Implementing a soil ammonium N fertilizer management for synchronizing potato N demands.

Potatoes, as a high-nitrogen (N)-demand crop, are strongly influenced by both the quantity and form of N supply. Previous studies have demonstrated that applying nitrate N prior to tuber formation and ammonium N post-tuber formation can substantially enhance potato yields and improve N fertilizer use efficiency. However, the ammonium N introduced into the soil undergoes nitrification, creating challenges in aligning the N supply form with the needs of potatoes. This study explored novel N regulation strategies aimed at augmenting potato yields and improving N fertilizer use efficiency. Two field experiments were conducted from 2020 to 2022. Experiment 1 involved four N gradients, namely no N, 150 kg N ha-1, 300 kg N ha-1, and 450 kg N ha-1. Soil samples were collected regularly to determine the transformation patterns of soil ammonium N during potato growth. Experiment 2 included three N management practices: farmer practice (Con), "nitrate followed by ammonium" with nitrification inhibitor (N-NI), and optimization (the soil ammonium N transformation-based split application of N fertilizer, Opt). The potato yield and N fertilizer use efficiency were compared to assess the performance of the optimized strategy. The results showed that 90 % of the ammonium N transformed 20 days after the basal dressing of N. When N fertilizer was applied as top dressing during the tuber formation and bulking stages, more than 90 % of ammonium N was transformed after 10 days. The optimized strategy resulted in a 20 % increase in potato yield, a 20 % increase in N fertilizer partial factor productivity, and a 12-20 % reduction in residual inorganic N in the 0-60 cm soil layer. This suggests that ammonium N applied as base fertilizer exhibits a relatively slow transformation rate, while applying ammonium N as top dressing during the tuber formation and bulking stages accelerates the transformation rate. The split application of ammonium N based on soil ammonium N transformation patterns can improve the alignment between the N supply form with the specific demands of potatoes.

Optimizing nutrient inputs by balancing spring wheat yield and environmental effects in the Hetao Irrigation District of China.

The Hetao Irrigation District is the primary spring wheat production region in China. However, overuse and unscientific use of chemical fertilizer have resulted in low nutrient use efficiency and potential risks to the environment. Balanced fertilization (BF), a 29.9-36.4% N fertilizer and 40% P fertilizer, was reduced, while a 72 kg K2O ha-1 K fertilizer was supplied and designed to resolve problems encountered during the field trial from 2019 to 2021. The results showed that the grain yield did not decrease significantly in the BF treatments compared in the local farmer practice (FP) treatment. The nitrogen fertilizer partial productivity (PFPN) and agronomic nitrogen efficiency (NAEN) increased 42.95-52.88% and 44.06-49.24% with BF compared to with the FP, respectively. Moreover, the BF treatments reduced nitrate leaching in the 0-100 cm soil layer and reduced the N surplus (Nsur) to approximately 160 kg N per hectare per year, dramatically reducing the environmental risk. The yield maintenance and nitrogen use efficiency increases were attributed to the lower nitrogen concentrations in the seedlings and the higher apparent N translocation efficiency (TR) from the stems and sheaths after anthesis in the BF treatments than in the FP treatments. Considering the yield, nutrient use efficiency, and environmental and economic benefits comprehensively, the BF1 treatment was considered the optimal fertilization scheme for Hetao spring wheat production.

Potato tuber degradation is regulated by carbohydrate metabolism: Results of transcriptomic analysis.

Tuber number is an essential factor determining yield and commodity in potato production. The initiation number has long been considered the sole determinant of the final total tuber number. In this study, we observed that tuber numbers at harvest were lower than at the tuber bulking stage; some formed tubers that were smaller than 3 cm degraded during development. Carbohydrate metabolism plays a crucial role in tuber degradation by coordinating the source-sink relationship. The contents of starch and sucrose, and the C:N ratio, are dramatically reduced in degradating tubers. Transcriptomic study showed that "carbohydrate metabolic processes" are Gene Ontology (GO) terms associated with tuber degradation. A polysaccharide degradation-related gene, LOC102601831, and a sugar transport gene, LOC102587850 (SWEET6a), are dramatically up-regulated in degradating tubers according to transcriptomic analysis, as validated by qRT-PCT. The terms "peptidase inhibitor activity" and "hydrolase activity" refer to the changes in molecular functions that degradating tubers exhibit. Nitrogen supplementation during potato development alleviates tuber degradation to a certain degree. This study provides novel insight into potato tuber development and possible management strategies for improving potato cultivation.

Death-Domain-Receptor 3 Deletion Normalizes Inflammatory Gene Expression and Prevents Ileitis in Experimental Crohn's Disease.

Background: TNF-like cytokine 1A (TL1A) and its functional receptor, death-domain-receptor-3 (DR3), are multifunctional mediators of effector and regulatory immunity. We aimed to evaluate the functional role and therapeutic potential of TL1A/DR3 signaling in Crohn's disease-like ileitis. Methods: Ileitis-prone SAMP1/YitFc (SAMP) and TNFΔARE/+ mice were rendered deficient for DR3 or TL1A by microsatellite marker-assisted backcrossing. Pathological and immunological characteristics were compared between control and knockout mice, and mucosal immunophenotype was analyzed by Nanostring microarray assay. The therapeutic effect of pharmacological TL1A neutralization was also investigated. Results: DR3 deficiency was associated with restoration of a homeostatic mucosal immunostat in SAMP mice through the regulation of several pro- and anti-inflammatory genes. This led to suppression of effector immunity, amelioration of ileitis severity, and compromised ability of either unfractionated CD4+ or CD4+CD45RBhi mucosal lymphocytes to transfer ileitis to severe combined immunodeficient mice recipients. TNF-driven ileitis was also prevented in TNFΔARE/+xDR3-/- mice, in association with decreased expression of the pro-inflammatory cytokines TNF and IFN-γ. In contrast to DR3, TL1A was dispensable for the development of ileitis although it affected the kinetics of inflammation, as TNFΔARE/+xTL1A-/- demonstrated delayed onset of inflammation, whereas administration of a neutralizing, anti-TL1A antibody ameliorated early but not late TNFΔARE/+ ileitis. Conclusion: We found a prominent pro-inflammatory role of DR3 in chronic ileitis, which is only partially mediated via interaction with TL1A, raising the possibility for additional DR3 ligands. Death-domain-receptor-3 appears to be a master regulator of mucosal homeostasis and inflammation and may represent a candidate therapeutic target for chronic inflammatory conditions of the bowel.

Death Receptor 3 Signaling Controls the Balance between Regulatory and Effector Lymphocytes in SAMP1/YitFc Mice with Crohn's Disease-Like Ileitis.

Death receptor 3 (DR3), a member of the tumor necrosis factor receptor (TNFR) superfamily, has been implicated in regulating T-helper type-1 (TH1), type-2 (TH2), and type-17 (TH17) responses as well as regulatory T cell (Treg) and innate lymphoid cell (ILC) functions during immune-mediated diseases. However, the role of DR3 in controlling lymphocyte functions in inflammatory bowel disease (IBD) is not fully understood. Recent studies have shown that activation of DR3 signaling modulates Treg expansion suggesting that stimulation of DR3 represents a potential therapeutic target in human inflammatory diseases, including Crohn's disease (CD). In this study, we tested a specific DR3 agonistic antibody (4C12) in SAMP1/YitFc (SAMP) mice with CD-like ileitis. Interestingly, treatment with 4C12 prior to disease manifestation markedly worsened the severity of ileitis in SAMP mice despite an increase in FoxP3+ lymphocytes in mesenteric lymph node (MLN) and small-intestinal lamina propria (LP) cells. Disease exacerbation was dominated by overproduction of both TH1 and TH2 cytokines and associated with expansion of dysfunctional CD25-FoxP3+ and ILC group 1 (ILC1) cells. These effects were accompanied by a reduction in CD25+FoxP3+ and ILC group 3 (ILC3) cells. By comparison, genetic deletion of DR3 effectively reversed the inflammatory phenotype in SAMP mice by promoting the expansion of CD25+FoxP3+ over CD25-FoxP3+ cells and the production of IL-10 protein. Collectively, our data demonstrate that DR3 signaling modulates a multicellular network, encompassing Tregs, T effectors, and ILCs, governing disease development and progression in SAMP mice with CD-like ileitis. Manipulating DR3 signaling toward the restoration of the balance between protective and inflammatory lymphocytes may represent a novel and targeted therapeutic modality for patients with CD.

Chemical signals and their regulations on the plant growth and water use efficiency of cotton seedlings under partial root-zone drying and different nitrogen applications.

Partial root-zone drying during irrigation (PRD) has been shown effective in enhancing plant water use efficiency (WUE), however, the roles of chemical signals from root and shoot that are involved and the possible interactions affected by nitrogen nutrition are not clear. Pot-grown cotton (Gossypium spp.) seedlings were treated with three levels of N fertilization and PRD. The concentrations of nitrate (NO3-), abscisic acid (ABA) and the pH value of leaf and root xylem saps, biomass and WUE were measured. Results showed that PRD plants produced larger biomass and higher WUE than non-PRD plants, with significant changes in leaf xylem ABA, leaf and root xylem NO3- concentrations and pH values, under heterogeneous soil moisture conditions. Simultaneously, high-N treated plants displayed larger changes in leaf xylem ABA and higher root xylem NO3- concentrations, than in the medium- or low-N treated plants. However, the WUE of plants in the low-N treatment was higher than that of those in the high- and medium-N treatments. PRD and nitrogen levels respectively induced signaling responses of ABA/NO3- and pH in leaf or root xylem to affect WUE and biomass under different watering levels, although significant interactions of PRD and nitrogen levels were found when these signal molecules responded to soil drying. We conclude that these signaling chemicals are regulated by interaction of PRD and nitrogen status to regulate stomatal behavior, either directly or indirectly, and thus increase PRD plant WUE under less irrigation.

Epithelial-specific Toll-like Receptor (TLR)5 Activation Mediates Barrier Dysfunction in Experimental Ileitis.

BACKGROUND: A large body of evidence supports a central role of TLR5 and its natural ligand, flagellin, in Crohn's disease (CD), with the precise mechanism(s) still unresolved. METHODS: We investigated the role of flagellin/TLR5 in SAMP1/YitFc (SAMP) mice, a spontaneous model of Crohn's disease-like ileitis. RESULTS: Ileal Tlr5 and serum antiflagellin IgG antibodies were increased in SAMP before the onset of inflammation and during established disease; these trends were abrogated in the absence of colonizing commensal bacteria. Irradiated SAMP receiving either wild-type (AKR) or SAMP bone marrow (BM) developed severe ileitis and displayed increased ileal Tlr5 compared with AKR recipients of either SAMP or AKR bone marrow, neither of which conferred ileitis, suggesting that elevated TLR5 in native SAMP is derived primarily from a nonhematopoietic (e.g., epithelial) source. Indeed, ileal epithelial TLR5 in preinflamed SAMP was increased compared with age-matched AKR and germ-free SAMP. TLR5-specific ex vivo activation of SAMP ileal tissues decreased epithelial barrier resistance, indicative of increased permeability, and was accompanied by altered expression of the tight junction proteins, claudin-3, occludin, and zonula occludens-1. CONCLUSIONS: Our results provide evidence that aberrant, elevated TLR5 expression is present in the ileal epithelium of SAMP mice, is augmented in the presence of the gut microbiome, and that TLR5 activation in response to bacterial flagellin results in a deficiency to maintain appropriate epithelial barrier integrity. Together, these findings represent a potential mechanistic pathway leading to the exacerbation and perpetuation of chronic gut inflammation in experimental ileitis and possibly, in patients with Crohn's disease.

A Novel Role for TL1A/DR3 in Protection against Intestinal Injury and Infection.

TNF-like cytokine 1A (TL1A) is expressed on APCs and provides costimulatory signals to activated lymphocytes that bear its functional receptor, death receptor 3 (DR3). TL1A/DR3 signaling is involved in the pathogenesis of human and experimental inflammatory bowel disease. In the current study, we investigated the role of this cytokine/receptor pair in acute intestinal injury/repair pathways. We demonstrate that intact DR3 signaling protected mice from acute dextran sodium sulfate colitis because DR3(-/-) mice showed more severe mucosal inflammation and increased mortality. DR3(-/-) mice were compromised in their ability to maintain adequate numbers of CD4(+)CD25(+)Foxp3(+) regulatory T cells in response to acute mucosal damage. This defect in immune regulation led to a nonspecific upregulation of effector proinflammatory pathways, which was most prominent for the Th17 immunophenotype. TL1A(-/-) mice were similarly more susceptible to dextran sodium sulfate colitis, although without mortality and with delayed kinetics compared with DR3(-/-) mice, and also displayed significantly reduced numbers of regulatory T cells. Infection of DR3(-/-) mice with Salmonella typhimurium was associated with defective microbial clearance and elevated bacterial load. Taken together, our findings indicate a novel protective role for the TL1A/DR3 axis in the regulation of mucosal homeostasis during acute intestinal injury/repair, which contrasts with its known pathogenic function during chronic intestinal inflammation.

AtDsPTP1 acts as a negative regulator in osmotic stress signalling during Arabidopsis seed germination and seedling establishment.

Dual-specificity protein phosphatases (DsPTPs) target both tyrosine and serine/threonine residues and play roles in plant growth and development. We have characterized an Arabidopsis mutant, dsptp1, which shows a higher seed germination rate and better root elongation under osmotic stress than the wild type. By contrast, its overexpression line, DsPTP1-OE, shows inhibited seed germination and root elongation; and its complemented line, DsPTP1-Com, resembles the wild type and rescues DsPTP1-OE under osmotic stress. Expression of AtDsPTP1 is enhanced by osmotic stress in seed coats, bases of rosette leaves, and roots. Compared with the wild type, the dsptp1 mutant shows increased proline accumulation, reduced malondialdehyde (MDA) content and ion leakage, and enhanced antioxidant enzyme activity in response to osmotic stress. AtDsPTP1 regulates the transcript levels of various dehydration-responsive genes under osmotic stress. Abscisic acid (ABA) accumulation in dsptp1 under osmotic stress is reduced with reduced expression of the ABA-biosynthesis gene NCED3 and increased expression of the ABA-catabolism gene CYP707A4. AtDsPTP1 also regulates the expression of key components in the ABA-signalling pathway. In conclusion, AtDsPTP1 regulates ABA accumulation, and acts as a negative regulator in osmotic stress signalling during Arabidospsis seed germination and seedling establishment.

The tumor necrosis factor-like cytokine 1A/death receptor 3 cytokine system in intestinal inflammation.

PURPOSE OF REVIEW: Tumor necrosis factor (TNF)-like cytokine 1A (TL1A) associates with the death receptor 3 (DR3) on activated lymphocytes and induces proinflammatory signals. The decoy receptor 3 (DcR3) competes for TL1A binding and inhibits functional signaling. This review focuses on the role of the TL1A/DR3/DcR3 cytokine system in inflammatory bowel diseases (IBDs). RECENT FINDINGS: TL1A may induce IFN-γ-mediated and IL-17-mediated proinflammatory pathways in IBDs by acting on DR3-expressing, CD4(+)CD161(+) lymphocytes, which are substantially enriched at the inflamed intestinal mucosa. In addition, TL1A/DR3 signaling results in expansion of the Treg pool with concomitant and transient inhibition of their suppressive function. Constitutive expression of TL1A in transgenic mice was associated with small intestinal inflammation, which was accompanied by colonic fibrosis both spontaneously and under colitogenic conditions. Recent human studies demonstrated that soluble TL1A and DcR3 are present in the systemic circulation in patients with active IBD and decline after successful anti-inflammatory treatment. SUMMARY: TL1A/DR3 interactions may participate in the pathogenesis of chronic intestinal inflammation and offer novel therapeutic targets for patients with ulcerative colitis and Crohn's disease.

The Tomato 14-3-3 protein TFT4 modulates H+ efflux, basipetal auxin transport, and the PKS5-J3 pathway in the root growth response to alkaline stress.

Alkaline stress is a common environmental stress, in particular in salinized soils. Plant roots respond to a variety of soil stresses by regulating their growth, but the nature of the regulatory pathways engaged in the alkaline stress response (ASR) is not yet understood. Previous studies show that PIN-FORMED2, an auxin (indole-3-acetic acid [IAA]) efflux transporter, PKS5, a protein kinase, and DNAJ HOMOLOG3 (J3), a chaperone, play key roles in root H(+) secretion by regulating plasma membrane (PM) H(+)-ATPases directly or by targeting 14-3-3 proteins. Here, we investigated the expression of all 14-3-3 gene family members (TOMATO 14-3-3 PROTEIN1 [TFT1]-TFT12) in tomato (Solanum lycopersicum) under ASR, showing the involvement of four of them, TFT1, TFT4, TFT6, and TFT7. When these genes were separately introduced into Arabidopsis (Arabidopsis thaliana) and overexpressed, only the growth of TFT4 overexpressors was significantly enhanced when compared with the wild type under stress. H(+) efflux and the activity of PM H(+)-ATPase were significantly enhanced in the root tips of TFT4 overexpressors. Microarray analysis and pharmacological examination of the overexpressor and mutant plants revealed that overexpression of TFT4 maintains primary root elongation by modulating PM H(+)-ATPase-mediated H(+) efflux and basipetal IAA transport in root tips under alkaline stress. TFT4 further plays important roles in the PKS5-J3 signaling pathway. Our study demonstrates that TFT4 acts as a regulator in the integration of H(+) efflux, basipetal IAA transport, and the PKS5-J3 pathway in the ASR of roots and coordinates root apex responses to alkaline stress for the maintenance of primary root elongation.

Class III peroxidases are activated in proanthocyanidin-deficient Arabidopsis thaliana seeds.

BACKGROUND AND AIMS: It has previously been shown that proanthocyanidins (PAs) in the seed coat of Arabidopsis thaliana have the ability to scavenge superoxide radicals (O2(-)). However, the physiological processess in PA-deficit seeds are not clear. It is hypothesized that there exist alternative ways in PA-deficient seeds to cope with oxidative stress. METHODS: The content of hydrogen peroxide (H2O2) and its relevance to the activities of superoxide dismutase (SOD), catalase (CAT) and peroxidases was investigated in both wild-type and PA-deficit mutant seeds. A biochemical staining approach was used to detect tissue localizations of peroxidase activities in PA-deficit mutant seeds. KEY RESULTS: PA-deficient mutants possess significantly lower levels of H2O2 than the wild-type, despite their higher accumulation of superoxide radicals. Screening of the key antioxidant enzymes revealed that peroxidase activity was significantly over-activated in mutant seeds. This high peroxidase activity was mainly confined to the seed coat zone. Interestingly, neither ascorbate peroxidase nor glutathione peroxidase, just the guaiacol peroxidases (class III peroxidases), was specifically activated in the seed coat. However, no significant difference in peroxidase activity was observed in embryos of either mutants or the wild-type, although gene expressions of several candidate peroxidases were down-regulated in the embryos of PA-deficient seeds. CONCLUSIONS: The results suggest that enhanced class III peroxidase activity in the seed coat of PA-deficient mutants is an adaptive strategy for seed development and survival.

Abscisic acid accumulation modulates auxin transport in the root tip to enhance proton secretion for maintaining root growth under moderate water stress.

Maintenance of root growth is essential for plant adaptation to soil drying. Here, we tested the hypothesis that auxin transport is involved in mediating ABA's modulation by activating proton secretion in the root tip to maintain root growth under moderate water stress. Rice and Arabidopsis plants were raised under a hydroponic system and subjected to moderate water stress (-0.47 MPa) with polyethylene glycol (PEG). ABA accumulation, auxin transport and plasma membrane H(+)-ATPase activity at the root tip were monitored in addition to the primary root elongation and root hair density. We found that moderate water stress increases ABA accumulation and auxin transport in the root apex. Additionally, ABA modulation is involved in the regulation of auxin transport in the root tip. The transported auxin activates the plasma membrane H(+)-ATPase to release more protons along the root tip in its adaption to moderate water stress. The proton secretion in the root tip is essential in maintaining or promoting primary root elongation and root hair development under moderate water stress. These results suggest that ABA accumulation modulates auxin transport in the root tip, which enhances proton secretion for maintaining root growth under moderate water stress.

PIN2 is required for the adaptation of Arabidopsis roots to alkaline stress by modulating proton secretion.

Soil alkalinity is a widespread environmental problem that limits agricultural productivity. The hypothesis that an auxin-regulated proton secretion by plasma membrane H(+)-ATPase plays an important role in root adaption to alkaline stress was studied. It was found that alkaline stress increased auxin transport and PIN2 (an auxin efflux transporter) abundance in the root tip of wild-type Arabidopsis plants (WT). Compared with WT roots, the pin2 mutant roots exhibited much reduced plasma membrane H(+)-ATPase activity, root elongation, auxin transport, and proton secretion under alkaline stress. More importantly, roots of the pks5 mutant (PKS5, a protein kinase) lacking PIN2 (a pks5/pin2 double mutant) lost the previous higher proton-secretion capacity and higher elongation rate of primary roots under alkaline stress. By using Arabidopsis natural accessions with a high proton-secretion capacity, it was found that their PIN2 transcription abundance is positively related to the elongation rate of the primary root and proton-secretion capacity under alkaline stress. Taken together, our results confirm that PIN2 is involved in the PKS5-mediated signalling cascade under alkaline-stress and suggest that PIN2 is required for the adaptation of roots to alkaline stress by modulating proton secretion in the root tip to maintain primary root elongation.

Smart role of plant 14-3-3 proteins in response to phosphate deficiency.

Higher plants adapt to phosphorus deficiency through a complex of biological processes. Among of them, two adaptive processes are very important for the response of higher plants to phosphorus deficiency. One is the enhancement of root growth by regulating carbohydrate metabolism and allocation, and the other is rhizosphere acidification to acquire phosphorus efficiently from soil. TFT6 and TFT7, two different members of tomato 14-3-3 gene family, play the distinct roles in the adaption of plants to phosphorus deficiency by taking part in the two processes respectively. TFT6 which acts mainly in leaves is involved in the systemic response to phosphorus deficiency by regulating leaf carbon allocation and increasing phloem sucrose transport to promote root growth, while TFT7 directly functions in root by activating root plasma membrane H (+) -ATPase to release more protons under phosphorus deficiency. Based on these results, we propose that 14-3-3 proteins play the smart role in response to phosphorus deficiency in higher plants.

Proanthocyanidins inhibit seed germination by maintaining a high level of abscisic acid in Arabidopsis thaliana.

Proanthocyanidins (PAs) are the main products of the flavonoid biosynthetic pathway in seeds, but their biological function during seed germination is still unclear. We observed that seed germination is delayed with the increase of exogenous PA concentration in Arabidopsis. A similar inhibitory effect occurred in peeled Brassica napus seeds, which was observed by measuring radicle elongation. Using abscisic acid (ABA), a biosynthetic and metabolic inhibitor, and gene expression analysis by real-time polymerase chain reaction, we found that the inhibitory effect of PAs on seed germination is due to their promotion of ABA via de novo biogenesis, rather than by any inhibition of its degradation. Consistent with the relationship between PA content and ABA accumulation in seeds, PA-deficient mutants maintain a lower level of ABA compared with wild-types during germination. Our data suggest that PA distribution in the seed coat can act as a doorkeeper to seed germination. PA regulation of seed germination is mediated by the ABA signaling pathway.

TFT6 and TFT7, two different members of tomato 14-3-3 gene family, play distinct roles in plant adaption to low phosphorus stress.

14-3-3 proteins are a large family of proteins but exact roles of their members in plant response to abiotic stresses are not clear, especially under nutrient deficiency. We investigated the expressions of all the tomato 14-3-3 gene family members (TFT1-TFT12) under low phosphorus stress (LP) and found that TFT6 belongs to the later responsive gene while TFT7 belongs to the early responsive gene. When the two genes were separately introduced into Arabidopsis and overexpressed, their plant growth under LP was much enhanced compared with wild-type plant. TFT6 overexpressing plants showed reduced starch synthase activity, reduced starch content but enhanced sucrose loading into phloem in the shoot under LP. TFT7 overexpressing plants had much enhanced H⁺ flux along their root tip and activity of plasma membrane H⁺-ATPase in the roots under LP. Our results suggest that TFT6 and TFT7 play different roles in plant adaption to LP. TFT6 acts mainly in leaves and is involved in the systemic response to LP by regulating leaf carbon allocation and increasing phloem sucrose transport to promote root growth, while TFT7 directly functions in root by activating root plasma membrane H⁺-ATPase to release more protons under LP.

Modulation of anti-oxidation ability by proanthocyanidins during germination of Arabidopsis thaliana seeds.

Proanthocyanidins (PAs) as the end products of flavonoid biosynthetic pathway mainly accumulate in seed coat but their biological function is largely unknown. We studied the anti-oxidation ability in seed coat and germination changes under externally applied oxidative stresses in PAs-deficient mutants of Arabidopsis. Germination of PAs-deficient mutant seeds was faster than that of wild-type under low or no oxidative stress, suggesting a PAs-induced inhibition of germination. When the applied oxidative stress was high, germination of PAs-deficient mutants was lower than that of wild-type, suggesting a loss of PAs-related anti-oxidation ability in the mutants. Using ABA signaling mutants, our studies demonstrated that both ABA signaling pathway and PAs were important for the response to serve oxidative stress during seed germination. However, the discrepancy of the response between abi mutants and PAs mutants to oxidative stress suggests that ABA signaling pathway may not play a major role in PAs' action in alleviating oxidative stress. Under low or no oxidative stress, germination was mainly determined by the ABA content in seed and the PAs-deficient mutant seeds germinated faster due to their lower ABA content than wild-type. However, oxidative injury inhibited germination when PAs-deficient seeds germinated under high oxidative stress. Wild-type exhibited higher germination under the high oxidative stress due to the PAs' anti-oxidation ability. Oxidative stress applied externally led to changes in endogenous PAs contents that coincided with the expression changes of PAs biogenesis genes. PAs modulated the activities of some key enzymes that controlled the levels of reactive oxygen species and the anti-oxidation capacity during the seed germination. This work suggests that PAs contribute to the adaptive mechanism that helps germination under environmental stresses by playing dual roles in both germination control and anti-oxidation reaction.

ABA signal in rice under stress conditions.

Ever since its discovery, abscisic acid (ABA) has been intensively studied due to its versatile functions in plant developmental and physiological processes. Many signaling details of ABA have been well elucidated and reviewed. The identification of ABA receptors is a great breakthrough in the field of ABA study, whereas the discovery of ABA transporter has changed our concept that ABA is delivered solely by passive transport. The intensity of ABA signaling pathway is well known to be controlled by multi-regulators. Nonetheless, the interaction and coordination among ABA biosynthesis, catabolism, conjugation and transportation are seldom discussed. Here, we summarize the biological functions of ABA in response to different stresses, especially the roles of ABA in plant defense to pathogen attack, and discuss the possible relationships of these determinants in controlling the specificity and intensity of ABA signaling pathway in the rice.

Ascorbic acid and reactive oxygen species are involved in the inhibition of seed germination by abscisic acid in rice seeds.

The antagonism between abscisic acid (ABA) and gibberellin (GA) plays a key role in controlling seed germination, but the mechanism of antagonism during this process is not known. The possible links among ABA, reactive oxygen species (ROS), ascorbic acid (ASC), and GA during rice seed germination were investigated. Unlike in non-seed tissues where ROS production is increased by ABA, ABA reduced ROS production in imbibed rice seeds, especially in the embryo region. Such reduced ROS also led to an inhibition of ASC production. GA accumulation was also suppressed by a reduced ROS and ASC level, which was indicated by the inhibited expression of GA biosynthesis genes, amylase genes, and enzyme activity. Application of exogenous ASC can partially rescue seed germination from ABA treatment. Production of ASC, which acts as a substrate in GA biosynthesis, was significantly inhibited by lycorine which thus suppressed the accumulation of GA. Consequently, expression of GA biosynthesis genes was suppressed by the low levels of ROS and ASC in ABA-treated seeds. It can be concluded that ABA regulates seed germination in multiple dimensions. ROS and ASC are involved in its inhibition of GA biosynthesis.