Modulation of environmental responses of plants by circadian clocks.

Circadian clocks are signalling networks that enhance an organism's relationship with the rhythmic environment. The plant circadian clock modulates a wide range of physiological and biochemical events, such as stomatal and organ movements, photosynthesis and induction of flowering. Environmental signals regulate the phase and period of the plant circadian clock, which results in an approximate synchronization of clock outputs with external events. One of the consequences of circadian control is that stimuli of the same strength applied at different times of the day can result in responses of different intensities. This is known as 'gating'. Gating of a signal may allow plants to better process and react to the wide range and intensities of environmental signals to which they are constantly subjected. Light signalling, stomatal movements and low-temperature responses are examples of signalling pathways that are gated by the circadian clock. In this review, we describe the many levels at which the circadian clock interacts with responses to the environment. We discuss how environmental rhythms of temperature and light intensity entrain the circadian clock, how photoperiodism may be regulated by the relationship between environmental rhythms and the phasing of clock outputs, and how gating modulates the sensitivity of the clock and other responses to environmental and physiological signals. Finally, we describe evidence that the circadian clock can increase plant fitness.

Marked changes in volume of mesophyll protoplasts of pea (Pisum sativum) on exposure to growth hormones.

The present study reports quick and significant changes induced by plant hormones in the volume of mesophyll protoplasts of pea (Pisum sativum). Four plant hormones: gibberellic acid (GA3), indole 3-acetic acid (IAA), abscisic acid (ABA)(+/-) and methyl jasmonate (MJ), caused marked changes in the volume of mesophyll protoplasts. GA3 and IAA increased the volume of the protoplasts (up to 90%) whereas the ABA and MJ decreased (by about 40%) the volume. Aquaporins or water channels appear to play an important role in swelling/shrinkage of the protoplasts as indicated by the suppression of volume changes by HgCl2 and reversal by mercaptoethanol. The possible role of secondary messengers in volume changes induced by GA3 was investigated by using selected pharmacological reagents. The GA3 induced swelling was restricted by GDP-beta-S (G-protein antagonist), U73122 (phospholipase C inhibitor), and TFP (calmodulin antagonist), but was not affected by 1-butanol (phospholipase D inhibitor), GTP-gamma-S (G-protein agonist), or verapamil (calcium channel blocker). The results suggest that the mesophyll protoplasts can be a simple and useful system for further studies on volume changes in plant tissues.

Cytoplasmic alkalization precedes reactive oxygen species production during methyl jasmonate- and abscisic acid-induced stomatal closure.

Signaling events during abscisic acid (ABA) or methyl jasmonate (MJ)-induced stomatal closure were examined in Arabidopsis wild type, ABA-insensitive (ost1-2), and MJ-insensitive mutants (jar1-1) in order to examine a crosstalk between ABA and MJ signal transduction. Some of the experiments were performed on epidermal strips of Pisum sativum. Stomata of jar1-1 mutant plants are insensitive to MJ but are able to close in response to ABA. However, their sensitivity to ABA is less than that of wild-type plants. Reciprocally, the stomata of ost1-2 are insensitive to ABA but are able to close in response to MJ to a lesser extent compared to wild-type plants. Both MJ and ABA promote H(2)O(2) production in wild-type guard cells, while exogenous application of diphenylene iodonium (DPI) chloride, an inhibitor of NAD(P)H oxidases, results in the suppression of ABA- and MJ-induced stomatal closure. ABA elevates H(2)O(2) production in wild-type and jar1-1 guard cells but not in ost1-2, whereas MJ induces H(2)O(2) production in both wild-type and ost1-2 guard cells, but not in jar1-1. MJ-induced stomatal closing is suppressed in the NAD(P)H oxidase double mutant atrbohD/F and in the outward potassium channel mutant gork1. Furthermore, MJ induces alkalization in guard cell cytosol, and MJ-induced stomatal closing is inhibited by butyrate. Analyses of the kinetics of cytosolic pH changes and reactive oxygen species (ROS) production show that the alkalization of cytoplasm precedes ROS production during the stomatal response to both ABA and MJ. Our results further indicate that JAR1, as OST1, functions upstream of ROS produced by NAD(P)H oxidases and that the cytoplasmic alkalization precedes ROS production during MJ or ABA signal transduction in guard cells.