994Co-Authors: John W PatrickAbstract:Key physiological characteristics of Turgor-dependent efflux of photosynthates were examined using excised coats and cotyledons of developing Phaseolus vulgaris (cv. Redland Poineer) and Vicia faba (cv. Coles Prolific) seed during the linear phase of seed fill. Exposure to solutions of high osmotic potential inhibited net uptake of [14C]sucrose by cotyledons at developmental stages less than 60% of their final dry weight. The effect could not be fully reversed by transferring cotyledons to solutions set at lower osmotic potentials. The inhibition became apparent at osmotic potentials that were higher than those that caused stimulation of efflux from seed coats. Net [14C]sucrose uptake by cotyledons at more advanced stages of development was unaffected by external osmotic potential. Specified tissue layers were removed from seed coats by pretreatment with pectinase. Efflux studies with the pectinase-modified coats of Phaseolus and Vicia seed demonstrated that the cellular site of Turgordependent efflux was the ground parenchyma and thin-wall parenchyma transfer cells, respectively. Coats subjected to long-term (hours) incubations, under hypo-osmotic conditions, exhibited the capacity for Turgor regulation. This was mediated by Turgor-dependent efflux of solutes. The solutes exchanged were of nutritional significance to the developing embryo. The relationship between efflux and coat Turgor was characterised by a Turgor-independent phase at low Turgors. Once Turgor exceeded a minimal value (set point), efflux increased in proportion to the magnitude of the Turgor deviation (error signal) from the set point. For coats of sink-limited seed of Vicia and Phaseolus, efflux exhibited apparent saturation at Turgors above 0.25 and 0.5 MPa respectively. The putative Turgor set point and slope of the Turgor-dependent component of efflux varied with seed development, the prevailing source/sink ratio and genetic differences in seed growth rate. The nature of these kinetic variations was compatible with the competitive ability of the seed. A Turgor homeostat model is proposed that incorporates the observed functional attributes of Turgor-dependent efflux. Operationally, the model provides a mechanistic basis for the integration of assimilate demand by the cotyledons with assimilate import into and unloading from the seed coat.
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Turgor‐dependent unloading of photosynthates from coats of developing seed of Phaseolus vulgaris and Vicia faba. Turgor homeostasis and set points
Physiologia Plantarum, 1994Co-Authors: John W PatrickAbstract:Key physiological characteristics of Turgor-dependent efflux of photosynthates were examined using excised coats and cotyledons of developing Phaseolus vulgaris (cv. Redland Poineer) and Vicia faba (cv. Coles Prolific) seed during the linear phase of seed fill. Exposure to solutions of high osmotic potential inhibited net uptake of [14C]sucrose by cotyledons at developmental stages less than 60% of their final dry weight. The effect could not be fully reversed by transferring cotyledons to solutions set at lower osmotic potentials. The inhibition became apparent at osmotic potentials that were higher than those that caused stimulation of efflux from seed coats. Net [14C]sucrose uptake by cotyledons at more advanced stages of development was unaffected by external osmotic potential. Specified tissue layers were removed from seed coats by pretreatment with pectinase. Efflux studies with the pectinase-modified coats of Phaseolus and Vicia seed demonstrated that the cellular site of Turgordependent efflux was the ground parenchyma and thin-wall parenchyma transfer cells, respectively. Coats subjected to long-term (hours) incubations, under hypo-osmotic conditions, exhibited the capacity for Turgor regulation. This was mediated by Turgor-dependent efflux of solutes. The solutes exchanged were of nutritional significance to the developing embryo. The relationship between efflux and coat Turgor was characterised by a Turgor-independent phase at low Turgors. Once Turgor exceeded a minimal value (set point), efflux increased in proportion to the magnitude of the Turgor deviation (error signal) from the set point. For coats of sink-limited seed of Vicia and Phaseolus, efflux exhibited apparent saturation at Turgors above 0.25 and 0.5 MPa respectively. The putative Turgor set point and slope of the Turgor-dependent component of efflux varied with seed development, the prevailing source/sink ratio and genetic differences in seed growth rate. The nature of these kinetic variations was compatible with the competitive ability of the seed. A Turgor homeostat model is proposed that incorporates the observed functional attributes of Turgor-dependent efflux. Operationally, the model provides a mechanistic basis for the integration of assimilate demand by the cotyledons with assimilate import into and unloading from the seed coat.
Weicai Yang - One of the best experts on this subject based on the ideXlab platform.
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the arabidopsis alkaline ceramidase tod1 is a key Turgor pressure regulator in plant cells
Nature Communications, 2015Co-Authors: Li Yu Chen, Weicai Yang, Zuoshun Tang, Wenjuan ZhangAbstract:Turgor pressure is critical for the growth of plant cells but the mechanisms regulating Turgor are poorly understood. Here, Chen et al. identify TOD1, an alkaline ceramidase, involved in sphingosine metabolism that regulates Turgor during pollen tube growth and stomatal closure.
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the arabidopsis alkaline ceramidase tod1 is a key Turgor pressure regulator in plant cells
Nature Communications, 2015Co-Authors: Li Yu Chen, Zuoshun Tang, Wenjuan Zhang, Dongqiao Shi, Jie Liu, Weicai YangAbstract:Turgor pressure plays pivotal roles in the growth and movement of walled cells that make up plants and fungi. However, the molecular mechanisms regulating Turgor pressure and the coordination between Turgor pressure and cell wall remodelling for cell growth remain poorly understood. Here, we report the characterization of Arabidopsis Turgor regulation Defect 1 (TOD1), which is preferentially expressed in pollen tubes and silique guard cells. We demonstrate that TOD1 is a Golgi-localized alkaline ceramidase. tod1 mutant pollen tubes have higher Turgor than wild type and show growth retardation both in pistils and in agarose medium. In addition, tod1 guard cells are insensitive to abscisic acid (ABA)-induced stomatal closure, whereas sphingosine-1-phosphate, a putative downstream component of ABA signalling and product of alkaline ceramidases, promotes closure in both wild type and tod1. Our data suggest that TOD1 acts in Turgor pressure regulation in both guard cells and pollen tubes.
Kathy Steppe - One of the best experts on this subject based on the ideXlab platform.
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Turgor time controls grass leaf elongation rate and duration under drought stress
Plant Cell and Environment, 2021Co-Authors: Jonas R Coussement, Selwyn L Y Villers, Hilde Nelissen, Dirk Inze, Kathy SteppeAbstract:The process of leaf elongation in grasses is characterized by the creation and transformation of distinct cell zones. The prevailing Turgor pressure within these cells is one of the key drivers for the rate at which these cells divide, expand and differentiate, processes that are heavily impacted by drought stress. In this article, a Turgor-driven growth model for grass leaf elongation is presented, which combines mechanistic growth from the basis of Turgor pressure with the ontogeny of the leaf. Drought-induced reductions in leaf Turgor pressure result in a simultaneous inhibition of both cell expansion and differentiation, lowering elongation rate but increasing elongation duration due to the slower transitioning of cells from the dividing and elongating zone to mature cells. Leaf elongation is, therefore, governed by the magnitude of, and time spent under, growth-enabling Turgor pressure, a metric which we introduce as Turgor-time. Turgor-time is able to normalize growth patterns in terms of varying water availability, similar to how thermal time is used to do so under varying temperatures. Moreover, additional inclusion of temperature dependencies within our model pioneers a novel concept enabling the general expression of growth regardless of water availability or temperature.
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daytime depression in temperature normalised stem co2 efflux in young poplar trees is dominated by low Turgor pressure rather than by internal transport of respired co2
New Phytologist, 2018Co-Authors: Roberto L Salomon, Veerle De Schepper, Maria Valbuenacarabana, Kathy SteppeAbstract:Summary Daytime decreases in temperature-normalised stem CO2 efflux (EA_D) are commonly ascribed to internal transport of respired CO2 (FT) or to an attenuated respiratory activity due to lowered Turgor pressure. The two are difficult to separate as they are simultaneously driven by sap flow dynamics. To achieve combined gradients in Turgor pressure and FT, sap flow rates in poplar trees were manipulated through severe defoliation, severe drought, moderate defoliation and moderate drought. Turgor pressure was mechanistically modelled using measurements of sap flow, stem diameter variation, and soil and stem water potential. A mass balance approach considering internal and external CO2 fluxes was applied to estimate FT. Under well-watered control conditions, both Turgor pressure and sap flow, as a proxy of FT, were reliable predictors of EA_D. After tree manipulation, only Turgor pressure was a robust predictor of EA_D. Moreover, FT accounted for < 15% of EA_D. Our results suggest that daytime reductions in Turgor pressure and associated constrained growth are the main cause of EA_D in young poplar trees. Turgor pressure is determined by both carbohydrate supply and water availability, and should be considered to improve our widely used but inaccurate temperature-based predictions of woody tissue respiration in global models.
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Daytime depression in temperature‐normalised stem CO2 efflux in young poplar trees is dominated by low Turgor pressure rather than by internal transport of respired CO2
New Phytologist, 2017Co-Authors: Roberto L Salomon, Veerle De Schepper, María Valbuena-carabaña, Kathy SteppeAbstract:Summary Daytime decreases in temperature-normalised stem CO2 efflux (EA_D) are commonly ascribed to internal transport of respired CO2 (FT) or to an attenuated respiratory activity due to lowered Turgor pressure. The two are difficult to separate as they are simultaneously driven by sap flow dynamics. To achieve combined gradients in Turgor pressure and FT, sap flow rates in poplar trees were manipulated through severe defoliation, severe drought, moderate defoliation and moderate drought. Turgor pressure was mechanistically modelled using measurements of sap flow, stem diameter variation, and soil and stem water potential. A mass balance approach considering internal and external CO2 fluxes was applied to estimate FT. Under well-watered control conditions, both Turgor pressure and sap flow, as a proxy of FT, were reliable predictors of EA_D. After tree manipulation, only Turgor pressure was a robust predictor of EA_D. Moreover, FT accounted for
Mary J Beilby - One of the best experts on this subject based on the ideXlab platform.
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Transport systems of Ventricaria ventricosa: Asymmetry of the hyper- and hypotonic regulation mechanisms
Journal of Membrane Biology, 2008Co-Authors: Marcus A. Bisson, Mary J BeilbyAbstract:Hyper- and hypotonic stresses elicit apparently symmetrical responses in the alga Ventricaria. With hypertonic stress, membrane potential difference (PD) between the vacuole and the external medium becomes more positive, conductance at positive PDs (Gmpos) increases and KCl is actively taken up to increase Turgor. With hypotonic stress, the membrane PD becomes more negative, conductance at negative PDs (Gmneg) increases and KCl is lost to decrease Turgor. We used inhibitors that affect active transport to determine whether agents that inhibit the K(+) pump and hypertonic regulation also inhibit hypotonic regulatory responses. Cells whose Turgor pressure was held low by the pressure probe (Turgor-clamped) exhibited the same response as cells challenged by hyperosmotic medium, although the response was maintained longer than in osmotically challenged cells, which regulate Turgor. The role of active K(+) transport was confirmed by the effects of decreased light, dichlorophenyldimethyl urea and diethylstilbestrol, which induced a uniformly low conductance (quiet state). Cells clamped to high Turgor exhibited the same response as cells challenged by hypo-osmotic medium, but the response was similarly transient, making effects of inhibitors hard to determine. Unlike clamped cells, cells challenged by hypo-osmotic medium responded to inhibitors with rapid, transient, negative-going PDs, with decreased Gmneg and increased Gmpos (linearized I-V), achieving the quiet state as PD recovered. These changes are different from those exerted on the pump state, indicating that different transport systems are responsible for Turgor regulation in the two cases.
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mechanosensory ion channels in chara the influence of cell Turgor pressure on touch activated receptor potentials and action potentials
Functional Plant Biology, 2001Co-Authors: Virginia A Shepherd, Teruo Shimmen, Mary J BeilbyAbstract:Chara cells produce receptor potentials (RPDs) in response to mechanical stimulation. We have used a mechanostimulatory device to compare characteristics of touch-activated RPDs and action potentials (APs) when cell Turgor pressure was changed. The device delivered a series of mechanical stimulations of increasing energy (F0.5, F1, F2, F3, F4, F5 and F6). Cells were alternately stimulated in artificial pondwater (APW) and a sorbitol series, in long-term experiments, involving up to six solution changes. The calculated cell Turgor pressures were about 0.6 MPa (APW), and 0.49 MPa, 0.37 MPa, 0.24 MPa and 0.12 MPa in 50, 100, 150 and 200 mM sorbitol–APW, respectively. In other experiments, cells were pre-conditioned in the sorbitol solutions, and then transferred to APW. All cells were allowed long recovery periods (40–60 min) after APs or solution transfers. Only small changes in cell conductance were observed in I–V and G–V analysis of unstimulated cells after reducing Turgor pressure from 0.59 MPa to 0.24 MPa. In APW, the RPDs increased in amplitude and duration with increased stimulus energy until the threshold RPD was reached, and an AP was triggered, usually between stimulus F4 and F5. Cells with decreased Turgor pressure became more sensitive to stimulation, giving threshold RPDs or APs with smaller stimulus (e.g. between F0.5 and F3). Conversely, an increase in cell Turgor pressure (return to APW) led to a decrease in sensitivity to stimulus. When Turgor pressure was greatly decreased (to 0.12 MPa), some cells became unresponsive or gave unusual responses. However, only the mechanical part of the touch response was affected by changing the cell Turgor pressure. The mean amplitudes of the subthreshold and threshold RPD (that triggers the AP), and of the touch-activated APs, were independent of cell Turgor pressure, although action potentials had smaller amplitude when Turgor was reduced to about 0.12 MPa. The amplitude of the subthreshold RPD was close to 20 mV, and the amplitude of the threshold RPD was close to 50 mV, in all cells. If tension of the cell wall–plasma membrane–cytoskeleton complex decreased along with decreased cell Turgor pressure, a given stimulus could stretch the complex to a greater extent, resulting in activation of more mechanosensory channels. The effect on the RPD of changes in cell Turgor pressure is discussed in relation to the mechanical properties of the cell wall–plasma membrane–cytoskeleton complex.
Anthony E. Walsby - One of the best experts on this subject based on the ideXlab platform.
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digital recordings of gas vesicle collapse used to measure Turgor pressure and cell water relations of cyanobacterial cells
Journal of Microbiological Methods, 2009Co-Authors: Daryl Philip Holland, Anthony E. WalsbyAbstract:Abstract The gas vesicles of the cyanobacterium Microcystis sp. collapse under pressures ranging from 0.65–1.10 MPa, determined from turbidity changes in a pressure nephelometer. In turgid cells, collapse occurs at a lower range of pressures; the difference is equal to the cell Turgor pressure. The Turgor pressure decreases, however, as gas vesicles collapse; this decrease is minimised by calculating the Turgor pressure in samples with few of their gas vesicles collapsed. Previously, pressure and turbidity were measured in discrete steps, using analogue meters, or continuously, using chart recorders: Turgor pressure was calculated from the mean or median collapse pressures. We describe modifications allowing continuous digital recording; the output was modelled with polynomial or sigmoid functions, the latter providing the best fit over the full collapse-pressure curve; Turgor pressure could then be calculated for any point on the collapse-pressure curve. The shape of the collapse-pressure curve was affected by the rate of pressure rise; curves were similar to those from step-wise methods when the pressure was raised at approximately 4 kPa s − 1 . Under a rapid, almost instantaneous, rise in pressure there was a larger initial decrease in Turgor and from the subsequent recovery the hydraulic conductivity of the cell surface could be calculated; the new method gave improved measurements of the cell volumetric elastic modulus. Following collapse of half the gas vesicles, cells recovered their full Turgor pressure after 3 h. This suggests Turgor homeostasis. These methods are applicable to other bacteria with gas vesicles, including Escherichia coli , if it could be genetically modified to express transgenic gas vesicles.
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Digital recordings of gas-vesicle collapse used to measure Turgor pressure and cell–water relations of cyanobacterial cells
Journal of Microbiological Methods, 2009Co-Authors: Daryl Philip Holland, Anthony E. WalsbyAbstract:Abstract The gas vesicles of the cyanobacterium Microcystis sp. collapse under pressures ranging from 0.65–1.10 MPa, determined from turbidity changes in a pressure nephelometer. In turgid cells, collapse occurs at a lower range of pressures; the difference is equal to the cell Turgor pressure. The Turgor pressure decreases, however, as gas vesicles collapse; this decrease is minimised by calculating the Turgor pressure in samples with few of their gas vesicles collapsed. Previously, pressure and turbidity were measured in discrete steps, using analogue meters, or continuously, using chart recorders: Turgor pressure was calculated from the mean or median collapse pressures. We describe modifications allowing continuous digital recording; the output was modelled with polynomial or sigmoid functions, the latter providing the best fit over the full collapse-pressure curve; Turgor pressure could then be calculated for any point on the collapse-pressure curve. The shape of the collapse-pressure curve was affected by the rate of pressure rise; curves were similar to those from step-wise methods when the pressure was raised at approximately 4 kPa s − 1 . Under a rapid, almost instantaneous, rise in pressure there was a larger initial decrease in Turgor and from the subsequent recovery the hydraulic conductivity of the cell surface could be calculated; the new method gave improved measurements of the cell volumetric elastic modulus. Following collapse of half the gas vesicles, cells recovered their full Turgor pressure after 3 h. This suggests Turgor homeostasis. These methods are applicable to other bacteria with gas vesicles, including Escherichia coli , if it could be genetically modified to express transgenic gas vesicles.
