Selenium excess can cause toxicity symptoms, e.g. root growth inhibition in non-hyperaccumulator plants such as Arabidopsis. Selenite-induced hormonal and signalling mechanisms in the course of development are poorly understood; therefore this study set out to investigate the possible hormonal and signalling processes using transgenic and mutant Arabidopsis plants. Significant alterations were observed in the root architecture of the selenite-treated plants, due to the loss of cell viability in the root apex. During mild selenite excess, the plants showed symptoms of the morphogenic response: primary root (PR) shortening and increased initiation of laterals, ensuring better nutrient and water uptake and stress acclimation. As well as lower meristem cell activity, the second reason for the Se-induced growth hindrance is the hormonal imbalance, since the in situ expression of the auxin-responsive DR5::GUS, and consequently the auxin levels, significantly decreased, while that of the cytokinin-inducible ARR5::GUS and the ethylene biosynthetic ACS8::GUS increased. It is assumed that auxin and ethylene might positively regulate selenium tolerance, since reduced levels of them resulted in sensitivity. Moreover, high cytokinin levels caused notable selenite tolerance. During early seedling development, nitric oxide (NO) contents decreased but hydrogen peroxide levels increased reflecting the antagonism between the two signal molecules during Se excess. High levels of NO in gsnor1-3, lead to selenite tolerance, while low NO production in nia1nia2 resulted in selenite sensitivity. Consequently, NO derived from the root nitrate reductase activity is responsible for the large-scale selenite tolerance in Arabidopsis.
In plant organs, Cu(2+) excess results in severe morphological responses during which the endogenous hormonal balance and signal transduction are affected. Auxin and NO negatively regulate each other's level and NO intensifies the metal-induced cotyledon expansion, but mitigates elongation processes under Cu(2+) exposure.
Nitric oxide improves copper tolerance via modulation of superoxide and hydrogen peroxide levels. This reflects the necessity of a well-coordinated interplay between NO and ROS during stress tolerance. Copper (Cu) excess causes toxicity and one probable consequence of this is the disturbance of cell redox state maintenance, inter alia, by reactive oxygen- (ROS) and nitrogen species (RNS). The objective of this paper was to examine the role of nitric oxide (NO) in Cu stress tolerance and its relationship with ROS in Arabidopsis. In agar-grown seedlings, concentration-dependent Cu accumulation was observed. The 5 μM Cu resulted in reduced cell viability in the NO overproducing nox1 and gsnor1-3 root tips compared to the wild-type (WT). In contrast, 25 and 50 μM Cu caused higher viability in these mutants, while in the NO-lacking nia1nia2 lower viability was detected than in the WT. The exogenous NO donor enhanced cell viability and scavenging endogenous NO decreased it in Cu-exposed WT seedlings. Besides, SNP in nia1nia2 roots led to the improvement of viability. The ascorbic acid-deficient mutants (vtc2-1, vtc2-3) possessing slightly elevated ROS levels proved to be Cu sensitive, while miox4 showing decreased ROS production was more tolerant to Cu than the WT. In nox1 and gsnor1-3, Cu did not induce superoxide formation, and H₂O₂ accumulation occurred only in the case of NO deficiency. Based on these, under mild stress NO intensifies cell injury, while in the case of severe Cu excess it contributes to better viability. ROS were found to be responsible for aggravation of Cu-induced damage. NO alleviates acute Cu stress via modulation of O₂(·-) and H₂O₂ levels reflecting the necessity of a well-coordinated interplay between NO and ROS during stress tolerance.
Heavy metals (HMs) are toxic pollutants, which can negatively affect the physiological processes of plants; moreover, HMs can be present in the food chain endangering people's health. The aim of this study was to investigate the early physiological events during HM exposure in the root tips of the food plant Pisum sativum L. Ten-day-old pea plants were treated with 100 lM CdCl 2 or CuSO 4 , in nutrient solution for 48 h. We studied the rapid formation of different reactive oxygen species (hydrogen peroxide H 2 O 2 and superoxide radical O 2 Á-) and reactive nitrogen species (nitric oxide NOÁ and peroxynitrite ONOO -) together with membrane damage and cell death in the meristem cells of pea roots using in vivo and in situ microscopic methods. In our experimental system, copper and cadmium induced the formation of H 2 O 2 and NO. Two hours of heavy metal treatments resulted in an increased O 2 Á-formation; however, later the level of this reactive molecule dramatically decreased. We found that high levels of NO were needed for ONOO -production under HM exposure. A fast loss of membrane integrity and decreased cell viability were detected in root tips of copper-treated plants. The effects of cadmium seemed to be slower compared to copper, but this non-essential metal also caused cell death. We concluded that viability decreased when NO and H 2 O 2 levels were simultaneously high in the same tissues. Using the NO scavenger it was also evidenced that NO generation is essential for cell death induction under copper or cadmium stress.
Selenite oppositely modifies cytokinin and nitric oxide metabolism in Arabidopsis organs. A mutually negative interplay between the molecules exists in selenite-exposed roots; and their overproduction causes selenite insensitivity. Selenium-induced phytotoxicity is accompanied by developmental alterations such as primary root (PR) shortening. Growth changes are provoked by the modulation of hormone status and signalling. Cytokinin (CK) cooperates with the nitric oxide (NO) in many aspects of plant development; however, their interaction under abiotic stress has not been examined. Selenite inhibited the growth of Arabidopsis seedlings and reduced root meristem size through cell division arrest. The CK-dependent pARR5::GUS activity revealed the intensification of CK signalling in the PR tip, which may be partly responsible for the root meristem shortening. The selenite-induced alterations in the in situ expressions of cytokinin oxidases (AtCKX4::GUS, AtCKX5::GUS) are associated with selenite-triggered changes of CK signalling. In wild-type (WT) and NO-deficient nia1nia2 root, selenite led to the diminution of NO content, but CK overproducer ipt-161 and -deficient 35S:CKX2 roots did not show NO decrease. Exogenous NO (S-nitroso-N-acetyl-DL-penicillamine, SNAP) reduced the pARR5::GFP and pTCS::GFP expressions. Roots of the 35S:CKX and cyr1 plants suffered more severe selenite-triggered viability loss than the WT, while in ipt-161 and gsnor1-3 no obvious viability decrease was observed. Exogenous NO ameliorated viability loss, but benzyladenine intensified it. Based on the results, selenite impacts development by oppositely modifying CK signalling and NO level. In the root system, CK signalling intensifies which possibly contributes to the nitrate reductase-independent NO diminution. A mutually negative CK-NO interplay exists in selenite-exposed roots; however, overproduction of both molecules worsens selenite sensing. Hereby, we suggest novel regulatory interplay and role for NO and CK in abiotic stress signalling.
Plants are able to dynamically adapt to their environment by reprogramming of their growth and development. Copper (Cu 2?) excess modifies shoot and root architecture of plants by a lesser known mechanism, therefore the involvement of a major hormone component (auxin) and a signal molecule (nitric oxide) in Cu 2?induced morphological responses were studied in Arabidopsis using microscopic methods. Auxin-inducible gene expression was visualized in DR5::GUS Arabidopsis and nitric oxide (NO) levels were detected by DAF-FM fluorophore in the stem and root system. Copper excess caused the inhibition of stem and root growth of Arabidopsis, during which cell elongation, division and expansion were also affected. The symptoms of stress-induced morphogenic response were found in the root system of 25 lM Cu 2?-treated plants. In both organs, the decrease of auxindependent gene expression was found, which can partly explain the growth inhibitions. Besides hormonal system, nitric oxide metabolism was also affected by Cu 2?. In root tips, copper excess induced NO generation, while NO content in lateral roots was not affected by the treatments. Using nia1nia2 mutants, nitrate reductase enzyme as a putative source of Cu 2?-induced NO was identified in Arabidopsis primary roots.
Hydroponic experiments were conducted to compare the effects of excess copper (Cu) on growth and photosynthesis in young Indian mustard (Brassica juncea) and oilseed rape (Brassica napus). We compared the effects of excess Cu on the two Brassica species at different physiological levels from antioxidant levels to photosynthetic activity. Nine-day-old plants were treated with Cu (10, 25 and 50 µM CuSO 4 ) for 7 and 14 days. Both species took up Cu from the external solution to a similar degree but showed slight root-to-shoot translocation. Furthermore, after seven days of treatment, excess Cu significantly decreased other microelement content, such as iron (Fe) and manganese (Mn), especially in the shoots of B. napus. As a consequence, the leaves of young Brassica napus plants showed decreased concentrations of photosynthetic pigments and more intense growth inhibition; however, accumulation of highly reactive oxygen species (hROS) were not detected. After 14 days of Cu exposure the reduction of Fe and Mn contents and shoot growth proved to be comparable in the two species. Moreover, a significant Cu-induced hROS accumulation was observed in both Brassica species. The diminution in pigment contents and photosynthetic efficiency were more pronounced in B. napus during prolonged Cu exposure. Based on all the parameters, B. juncea appears to be more resistant to excess Cu than B. napus, rendering it a species with higher potential for phytoremediation.Keywords: Brassica juncea -Brassica napus -copper -oxidative stress -phytoremediation -photosynthesis INTRODUCTIONAmong heavy metals, copper in trace amounts is essential for plant life but it becomes toxic at higher concentrations. In excess, this heavy metal seriously inhibits leaf expansion at the early growth stage and it causes changes in physiological processes such as transpiration, photosynthetic electron transport and biosynthesis of chlorophyll [30]. Indeed, photosynthesis is the most heavy metal-sensitive process [1] since * Corresponding author; e-mail address: fglgbr@gmail.com + These authors contributed equally to this work. 206Gábor FeiGl et al. Biologica Hungarica 66, 2015 excess Cu can, inter alia, affect photosynthetic electron transport on the reducing side of PSI at the level of ferredoxin. In addition, it can alter the PSII on the oxidising side by inhibiting the electron transport at P680 as well as by inactivating some PSII reaction centres [41]. A few studies indicate that excess Cu can impair the PSII electron transport on its reducing side by affecting the rate of electron transfer from tyrosine (Y Z ) to the oxidized primary donor P680 + [16]. ActaAt the molecular level, excess Cu is able to induce the formation of reactive oxygen species (ROS) via the Fenton or Haber-Weiss reactions which subsequently damage proteins, nucleic acids and lipids [14]. This effect of excess Cu was supported by the positive correlation between Cu-treatment and the production of hydroxyl radicals in Arabidopsis [9]. Besides, excess Cu can indirectly cause oxida...
The Arabidopsis AtCRK5 protein kinase is involved in the establishment of the proper auxin gradient in many developmental processes. Among others, the Atcrk5-1 mutant was reported to exhibit a delayed gravitropic response via compromised PIN2-mediated auxin transport at the root tip. Here, we report that this phenotype correlates with lower superoxide anion (O2•−) and hydrogen peroxide (H2O2) levels but a higher nitric oxide (NO) content in the mutant root tips in comparison to the wild type (AtCol-0). The oxidative stress inducer paraquat (PQ) triggering formation of O2•− (and consequently, H2O2) was able to rescue the gravitropic response of Atcrk5-1 roots. The direct application of H2O2 had the same effect. Under gravistimulation, correct auxin distribution was restored (at least partially) by PQ or H2O2 treatment in the mutant root tips. In agreement, the redistribution of the PIN2 auxin efflux carrier was similar in the gravistimulated PQ-treated mutant and untreated wild type roots. It was also found that PQ-treatment decreased the endogenous NO level at the root tip to normal levels. Furthermore, the mutant phenotype could be reverted by direct manipulation of the endogenous NO level using an NO scavenger (cPTIO). The potential involvement of AtCRK5 protein kinase in the control of auxin-ROS-NO-PIN2-auxin regulatory loop is discussed.
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