• Temperature has a direct effect at the cellular level on an organism. For instance, in the case of biomembranes, cooling causes lipids to lose entropy and pack closely together. Reducing temperature should, in the absence of other factors, increase the viscosity of a lipid membrane. We have investigated the effect of temperature variation on plasma membrane (PM) viscosity. • We used dispersion tracking of photoactivated green fluorescent protein (GFP) and fluorescence recovery after photobleaching in wild-type and desaturase mutant Arabidopsis thaliana plants along with membrane lipid saturation analysis to monitor the effect of temperature and membrane lipid composition on PM viscosity. • Plasma membrane viscosity in A. thaliana is negatively correlated with ambient temperature only under constant-temperature conditions. In the more natural environment of temperature cycles, plants actively manage PM viscosity to counteract the direct effects of temperature. • Plasma membrane viscosity is regulated by altering the proportion of desaturated fatty acids. In cold conditions, cell membranes accumulate desaturated fatty acids, which decreases membrane viscosity and vice versa. Moreover, we show that control of fatty acid desaturase 2 (FAD2)-dependent lipid desaturation is essential for this homeostasis of membrane viscosity. Finally, a lack of FAD2 function results in aberrant temperature responses.
Calcium is well established as a key signalling molecule in plant and animals systems. Stimuli such as heat, cold, touch and ozone (O3) cause an increase in cytosolic calcium concentration [Ca2+]cyt in plants. O3 is a reactive oxygen species (ROS) and acts as a pollutant in the troposphere, whereas stratospheric ozone protects the earth from damaging ultra violet radiation. ROS are able to cause damage to plant cell components, effects include lipid peroxidation, reduced transpiration, a decrease in photosynthesis and a reduction in productivity. We have been studying the early molecular events in the response of Arabidopsis thaliana to O3 focusing on the role of calcium ions. Arabidopsis thaliana transformed with the photoprotein apoaequorin have been used to measure changes in [Ca2+]cyt during fumigation with O3. Elevations in [Ca2+]cyt occur in a dose dependent manner and a ‘calcium signature’ characteristic of O3 exposure is seen. Increases in antioxidant defences also occur following O3 exposure, however the signal transduction pathways leading from the perception of O3 stress and adaptation to the stress are poorly understood. The ozone induced increase in [Ca2+]cyt has been implicated in the induction of the antioxidant gene glutathione-S-transferase tau 5 (GSTU5) (Clayton et al. (1999) The Plant Journal 17(5) 575-579) . This study provides a continuation of this work. A pharmacological analysis of the calcium signature in response to O3 has been undertaken. Two inhibitors of calcium release pathways, lanthanum, a plasma membrane channel blocker and ruthenium red, an intracellular calcium channel blocker, have been used, as has the calcium chelator EGTA. The calcium response following treatment with inhibitors of other signalling molecules and components of signal transduction pathways has also been investigated. These include the cADPR inhibitor nicotinamide and the phospholipase C inhibitor 2-APB. The research has been extended to include an analysis of the effect of these inhibitors on GSTU5 expression in response to ozone. In addition a genetic analysis of the ozone-calcium signature has been performed using the calcium transport mutant ACA3 transformed with apoaequorin. This has a plasma membrane autoinihibited calcium ATPase gene knocked out. Theere is little difference between the mutant and wild type response to O3, suggesting redundancy within the system or that an alternative source of calcium is involved in the ozone response
Previous studies have suggested a role for jasmonates in the promotion of stomatal closure ([Raghavendra and Reddy, 1987][1]; [Gehring et al., 1997][2]). This report describes whole-cell patch-clamp experiments that demonstrate that methyl jasmonate (Me-JA) has concentration-dependent effects on
Summary Ozone is responsible for more crop losses than any other air pollutant. The changes in gene expression, which occur in plants in response to ozone, have been well characterized, yet little is known about how ozone is perceived or the signal transduction steps that follow. The earliest characterized response to ozone is an elevation in cytosolic‐free calcium, which takes place within seconds of exposure. In this study, the calcium response to ozone was investigated in Arabidopsis thaliana seedlings using a variety of fumigation protocols. Ozone elicited distinct calcium responses in the aerial tissue and roots of seedlings. The calcium response in the cotyledons and leaves was biphasic and sensitive to the rate at which the ozone concentration increased. The response in the root was monophasic and insensitive to the rate of increase in ozone concentration. Experiments utilizing inhibitors of antioxidant metabolism demonstrated that the magnitude of the first peak in calcium in the aerial tissues was dependent upon the redox status of the plant. Seedlings were shown to be able to distinguish between ozone and hydrogen peroxide, producing a calcium signal in response to one of these reactive oxygen species (ROS) when they had become refractory to the other. Pre‐treatment with ozone altered the calcium response to hydrogen peroxide and vice versa, indicating that the calcium response to a given ROS may reflect the stress history of the plant. These data suggest ROS signalling is more sophisticated than previously realized and raise questions over current models of ozone perception.
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