Here, we review information on how plants face redox imbalance caused by climate change, and focus on the role of nitric oxide (NO) in this response. Life on Earth is possible thanks to greenhouse ...effect. Without it, temperature on Earth’s surface would be around -19°C, instead of the current average of 14°C. Greenhouse effect is produced by greenhouse gasses (GHG) like water vapor, carbon dioxide (CO
2
), methane (CH
4
), nitrous oxides (N
x
O) and ozone (O
3
). GHG have natural and anthropogenic origin. However, increasing GHG provokes extreme climate changes such as floods, droughts and heat, which induce reactive oxygen species (ROS) and oxidative stress in plants. The main sources of ROS in stress conditions are: augmented photorespiration, NADPH oxidase (NOX) activity, β-oxidation of fatty acids and disorders in the electron transport chains of mitochondria and chloroplasts. Plants have developed an antioxidant machinery that includes the activity of ROS detoxifying enzymes e.g., superoxide dismutase (SOD), ascorbate peroxidase (APX), catalase (CAT), glutathione peroxidase (GPX), and peroxiredoxin (PRX), as well as antioxidant molecules such as ascorbic acid (ASC) and glutathione (GSH) that are present in almost all subcellular compartments. CO
2
and NO help to maintain the redox equilibrium. Higher CO
2
concentrations increase the photosynthesis through the CO
2
-unsaturated Rubisco activity. But Rubisco photorespiration and NOX activities could also augment ROS production. NO regulate the ROS concentration preserving balance among ROS, GSH, GSNO, and ASC. When ROS are in huge concentration, NO induces transcription and activity of SOD, APX, and CAT. However, when ROS are necessary (e.g., for pathogen resistance), NO may inhibit APX, CAT, and NOX activity by the S-nitrosylation of cysteine residues, favoring cell death. NO also regulates GSH concentration in several ways. NO may react with GSH to form GSNO, the NO cell reservoir and main source of S-nitrosylation. GSNO could be decomposed by the GSNO reductase (GSNOR) to GSSG which, in turn, is reduced to GSH by glutathione reductase (GR). GSNOR may be also inhibited by S-nitrosylation and GR activated by NO. In conclusion, NO plays a central role in the tolerance of plants to climate change.
Nitric oxide (NO), a gaseous, redox-active small molecule, is gradually becoming established as a central regulator of growth, development, immunity and environmental interactions in plants. A major ...route for the transfer of NO bioactivity is S-nitrosylation, the covalent attachment of an NO moiety to a protein cysteine thiol to form an S-nitrosothiol (SNO). This chemical transformation is rapidly emerging as a prototypic, redox-based post-translational modification integral to the life of plants. Here we review the myriad roles of NO and SNOs in plant biology and, where known, the molecular mechanisms underpining their activity.
Iron is an essential and commonly limited nutrient for plants. To increase the uptake of iron during times of low iron supply, plants, except the grasses, activate a set of physiological and ...morphological responses in their roots that include iron reduction, soil acidification, Fe(II) transport and proliferation of root hairs. It is not known how root cells sense and transduce the changes that occur after the onset of iron deficiency. This work presents evidence that nitric oxide (NO) is produced rapidly in the root epidermis of tomato plants (Solanum lycopersicum) that are grown in iron-deficient conditions. The scavenging of NO prevented iron-deficiency-induced upregulation of the basic helix-loop-helix transcription factor FER, the ferric-chelate reductase LeFRO1 and the Fe(II) transporter LeIRT1 genes. On the other hand, exogenous application of the NO donor S-nitrosoglutathione enhanced the accumulation of FER, LeFRO1 and LeIRT1 mRNA in roots of iron-deficient plants. The activity of the root ferric-chelate reductase and the proliferation of root hairs induced by iron deficiency were stimulated by NO supplementation and suppressed by NO scavenging. Nitric oxide was ineffective in inducing iron-deficiency responses in the tomato fer mutant, which indicates that the FER protein is necessary to mediate the action of NO. Furthermore, NO supplementation improved plant growth under low iron supply, which suggests that NO is a key component of the regulatory mechanisms that control iron uptake and homeostasis in plants. In summary, the results of this investigation indicate that an increase in NO production is an early response of roots to iron deprivation that contributes to the improvement of iron availability by (i) modulating the expression of iron uptake-related genes and (ii) regulating the physiological and morphological adaptive responses of roots to iron-deficient conditions.
Specialized guard cells modulate plant gas exchange through the regulation of stomatal aperture. The size of the stomatal pore is a direct function of the volume of the guard cells. The transport of ...solutes across channels in plasma membrane is a crucial process in the maintenance of guard cell water status. The fine tuned regulation of that transport requires an integrated convergence of multiple endogenous and exogenous signals perceived at both the cellular and the whole plant level. Gasotransmitters are novel signaling molecules with key functions in guard cell physiology. Three gasotransmitters, nitric oxide (NO), carbon monoxide (CO), and hydrogen sulfide (H₂S) are involved in guard cell regulatory processes. These molecules are endogenously produced by plant cells and are part of the guard cells responses to drought stress conditions through ABA-dependent pathways. In this review, we summarize the current knowledge of gasotransmitters as versatile molecules interacting with different components of guard cell signaling network and propose them as players in new paradigms to study ABA-independent guard cell responses to water deficit.
Here, the link between UV-B stimulus and the abscisic acid (ABA)-induced nitric oxide (NO) synthesis pathway was studied in leaves of maize (Zea mays). The ABA concentration increased by 100% in UV-B ...irradiated leaves. Leaves of viviparous 14 (vp14), a mutant defective in ABA synthesis, were more sensitive to UV-B-induced damage than those of the wild type (wt). ABA supplementation attenuated UV-B-induced damage in both the wt and vp14. The hydrogen peroxide (H₂O₂) concentration increased in the irradiated wt, but changed only slightly in vp14. This increase was prevented by diphenylene iodonium (DPI), an inhibitor of NADPH oxidase (pNOX). NO was detected using the fluorophore 4,5-diamino-fluorescein diacetate (DAF-2DA). DAF-2DA fluorescence increased twofold in UV-B-irradiated wt leaves but not in vp14 leaves. H₂O₂ and NO production was restored in vp14 plants supplied with 100 μM ABA. Catalase, DPI and the NO synthase (NOS) inhibitor NG-nitro-L-arginine methyl ester (L-NAME) partially blocked UV-B-induced NO accumulation, suggesting that H₂O₂ as well as NOS-like activity is required for a full plant response to UV-B. NO protects against UV-B-induced cell damage. Our results suggest that UV-B perception triggers an increase in ABA concentration, which activates pNOX and H₂O₂ generation, and that an NOS-like-dependent mechanism increases NO production to maintain cell homeostasis and attenuate UV-B-derived cell damage.
Low UV-B fluence is a signaling stimulus that regulates various physiological processes and induces photomorphogenic responses in plants. The specific UV-B receptor UVR8 is a key component in these ...processes. Although UVR8 sequence is conserved, few homologs have been cloned and reported to be functional. Here we show the cloning and functional analysis of
Zea mays
UVR8 (
Zm
UVR8).
Zm
UVR8 presents 73% of identity with
At
UVR8, maintaining the key tryptophan responsible of UV-B perception.
Zm
UVR8 also contains the VP domain, involved in the interaction with the proteins CONSTITUTIVELY PHOTOMORPHOGENIC 1 (COP1) and REPRESSOR OF UV-B PHOTOMORPHOGENESIS 1 (RUP1). Whereas
UVR8
was expressed in non-irradiated
Arabidopsis
and maize leaves, after 2 h of UV-B irradiation, its expression was reduced. The expression of chalcone synthase (
CHS
), involved in flavonoid biosynthesis and regulated by UVR8, was increased in irradiated
Arabidopsis
and maize leaves.
Arabidopsis uvr8-1
null mutant was complemented with
Zm
UVR8 driven by the CaMV-35S promoter and fused to eGFP.
Zm
UVR8-eGFP fusion was mainly localized in nuclei of transgenic lines, irrespective of UV-B treatments. UV-B suppressed hypocotyl elongation in wild type (WT)
Arabidopsis
plants, whereas in
uvr8-1
hypocotyl growth was observed. However, hypocotyl elongation was reduced in UV-B irradiated transgenic lines complemented with
Zm
UVR8. Moreover,
CHS
and transcription factor
HY5
(ELONGATED HYPOCOTYL 5) expression were also restored in these plants. These results confirm that
Zm
UVR8 is similar enough to
At
UVR8 to restore UV-B perception and signaling in
Arabidopsis
mutant
uvr8-1
, thus being a functional UV-B photoreceptor. That reinforce the importance of UVR8 as a functional UV-B-responsive regulator in land plants.
Iron is an essential micronutrient required for a wide variety of cellular functions in plant growth and development. Chlorosis is the first visible symptom in iron-deficient plants. Glutathione ...(GSH) and ascorbic acid (ASC) are multifunctional metabolites playing important roles in redox balancing. In this work, it was shown that GSH and ASC treatment prevented chlorosis and the accumulation of reactive oxygen species induced by iron deficiency in Arabidopsis leaves. In iron deficiency, GSH and ASC increased the activity of the heme protein ascorbate peroxidase at a similar level to that found in iron-sufficient seedlings. GSH was also able to preserve the levels of the iron–sulfur protein ferredoxin 2. GSH content decreased 25% in iron-deficient Arabidopsis seedlings, whereas the ASC levels were not affected. Taken together, these results showed that GSH and ASC supplementation protects Arabidopsis seedlings from iron deficiency, preserving cell redox homeostasis and improving internal iron availability.
Ultraviolet-B (UV-B) is present in sunlight (280-315 nm) and has diverse effects on living organisms. Low fluence rate of exposure induces a specific photomorphogenic response regulated by the UV-B ...response locus 8 (UVR8) receptor. UVR8 was first described in
In the absence of stimuli it is located in the cytoplasm as a homodimer. However, upon UV-B irradiation, it switches to a monomer and interacts with the ubiquitin ligase E3 COP1 via the UVR8 β-propeller domain and the VP core. This induces the expression of the transcription factor HY5 leading to changes in the expression of genes associated with UV-B acclimation and stress tolerance. UVR8 senses UV-B through tryptophan residues being Trp233 and 285 the most important. Based on the comparison and analysis of UVR8 functionally important motifs, we report a comprehensive phylogeny of UVR8, trying to identify UVR8 homologs and the ancestral organism where this gene could be originated. Results obtained showed that
are the first organisms from the
group where UVR8 appears. UVR8 is present in green algae, bryophytes, lycophytes, and angiosperms. All the sequences identified contain tryptophans 233 and 285, arginines involved in homodimerization and the VP domain suggesting they are true UVR8 photoreceptors. We also determined that some species from bryophytes and angiosperms contain more than one UVR8 gene copy posing the question if UVR8 could constitute a gene family in these species. In conclusion, we described the functional conservation among UVR8 proteins from green algae to higher plants.
UV RESISTANCE LOCUS8 (UVR8) signaling involves CONSTITUTIVELY PHOTOMORPHOGENIC1, the ELONGATED HYPOCOTYL5 (HY5) transcription factor, and the closely related HY5 HOMOLOG. Some UV-B responses mediated ...by UVR8 are also regulated by nitric oxide (NO), a bioactive molecule that orchestrates a wide range of processes in plants. In this study, we investigated the participation of the UVR8 pathway and its interaction with NO in UV-B-induced stomatal movements in Arabidopsis (Arabidopsis thaliana). Stornata in abaxial epidermal strips of Arabidopsis ecotype Landsberg erecta closed in response to increasing UV-B fluence rates, with maximal closure after 3-h exposure to 5.46 µmol m⁻² s⁻¹ UV-B. Both hydrogen peroxide (H₂O₂) and NO increased in response to UV-B, and stomatal closure was maintained by NO up to 24 h after the beginning of exposure. Stornata of plants expressing bacterial NO dioxygenase, which prevents NO accumulation, did not close in response to UV-B, although H₂O₂ still increased. When the uvr8-l null mutant was exposed to UV-B, stornata remained open, irrespective of the fluence rate. Neither NO nor H₂O₂ increased in stornata of the uvr8-1 mutant. However, the NO donor S-nitrosoglutathione induced closure of uvr8-1 stornata to the same extent as in the wild type. Experiments with mutants in UVR8 signaling components implicated CONSTITUTIVELY PHOTOMORPHOGENICl, HY5, and HY5 HOMOLOG in UV-B-induced stomatal closure. This research provides evidence that the UVR8 pathway regulates stomatal closure by a mechanism involving both H₂O₂ and NO generation in response to UV-B exposure.
The activation of phosphoinositide-specific phospholipase C (PI-PLC) is one of the earliest responses triggered by the recognition of several microbe-associated molecular patterns (MAMPs) in plants. ...The Arabidopsis (Arabidopsis thaliana) PI-PLC gene family is composed of nine members. Previous studies suggested a role for PLC2 in MAMP-triggered immunity, as it is rapidly phosphorylated in vivo upon treatment with the bacterial MAMP flg22. Here, we analyzed the role of PLC2 in plant immunity using an artificial microRNA to silence PLC2 expression in Arabidopsis. We found that PLC2-silenced plants are more susceptible to the type III secretion system-deficient bacterial strain Pseudomonas syringae pv tomato (Pst) DC3000 hrcC⁻ and to the nonadapted pea (Pisum sativum) powdery mildew Erysiphe pisi. However, PLC2-silenced plants display normal susceptibility to virulent (Pst DC3000) and avirulent (Pst DC3000 AvrRPM1) P. syringae strains, conserving typical hypersensitive response features. In response to flg22, PLC2-silenced plants maintain wild-type mitogen-activated protein kinase activation and PHI1, WRKY33, and FRK1 immune marker gene expression but have reduced reactive oxygen species (ROS)-dependent responses such as callose deposition and stomatal closure. Accordingly, the generation of ROS upon flg22 treatment is compromised in the PLC2-defficient plants, suggesting an effect of PLC2 in a branch of MAMP-triggered immunity and nonhost resistance that involves early ROS-regulated processes. Consistently, PLC2 associates with the NADPH oxidase RBOHD, suggesting its potential regulation by PLC2.
PDF
