JXB Advance Access originally published online on September 18, 2006
Journal of Experimental Botany 2007 58(2):211-219; doi:10.1093/jxb/erl117
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
RESEARCH PAPER |
Dynamic analysis of ABA accumulation in relation to the rate of ABA catabolism in maize tissues under water deficit
1College of Agronomy and Biotechnology, State Key Laboratory of Plant Physiology and Biochemistry, China Agricultural University, Beijing, China
2Department of Biological Sciences, Lancaster Environment Centre, University of Lancaster, Lancaster LA1 4YQ, UK
3Department of Biology, Hong Kong Baptist University, Kowloon Tong, Hong Kong
To whom correspondence should be addressed. E-mail: Jiaws{at}cau.edu.cn or jzhang{at}hkbu.edu.hk
Received 26 May 2006; Accepted 14 July 2006
 |
Abstract |
|---|
 Top Abstract IntroductionMaterials and methodsResultsDiscussionReferences |
|---|
The plant hormone abscisic acid (ABA) accumulates in plant tissues which experience water deficit (stress ABA). This study analysed its accumulation as a function of both synthesis and catabolism in maize tissues. By following the disappearance of the stress ABA when ABA synthesis was blocked by nordihydroguaiaretic acid (NDGA), the rate of the catabolism of stress ABA was determined. When compared with the catabolic rate of baseline (non-stress) ABA, stress ABA showed a catabolic rate >11 times higher. With such an elevated catabolic rate, it is proposed that the xanthophyll precursor pool may not be able to sustain the ABA accumulation, and such a proposition has been substantiated by further experiments where fluridone is used to limit the availability of upstream ABA precursors. When fluridone was used, stress ABA accumulation could only be sustained for a few hours, i.e.
5 h for leaf and 1 h for root tissues. In detached roots, stress ABA accumulation could not be sustained even if fluridone was not used, suggesting that stress ABA accumulation in root systems requires the continuous import of ABA precursors from the shoots. Such an assumption was substantiated by the observation that defoliation or shading significantly reduced ABA accumulation in intact roots. The present study suggests that ABA catabolism is rapid enough to play an important role in the regulation of ABA accumulation. Key words: ABA accumulation, ABA precursors, catabolism, maize, water deficit
|
Introduction |
|---|
|
TopAbstractIntroductionMaterials and methodsResultsDiscussionReferences |
|---|
Abscisic acid (ABA) is a well-known stress hormone, which plays important roles in mediating the plant's responses to environmental stress (Davies and Zhang, 1991; Sauter et al., 2001). One basis of ABA acting as a stress signal, mediating such responses, is that accumulation of ABA can be induced rapidly in response to stresses such as soil drying. Both ABA biosynthesis and catabolism are complex processes involving many steps and enzymes. To date, most of the genes or enzymes in the ABA biosynthetic pathway have been identified and 9-cis-epoxycarotenoid dioxygenase (NCED) has been established as the key enzyme in the ABA biosynthesis pathway (Leon-Kloosterziel et al., 1996; Marin et al., 1996; Burbidge et al., 1997; Tan et al., 1997; Schwartz et al., 1997, 2003; Liotenberg et al., 1999; Qin and Zeevaart, 1999; Chernys and Zeevaart, 2000; Taylor et al., 2000; Cheng et al., 2002; Seo and Koshiba, 2002; Xiong and Zhu, 2003). In contrast to ABA biosynthesis, the genes and enzymes in ABA catabolism and its regulation remain largely unknown (Cutler and Krochko, 1999; Seo and Koshiba, 2002; Xiong and Zhu, 2003). Recently, the gene CYP707As encoding (+)-abscisic acid 8'-hydroxylase, a key enzyme responsible for ABA catabolism, was also identified in Arabidopsis (Saito et al., 2004).
While the molecular mechanisms for ABA biosynthesis have been well established, ABA accumulation will not only depend on an accelerated ABA biosynthesis under water deficit, but will also be a function of the rate of ABA catabolism and conjugation. In previous studies, the rate of ABA catabolism was assessed (Jia et al., 1996; Jia and Zhang, 1997), and the studies revealed that the rate of ABA catabolism was quite fast, for example, in maize seedlings >80% of the native ABA could be metabolized within <3 h. Although the rate of ABA conjugation was not accurately determined, the studies showed that the catabolism of ABA is probably the main factor controlling the disappearance of ABA (Jia et al., 1996; Jia and Zhang, 1997) in non-stressed conditions. However, to date, little is known about the roles of ABA catabolism in ABA accumulation under water-deficit conditions.
Water deficit-induced ABA accumulation is triggered by the activation of the NCED gene, and such activation is a transient process, i.e. soon after NCED is up-regulated the transcription activity returns to a base level again (Qin and Zeevaart, 1999). If the ABA catabolic rate is kept unchanged or becomes lower under water deficit, a transient activation of NCED activity would be able to produce an ABA accumulation, even when NCED activity returns to the base level. In such a case, the ABA accumulation capacity should be controlled by the degree and time of NCED activation. In contrast, if the catabolic rate of ABA increased under water deficit, to trigger an ABA accumulation and sustain the accumulation in a steady state, a sustained activation of NCED activity would be needed because the accelerated rate of catabolism would otherwise decrease the ABA content. It is therefore possible that ABA catabolism could play a crucial role in ABA accumulation.
The catabolic rate of ABA was previously determined under hydrated conditions using an isotope tracing method (Jia et al., 1996; Jia and Zhang, 1997). The catabolic rate for water deficit-induced ABA (defined as stress ABA) is still not known. In this study, a method has been developed to quantify the rate of catabolism of stress ABA. Based on the analysis of the catabolic rate, ABA accumulation has been analysed in relation to the sizes of the ABA precursor pools in shoots and roots. Our results strongly suggested that ABA catabolism plays a critical role in the regulation of ABA accumulation, thereby helping to explain plant adaptation to a variable environment.
|
Materials and methods |
|---|
|
TopAbstractIntroductionMaterials and methodsResultsDiscussionReferences |
|---|
Plant materials
Maize (Zea mays, cv. Zhongyou 1) were sown in trays of sand and watered with full-strength Hoagland's solution. The seedlings were grown for
4 d after germination at 28 °C in a greenhouse. For the experiment with detached roots, when the coleoptiles were 3 cm long, the primary roots were carefully washed out from the sand, and root tips (15 mm long) were excised as tissue samples. For experiments with detached leaves, the first and fully elongated leaves were used. In the experiment where attached roots and leaves were used, seedlings were at the four-leaf stage with the first leaves fully expanded.
Dehydration of detached leaves and roots
Dehydration of roots was achieved through air-drying. Root tips were allowed to lose water on the laboratory bench with gently moving air at room temperature (at 25 °C). After 15–20 min and when the root tips were 60% of their original fresh weight, the samples were sealed in aluminium foil and incubated in a moist chamber at 25 °C for various times before they were sampled for ABA content. To study water deficit-induced ABA accumulation in leaf tissues, detached leaves were cut into 5 mmx5 mm squares and placed in gently moving air at room temperature. When leaves lost 20% of their fresh weight in 30 min, the samples were then sealed in foil and incubated at room temperature for various times before they were sampled for ABA content. After incubation, the root or leaf samples were freeze-dried and stored in a desiccator pending ABA analysis.
Determination of the rate of catabolism of stress ABA
ABA can accumulate to a high level under water deficit. Because of this, the catabolic rate can be determined by following the disappearance of stress ABA under water deficit. To do this, a key requirement is to block further ABA accumulation completely while the disappearance of the stress ABA is being followed.
Moreover, the blockage of ABA biosynthesis should be fast and complete enough in order to maintain stress ABA not metabolized during the permeation of the inhibitor into cells. Preliminary tests showed that nordihydroguaiaretic acid (NDGA) was an ideal inhibitor of the NCED enzyme with regard to its permeation speed and capability to block ABA biosynthesis (Creelman et al., 1992). Because the inhibitory effect of NDGA is concentration dependent, the most suitable concentration of NDGA had to be determined, i.e. the lowest concentration which completely blocks ABA accumulation. To measure the half-life of stress ABA, detached leaves were cut into 5 mmx5 mm squares and dehydrated as described above. After incubation for 6 h, the leaf squares were vacuum infiltrated with 100 µM NDGA for 10 min and rapidly dehydrated again to their original weight within 15 min. Samples were then incubated as above and sampled for the determination of ABA content at different time points. To measure the half-life of stress ABA for a longer period, intact leaves were allowed to dehydrate by withholding watering to allow about the same degree of dehydration as for detached leaves. Seedlings were then put in a 100% humidity environment and incubated for 48 h, following which catabolism was determined as for detached leaves. Control samples were treated as above but with distilled water instead of NDGA solution. The catabolic rate of stress ABA was evaluated according to the time-course of the decrease in stress ABA content.
Determination of the rate of catabolism of non-stress ABA
While NDGA could completely block the synthesis of stress ABA, it could not completely block non-stress ABA biosynthesis in non-stressed plants. To determine the catabolic rate of the non-stress ABA, an isotope tracing method was adopted, which has been described previously (Jia et al., 1996; Jia and Zhang, 1997). Briefly, [3H]ABA was loaded into cells by feeding the detached seedlings with artificial xylem sap containing 200 µmol m–3 (±)-cis-trans-[3H]ABA (batch 29 from Amersham; the specific radioactivity was adjusted to 7.4x1012 Bq mol–1) under the following conditions: temperature 25 °C, humidity 60%, and a light intensity of 300 µmol m–2 s–1. Total radioactivity of 15–60 Bq mg–1 dried leaf mass (or 3.5–14.0 pg ABA mg–1 dry weight) could be loaded within 20 min, which was enough for ABA antibody capture and the detection of radioactivity. Uncatabolized [3H]ABA was separated with the ABA antibody Mac 252 (kindly provided by Dr SA Quarrie) and quantified using a liquid scintillation counter. The catabolic rate of native ABA was then determined by following the disappearance of [3H]ABA loaded into cells.
ABA accumulation in relation to the size of the ABA precursor pool
Fluridone is an inhibitor of carotenoid biosynthesis (Gamble and Mullet, 1986; Popova and Riddle, 1996). To estimate the relative pool size of ABA precursors in relation to ABA accumulation capacity, fluridone was used to block the conversion step upstream of the precursor pool. For such a purpose, detached leaf and root samples were vacuum infiltrated with 50 µM fluridone solution (a gift from SePRO Corp., Carmel, IN, USA), incubated for 30 min, and then subjected to dehydration treatment as described above.
To study the pool size of ABA precursors in relation to a relatively long-term ABA accumulation, experiments were carried out with attached leaves. When the first leaves were fully expanded, fluridone was fed into root systems of intact plants incubated in 200 µM fluridone solution for 1 h under the following conditions: PHAR 600 µmol–1 m–2 s–1, temperature 28 °C, and relative humidity 60%. After fluridone treatment, plants were immediately dehydrated as described below. For dehydration of attached leaves, plants were transferred into soil with a water content of 0.13 g g–1 (at permanent wilting point). The plants were allowed to lose water at 28 °C. When the leaf water potential decreased to –0.8 MPa, the plants were incubated in a growth chamber with the following conditions: PHAR 200 µmol m–2 s–1, temperature 25 °C, and relative humidity 95%. At various times of incubation, some leaves were detached and immediately frozen in liquid nitrogen for ABA analysis.
Effects of defoliation and shading on ABA accumulation in roots
Experiments were carried out to investigate the role of the shoot in the accumulation of ABA in roots. To assess the impact of defoliation, plants were dehydrated first by withholding watering. When the water potential of the leaves decreased to –0.8 MPa and the mature leaves showed initial wilting, all leaves were removed. Half of the intact plants were left as controls. At specific times after the defoliation, the root tips were collected for ABA analysis. To assess the impact of a shading treatment, young seedlings were shaded at 50 µmol m–2 s–1 for 2 or 3 d, and the root tips were then collected and dehydrated for ABA synthesis as described above. Non-shaded controls were also assessed.
ABA analysis
Aqueous extracts of ground root or leaf tissues (10 mg of freeze-dried sample in 1 ml of distilled water and shaken at 4 °C for 24 h) were used for the ABA assay without further purification. ABA analyses were carried out using the radioimmumoassay (RIA) method as described by Quarrie et al. (1988). The monoclonal antibody (Mac 252) was provided by Dr SA Quarrie. A 50 ml aliquot of crude extracts was mixed with 200 µl of phosphate-buffered saline (pH 6.0), 100 µl of diluted antibody solution, and 100 ml of [3H]ABA (8000 cpm) solution. The reaction mixture was incubated at 4 °C for 45 min and the bound radioactivity was measured in 50% saturated (NH4)2SO4-precipitated pellets with a liquid scintillation counter.
|
Results |
|---|
|
TopAbstractIntroductionMaterials and methodsResultsDiscussionReferences |
|---|
Effect of NDGA on ABA accumulation and determination of the catabolic rate for stress ABA
Figure 1 shows the dose-dependent inhibitory effect of NDGA on ABA accumulation. Water stress-induced ABA accumulation is very sensitive to NDGA. The concentration for half-inhibition is only
20 µM, and at 100 µM ABA accumulation could be totally blocked. Therefore, 100 µM NDGA was then used for the assessment of the catabolic rate of stress ABA.
|
Figure 2 shows the change in content of stress ABA after ABA accumulation was blocked by NDGA. While stress ABA remained at an elevated steady level in the control experiment, blocking of sustained ABA accumulation by NDGA led to a rapid decrease in stress ABA accumulation for both short-term (6 h, Fig. 2A) and long-term stresses (48 h, Fig. 2B), suggesting that such a method is suitable for the determination of the catabolic rate of stress ABA.
|
The curve for ABA catabolism could be modelled by the following equation:
 | (1) |
 | (2) |
 | (3) |
 | (4) |
According to equation (4), a catabolic rate of 2952 pmol ABA g–1 fresh weight (FW) h–1 for stress ABA at the steady state (i.e. at zero time) was calculated in detached leaf tissues (Fig. 2)
For a stress period of 48 h (Fig. 2B), the catabolism of the stress ABA could be modelled as:
 | (5) |
Determination of the catabolic rate for non-stress ABA
Figure 3 shows the catabolic curve for the baseline (non-stress) ABA. The data were obtained by following the disappearance of [3H]ABA loaded into fully hydrated leaf tissues. The curve could be modelled by equation (1) described above, with the remaining percentage of the total fed [3H]ABA (y) present:
 | (6) |
|
ABA accumulation in relation to the pool of ABA precursors in roots and leaves
With the high catabolic rate of stress ABA suggested by this study, an elevated rate of ABA biosynthesis must be established if substantial ABA accumulation is to be achieved under water deficit. Under these conditions, it seems possible that the size of the ABA precursor pool could become a limiting factor for sustained stress ABA accumulation. To test such a hypothesis, stress ABA biosynthesis was investigated in relation to the size of the xanthophyll pool (Fig. 4). Fluridone was used to block the new biosynthesis of xanthophyll. During the first 5 h there was no significant difference in the stress ABA levels between fluridone-treated and non-fluridone-treated leaf tissues (Fig. 4A). After 5 h, when ABA accumulation in control plants reached a steady state, the fluridone-treated leaves showed a gradual decline in stress ABA content, suggesting that the precursor pool could only sustain the ABA accumulation for an initial several hours, and that an accelerated synthesis of ABA precursors should be required for sustained ABA accumulation. Compared with the detached leaf tissues, the ABA accumulation in detached root tissues was much more sensitive to fluridone treatment (Fig. 4B). In
1 h, the fluridone treatment significantly reduced ABA accumulation, suggesting that the precursor pool in detached roots could not sustain ABA accumulation for more than a few hours (Fig. 4B). Interestingly, the time-course curves in detached root tissues were very different when compared with those of leaf tissues. They peaked at 5 h and declined rapidly afterwards, even in the absence of any fluridone treatment (Fig. 4B).
|
Is the ABA precursor pool size a limiting factor for ABA accumulation in detached leaves, if they are allowed to dehydrate for prolonged periods (i.e. for several days)? To mimic field conditions, intact plants were allowed to dry in the light for days and their ABA production with or without fluridone treatment was followed (Fig. 5). During the first 5 h there was no significant difference in the ABA levels between fluridone-treated and non-fluridone-treated plants (Fig. 5). However, compared with the situation with detached leaves, the time needed to reach a steady-state ABA content was much longer (>20 h in attached leaves and <8 h in detached leaves). After the initial hour, the difference in stress ABA contents between the fluridone and non-fluridone treatments became substantial. The stress ABA accumulation in attached leaves was much more than that in detached leaves, suggesting that the ABA precursor pool was much more quickly refilled at high PHAR. The shaded area in Fig. 5 shows the stress ABA accumulation that might be attributed to the initial ABA precursor pool. The dotted line shows a hypothetical stress ABA level according to equation (1) if no new ABA was produced due to a complete blockage of ABA precursors. Apparently fluridone did not completely block the synthesis of ABA precursors.
|
The influence of the shoot on ABA accumulation in roots
As shown in Fig. 4B, ABA accumulation in detached root tissues could not sustain a steady-state ABA content. This observation is not consistent with the proposal that, in field conditions, stressed roots can maintain a high ABA content for days (Davies and Zhang, 1991). In the present study, ABA accumulation was also followed over a much longer time period (72 h) in attached roots in drying soil. As expected, ABA accumulation was maintained at a steady level for days in attached roots (Fig. 6). Interestingly, defoliation led to a significant decrease in sustained ABA accumulation (Fig. 6). A further experiment showed that, while shading had no significant effect on the baseline ABA level in roots, plants shaded for 48 or 72 h showed reduced ABA accumulation in roots when compared with the non-shaded controls (Fig. 7). These results indicate that, to maintain the sustained ABA accumulation in attached roots, photosynthesis and active phloem transport to roots are required.
|
|
|
Discussion |
|---|
|
TopAbstractIntroductionMaterials and methodsResultsDiscussionReferences |
|---|
The ABA content of plants should be determined by a dynamic relationship between the rates of biosynthesis and catabolism of the molecule (Zeevaart, 1980, 1983; Zeevaart and Creelman, 1988). Using an 18O-labelling method (Creelman et al., 1987), a half-life of 15.5 h for ABA in Xanthium leaves was calculated. In the present study, a half-life of 0.88 h for non-stress ABA compared with a half life of
1 h for stress ABA (1.01 and 1.11 h for the 6 h and 48 h stress periods, respectively) was measured. Although the plant species used in these studies were different, the discrepancy in the half-life between the work of Creelman et al. (1987) and the present study might result from the different methods used. The 18O-labelling method will not take account of the effect of biosynthesis on the disappearance of stress ABA, thus leading to a much longer apparent half-life for ABA catabolism.
ABA catabolism was determined previously using a [3H]ABA tracing method, and it was found that the half-life for [3H]ABA fed to maize seedlings was 1 h (Jia et al., 1996; Jia and Zhang, 1997; Zhang et al., 1997). These earlier studies used maize leaves in a fully hydrated state, in which the ABA catabolism may not be the same as the catabolism of stress ABA. In the present study, two different methods were used to determine the catabolic rates for non-stress (baseline) and stress ABA. The catabolic assay of stress ABA is based on the inhibition of ABA biosynthesis by NDGA. Figure 1 shows that the inhibition of ABA accumulation is dependent on the NDGA concentration. For NDGA treatment at 100 µM, the ABA level accumulated was only 500 pmol g–1, which was near the baseline ABA level (normally 300–400 pmol g–1 FW), indicating that NDGA could basically inhibit the ABA accumulation. To inhibit ABA biosynthesis to a much lower level or even lower than the baseline ABA, the NDGA concentration used should be much higher, which might cause some adverse effects on cells. Thus, 100 µM is the perfect concentration used to determine the catabolic rate of stress ABA. Interestingly, the difference in half-life determined with the two different methods was not substantial, 0.88 h for baseline ABA and 1 h for stress ABA. The high value of r2 (>0.98 for both baseline and stress ABA, Figs 2, 3) strongly suggests that the catabolism of both baseline and stress ABA comply with the laws of exponential decay, which means the catabolic rate is proportional to the amount of ABA accumulated. In such a situation, the absolute rate of ABA catabolism should be significantly increased under water-deficit conditions with high ABA accumulation. The present results suggested that the increase could be >11 times. The conclusions of the present study are supported by an earlier observation that dehydration caused a steady and massive increase in the conversion of ABA to phaseic aicd in detached Phaseolus leaves (Pierce and Raschke, 1981), and a more recent observation that the gene CYP707As encoding (+)-abscisic acid 8'-hydroxylase could be activated under water deficit (Saito et al., 2004).
NCED is thought to be the key enzyme responsible for water deficit-induced ABA accumulation. In Arabidopsis, it was observed that the activation of NCED gene was very fast (within only 15–30 min after dehydration treatment); more interestingly, the transcript returned to its base level again after a few hours (4 h) (Qin and Zeevaart, 1999; Thompson et al., 2000). The present study shows that water deficit-induced ABA accumulation shows a saturation trend, i.e. the elevated level of ABA accumulation will be sustained at a plateau (Figs 5, 6). When the rate of biosynthesis of ABA is equivalent to the catabolic rate, the ABA content should be approximately constant (assuming no substantial import and/or export from other plant parts). Under water deficit, therefore, to sustain an elevated level of ABA, the synthetic rate of ABA should be activated to at least match an activated catabolic rate (11-fold in the present study). Based on such an analysis, it seems that the NCED gene should be activated for a sustained period or, alternatively, the elevated NCED activity could be sustained due to some post-transcription mechanism.
It is well known that, in the leaves, the ABA precursor pool can be very large. The levels of 9'-cis-neoxanthin and all-trans-violaxanthin are estimated to be 20- to 100-fold higher than the levels of ABA (Li and Walton, 1987, 1990; Norman et al., 1990; Parry et al., 1990; Parry and Horgan, 1991). Because of this, it is generally thought that the ABA precursor pool should be able to satisfy stress ABA accumulation, and therefore NCED might be the only enzyme that controls the ABA accumulation. As discussed above, to sustain a steady ABA content, the biosynthetic rate of ABA should be sustained at an elevated level, which might eventually lead to a depletion of the ABA precursor pool and limit further ABA accumulation. To test this hypothesis, fluridone was used to cut off the inflow of xanthophylls from the upstream pathway (Fig. 8). As expected, when the inflow of the xanthophyll precursor was cut off, after 5 h and 1 h, respectively, for leaves and roots, a significant decrease was found in the ABA accumulation compared with the control (non-fluridone treatment) (Figs 4, 5). This result suggests that the initial ABA precursor pool may play an important role only in ABA accumulation (as shown in the shaded area in Fig. 5).
|
When compared with leaves, stress ABA accumulation in detached roots declined rapidly from its maximum, even in the absence of fluridone treatment (Fig. 4). A reasonable explanation for this result is that detached roots are not able to satisfy the stress demand of ABA accumulation with their own limited precursor or substrate pool. To sustain ABA accumulation, it is necessary to import substrates from the shoot to the root. Besides direct biosynthesis, relocation of ABA may also play important roles in the regulation of ABA content in different organs or tissues (Hartung et al., 2002). It has been reported that ABA synthesized in leaves can be loaded in the phloem and transported to the roots, where it can be recirculated to the xylem vessels (Jeschke et al., 1997; Sauter et al., 2001). Some earlier studies also observed that the presence of shoots was essential for continuous ABA export from roots in drying soil (Zhang and Davies, 1989; Neales and Mcleod, 1991; Liang et al., 1997). It was observed here that defoliation caused a rapid decrease in stress ABA levels (Fig. 6), and that shading led to a decline in ABA accumulation in the root system (Fig. 7). This result suggested that, besides the direct import of ABA from shoot to root, the import of ABA precursor or substrate from shoot to root should also play important roles in root ABA accumulation, and because the content of ABA precursor is much higher than that of ABA, the precursor import might play more important roles in the ABA accumulation of roots. It is interesting to understand the rate and its regulation of ABA import from shoot to root. Using a [3H]ABA tracing method, the rate of ABA export from maize leaves was quantified (Jia and Zhang, 1997) and it was found that the rate of ABA export was much lower than the rate of catabolism of ABA. Furthermore, water deficit appeared to reduce the rate of ABA export from leaves. Although the ABA transport from root to shoot can play an important role in plant adaptive responses at the earlier stage of soil drying when no decrease in leaf turgor occurs (Davies and Zhang, 1991), when ABA starts to accumulate, ABA catabolism should also play a crucial role in the regulation of ABA content.
In summary, the present results show how stress ABA accumulation can be controlled by a dynamic equilibrium between ABA biosynthesis and catabolism. Initially, the ABA precursor pool allows ABA accumulation to be rapidly triggered without the necessity for the upstream enzymes to be involved, but a sustained ABA accumulation requires an activated and accelerated production of ABA precursors in both roots and leaves. The existence of a large ABA precursor pool can ensure a sensitive plant response to soil drying, while, on the other hand, the significant activation of ABA catabolism can restrict excessive ABA accumulation and therefore avoid any possible adverse effects on development physiology. In addition, the much increased catabolic rates should degrade the stress ABA rapidly to the base level and thus enable plants to recover functional capability quickly once the water deficit is relieved.
|
Acknowledgements |
|---|
This work was supported by the State Basic Research and Development Plan of China (2003CB114300), the National Natural Science Funds of China (30470160), and the Research Grant Council of Hong Kong (HKBU 2165/05M).
|
Footnotes |
|---|
* These authors contributed equally to this work.
|
Abbreviations |
|---|
ABA, abscisic acid; NCED, 9-cis-epoxycarotenoid dioxygenase; NDGA, nordihydroguaiaretic acid.
|
References |
|---|
|
TopAbstractIntroductionMaterials and methodsResultsDiscussionReferences |
|---|
Burbidge A, Grieve T, Jackson A, Thompson A, Taylor I. (1997) Structure and expression of a cDNA encoding a putative neoxanthin cleavage enzyme, isolated from a wilt-related tomato library. Journal of Experimental Botany 48 2111–2112.
Cheng WH, Endo A, Zhou L, Penney J, Chen HC, Arroyo A, Leon P, Nambara E, Asami T, Seo M. (2002) A unique short-chain dehydrogenase/reductase in Arabidopsis glucose signalling and abscisic acid biosynthesis and functions. The Plant Cell 14 2723–2743.
Chernys JT and Zeevaart JAD. (2000) Characterization of the 9-cis-epoxycarotenoid dioxygenase gene family and the regulation of abscisic acid biosynthesis in avocado. Plant Physiology 124 343–353.
Creelman RA, Bell E, Mullet JE. (1992) Involvement of a lipoxygenase-like enzyme in abscisic acid biosynthesis. Plant Physiology 99 1258–1260.
Creelman RA, Gage DA, Stults JT, Zeevaart JAD. (1987) Abscisic acid biosynthesis in leaves and roots of Xanthium strumarium.. Plant Physiology 85 726–732.
Cutler A and Krochko J. (1999) Formation and breakdwon of ABA. Trends in Plant Science 4 472–478.[CrossRef][Web of Science][Medline]
Davies WJ and Zhang J. (1991) Root signals and the regulation of growth and development of plants in drying soil. Annual Review of Plant Physiology and Plant Molecular Biology 42 55–76.[CrossRef][Web of Science]
Gamble PE and Mullet JE. (1986) Inhibition of carotenoid accumulation and abscisic acid biosynthesis in fluridone-treated dark-grown barley. European Journal of Biochemistry 160 117–121.[Web of Science][Medline]
Hartung W, Sauter A, Hose E. (2002) Abscisic acid in the xylem: where does it come from, where does it go to? Journal of Experimental Botany 53 27–32.
Jeschke WD, Holobradá M, Hartung W. (1997) Growth of Zea mays L. plants with their seminal roots only. Effects on plant development, xylem transport, mineral nutrition and the flow and distribution of abscisic acid (ABA) as a possible shoot to root signal. Journal of Experimental Botany 48 1229–1239.
Jia W and Zhang J. (1997) Comparison of exportation and metabolism of xylem-delivered ABA in maize leaves at different water status and xylem sap pH. Plant Growth Regulation 21 43–49.
Jia W, Zhang J, Zhang DP. (1996) Metabolism of xylem-delivered ABA in relation to ABA flux and concentration in leaves of maize and Commelina communis.. Journal of Experimental Botany 47 1085–1091.
Leon-Kloosterziel KM, Gil MA, Ruijs GJ, Jacobsen SE, Olszewski NE, Schwartz SH, Zeevaart JA, Koornneef M. (1996) Isolation and characterization of abscisic acid-deficient Arabidopsis mutants at two new loci. The Plant Journal 10 655–666.[CrossRef][Web of Science][Medline]
Li Y and Walton DC. (1987) Xanthophylls and abscisic acid biosynthesis in water-stressed bean leaves. Plant Physiology 85 910–915.
Li Y and Walton DC. (1990) Violaxanthin is an abscisic acid precursor in water-stressed dark-grown bean leaves. Plant Physiology 92 551–559.
Liang J, Zhang J, Wong MH. (1997) How do roots control xylem sap ABA concentration in response to soil drying? Plant, Cell and Physiology 38 10–16.
Liotenberg S, North H, Marion-Poll A. (1999) Molecular biology of abscisic acid biosynthesis in plants. Plant Physiology and Biochemistry 37 341–350.
Marin E, Nussaume L, Quesada A, Gonneau M, Sotta B, Hugueney P, Frey A, Marion-Poll A. (1996) Molecular identification of zeaxanthin epoxidase of Nicotiana plumbaginifolia, a gene involved in abscisic acid biosynthesis and corresponding to the ABA locus of Arabidopsis thaliana.. EMBO Journal 15 2331–2342.[Web of Science][Medline]
Neales TF and Mcleod AL. (1991) Do leaves contribute to the abscisic acid present in the xylem sap of drought sunflower plants? Plant, Cell and Environment 14 979–986.[CrossRef]
Norman SM, Maier VP, Pon DL. (1990) Abscisic acid accumulation and carotenoid and chlorophyll content in relation to water stress and leaf age of different types of citrus. Journal of Agricultural and Food Chemistry 38 1326–1334.[CrossRef]
Parry AD, Babiano MJ, Horgan R. (1990) The role of cis-carotenoids in abscisic acid biosynthesis. Planta 182 118–128.[Web of Science]
Parry AD and Horgan R. (1991) Carotenoids and abscisic acid biosynthesis in higher plants. Physiologia Plantarum 82 320–326.[CrossRef]
Pierce M and Raschke K. (1981) Synthesis and metabolism of abscisic acid in detached leaves of Phaseolus vulgaris L. after loss and recovery of turgor. Planta 153 156–165.[CrossRef]
Popova LP and Riddle KA. (1996) Development and accumulation of ABA in fluridone-treated and drought-stressed Vicia faba plants under different light conditions. Physiologia Plantarum 98 791–797.[CrossRef]
Qin XQ and Zeevaart JAD. (1999) The 9-cis-epoxycarotenoid cleavage reaction is the key regulatory step of abscisic acid biosynthesis in water-stressed bean. Proceedings of the National Academy of Sciences, USA 96 15354–15361.
Quarrie SA, Whitford PN, Appleford NEJ, Wang TL, Cook SK, Henson IE, Loveys BR. (1988) A monoclonal antibody to (S)-abscisic acid: its characterization and use in a radioimmunoassay for measuring abscisic acid in crude extracts of cereal and lupin leaves. Planta 173 330–339.[CrossRef][Web of Science]
Saito S, Hirai N, Matsumoto C, Ohigashi H, Ohta D, Sakata K, Masaharu M. (2004) Arabidopsis CYP707As encode (+)-abscisic acid 8'-hydroxylase, a key enzyme in the oxidative catabolism of abscisic acid. Plant Physiology 134 1439–1449.
Sauter A, Davies WJ, Hartung W. (2001) The long-distance abscisic acid signal in the droughted plant: the fate of the hormone on its way from root to shoot. Journal of Experimental Botany 52 1991–1997.
Schwartz SH, Qin X, Zeevaart JAD. (2003) Elucidation of the indirect pathway of abscisic acid biosynthesis by mutants, genes, and enzymes. Plant Physiology 131 1591–1601.
Schwartz SH, Tan BC, Gage DA, Zeevaart JAD, McCarty DR. (1997) Specific oxidative cleavage of carotenoids by Vp14 of maize. Science 276 1872–1874.
Seo M and Koshiba T. (2002) Complex regulation of ABA biosynthesis in plants. Trends in Plant Science 7 41–48.[CrossRef][Web of Science][Medline]
Tan BC, Schwartz SH, Zeevaart JAD, McCarty DR. (1997) Genetic control of abscisic acid biosynthesis in maize. Proceedings of the National Academy of Sciences, USA 94 12235–12240.
Taylor IB, Burbidge A, Thompson AJ. (2000) Control of abscisic acid synthesis. Journal of Experimental Botany 51 1563–1574.
Thompson AJ, Jackson AC, Parker RA, Morpeth DR, Burbidge A, Taylor IB. (2000) Abscisic acid biosynthesis in tomato: regulation of zeaxanthin epoxidase and 9-cis-epoxycarotenoid dioxygenase mRNAs by light/dark cycles, water stress and abscisic acid. Plant Molecular Biology 42 833–845.[CrossRef][Web of Science][Medline]
Xiong L and Zhu JK. (2003) Regulation of abscisic acid biosynthesis. Plant Physiology 133 29–36.
Zeevaart JAD. (1980) Changes in the levels of abscisic acid and its metabolites in excised leaf blades of Xanthium strumarium during and after water stress. Plant Physiology 66 672–678.
Zeevaart JAD. (1983) Metabolism of abscisic acid and its regulation in Xanthium leaves during and after water stress. Plant Physiology 71 477–481.
Zeevaart JAD and Creelman RA. (1988) Metabolism and physiology of abscisic acid. Annual Review of Plant Physiology and Plant Molecular Biology 39 439–473.[CrossRef][Web of Science]
Zhang J and Davies WJ. (1989) Sequential responses of whole plant water relations towards prolonged soil drying and the mediation by xylem sap ABA concentration in the regulation of stomatal behaviour of sunflower plants. New Phytologist 113 167–174.[CrossRef]
Zhang J, Jia W, Zhang DP. (1997) Effect of leaf water status and xylem pH on metabolism of xylem-transported abscisic acid. Plant Growth Regulation 21 51–58.
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  G. Zhu, N. Ye, and J. Zhang Glucose-Induced Delay of Seed Germination in Rice is Mediated by the Suppression of ABA Catabolism Rather Than an Enhancement of ABA Biosynthesis Plant Cell Physiol., March 1, 2009; 50(3): 644 - 651. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||