Modulation Of Gst Activity In The Plant

GSTs are expressed in plants in a tissue specific manner, and reports are available on heterogeneous expression of isoenzymes in single leaves. The reason for this is probably found in an age specific expression of GST that has been pointed out in the context of inducibility of the enzymes under ethylene and during senescence. Maize leaves exhibit high GST activity toward atrazine in early development, but after the age of 14 days this activity is lost and not regained during leaf ageing (Hatton et al. 1996).

In this context, another question is raised by the observation that het-erodimeric GSTs might appear under certain stress conditions. Hetero-dimeric GSTs have been described to possess mixed activities and specifici ties referring to the respective homodimers. Dimerization of subunits has been reported to occur spontaneously, but in artificial systems expressing the subunits heterologously, attempts failed to combine them randomly and to regain the expected activities (Dixon et al. 1999). The preliminary conclusion is that only subunit members of the distinct gene families will reconstitute to holoenzymes. However, as no database is available on the mechanism of induction or spontaneous rearrangement of GST subunits, this phenomenon might provide surprising future insights. The effect of subunit rearrangement on total GST activity might be massive.

Comparable to animal GST, plant GST activity may be enhanced by various xenobiotics, antidotes or natural compounds via the induction of distinct isoforms of the enzyme (Wiegand et al. 1986, Debus and Schröder 1990, Anderson and Gronwald 1991, Schröder et al. 1993).

An important property of GSTs is their inducibility by herbicide antidotes (safeners). This reaction has mostly been ascribed to monocotyledons and it is the decisive step conferring herbicide tolerance to many agricultural crops, but has also been observed in conifers. Wheat possesses more than eight GST isoforms when safener-treated. Five of them are heterodimeric and solely detected after the safener application.

Table 3. Sequence of steps leading to safener-induced herbicide tolerance (from Izryk and Fuerst 1997, modified).

Step 1:

Absorption of safener by seedlings into root and/or shoot

Step 2:

Metabolism of safener to active form hy phase 1 enzymes

Step 3:

Specific signal recognition and signal transduction

Step 4:

Increased transcription of GSH synthesis and GST genes

Step 5:

Increased levels of GSi I and GST isoforms

Step 6:

Increased herbicide conjugation

Result:

Enhanced whole-plant tolerance to herbicides

A hypothetical sequence of the events leading to an increase of herbicide tolerance in crops after safener application has been proposed by Izryk and Fuerst (1997), Table 3. From this it seems likely that several reactions take place in a more or less coordinate manner and may require a cascade process triggered by still unknown receptors somewhere in the cell. Halogenated air pollutants seem to act in a similar if not the same way on glutathione and GST in conifers. Unfortunately, the data basis is quite narrow, and only few reviews cover this subject (see Schroder 1998a,b).

Oxidative stress, but also anoxia and follow-up reactions like H202 evolution and the like are also known as inducers of plant GST (Table 4). Moreover, phytohormones and pathogens may act as inducers (Droog & al. 1993,

Mauch & Dudler 1993, Zhou & Goldsborough 1993). Natural and synthetic auxins seem to be very specific inducers of GSTs of the tau class in many plants, whereas theta gene products remain uninduced. Even more puzzling, it has been observed that in some cases gene activation is strictly specific for a single inducer, but in many cases evidence exists that seemingly unrelated and multiple stresses may as well lead to the activation of a single gene or a whole bundle of genes.

Experimental evidence points to a transcriptional regulation of the activation process, although the precise mechanisms have not been elucidated yet. Similar to safener-mediated induction, a reaction cascade has been postulated that is driven by a surplus of oxidative processes in the cytosol (Daniel 1993).

Table 4. Inducers of GST genes.

Inducers of gst genes

Abscisic acid

dithiothreithol

gibcrcllic acid

oxidative stress

Anaerobiosis

elicitors

gsh

ozone

Auxins

ethacrynic acid

h2o2

pathogens

Auxin analogs

cthanol

heavy metals

salicylic acid

Chlorocarbons

ethylene

herbicides

safeners

Cytokinins

flooding

iastnonic acid

substrates

This may be true for a number of GST, but is surely not valid for all iso-forms. Some promoters of GST have been found to contain regulatory elements such as ocs (octopine synthase, Zhang and Singh 1994). These ocs elements seem to respond to electrophilic compounds in a manner analogous to the AP-1 elements of animals. Therefore, ocs elements may be involved in the observed changes in gene expression.

GST activities have been shown to be induced within few hours after contact with xenobiotics or hormones or the onset of stress. It seems that two mechanisms, activation and true induction are possible. The basis for rapid activation might be binding of activators at non-catalytic sites and/or the formation of heterodimers. Induction is thought to proceed via gene activation and de novo synthesis of protein (Schröder and Pflugmacher 1996).

In principle the inducibility of enzymes is nothing special, but it has to be considered that GSTs play a central role in the adaptive answers of an organism toward numerous stimuli. This even more as various inducers themselves are substrates of GSTs or become substrates after activation. Hence it sounds likely that GST occupy a key position for the induction of other related enzymes such as chinone reductases, glucosyl transferases and enzymes of glutathione synthesis as well as on the glutathione conjugate pump in the tonoplast.

In this context it has been speculated that GST and other phase II enzymes are induced by GST substrates (=electrophiles) but that the resulting GS-conjugates themselves interact with the homeostasis of glutathione pools (Hayes & Pulford 1995). On the contrary, studies with onion showed that GS conjugates have a pivotal role in the course of the intracellular signalling processes responsible for the activation of cellular defence, whereas y-glutamylcysteine conjugates of the same compounds were somewhat inactive (Schröder and Stampfl 1999). These authors hypothesized that some glutathione conjugates serve as signal molecules being transported to the nucleus. Signal inactivation would be achieved by sequestering the conjugate in the vacuole.

Whereas most investigations on safeners and inducers focus on activation of GST, it is interesting to see that also inhibition and loss of GST activities may be encountered under the influence of xenobiotics. This has been shown repeatedly in conifers under the influence of air pollutants and other foreign compounds. Of course, such a loss of detoxification capacity for a series of electrophilic xenobiotics may have consequences on the fitness of plants in the environment and on their susceptibility for other stressors.

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