A NAC transcription factor represses a module associated with xyloglucan content and regulates aluminum tolerance.

The transcriptional regulation of aluminum (Al) tolerance in plants is largely unknown, although Al toxicity restricts agricultural yields in acidic soils. Here, we identified a NAM, ATAF1/2, and cup-shaped cotyledon 2 (NAC) transcription factor that participates in Al tolerance in Arabidopsis (Arabidopsis thaliana). Al substantially induced the transcript and protein levels of ANAC070, and loss-of-function mutants showed remarkably increased Al sensitivity, implying a beneficial role of ANAC070 in plant tolerance to Al toxicity. Further investigation revealed that more Al accumulated in the roots of anac070 mutants, especially in root cell walls, accompanied by a higher hemicellulose and xyloglucan level, implying a possible interaction between ANAC070 and genes that encode proteins responsible for the modification of xyloglucan, including xyloglucan endo-transglycosylase/hydrolase (XTH) or ANAC017. Yeast 1-hybrid analysis revealed a potential interaction between ANAC070 and ANAC017, but not for other XTHs. Furthermore, dual-luciferase reporter assay, RT-qPCR, and GUS analysis revealed that ANAC070 could directly repress the transcript levels of ANAC017, and knockout of ANAC017 in the anac070 mutant partially restored its Al sensitivity phenotype, indicating that ANAC070 contributes to Al tolerance mechanisms other than suppression of ANAC017 expression. Further analysis revealed that the core transcription factor SENSITIVE TO PROTON RHIZOTOXICITY 1 (STOP1) and its target genes, which control Al tolerance in Arabidopsis, may also be involved in ANAC070-regulated Al tolerance. In summary, we identified a transcription factor, ANAC070, that represses the ANAC017-XTH31 module to regulate Al tolerance in Arabidopsis.

Auxin acts upstream of nitric oxide to regulate cell wall xyloglucan and its aluminium-binding capacity in Arabidopsis thaliana.

MAIN CONCLUSION: Auxin acts upstream of NO through NOA and XXT5 pathways to regulate the binding capacity of the root cell wall to Al. In our previous study, we identified an unknown mechanism by which 1-naphthaleneacetic acid (NAA) decreased the fixation of aluminum (Al) in the cell wall. Here, we observed that external application of the nitric oxide (NO) donor S-nitrosoglutathion (GSNO) increased the inhibition of Al on root elongation. Further analysis indicated that GSNO could induce Al accumulation in the roots and root cell walls, which is consistent with lower xyloglucan content. In comparison to the Columbia-0 (Col-0) wild type (WT), endogenous NO-reduced mutants noa1 (NOA pathway) and nia1nia2 (NR pathway) were more resistant to Al, with lower root Al content, higher xyloglucan content, and more Al accumulation in the root cell walls. By contrast, the xxt5 mutant with reduced xyloglucan content exhibited an Al-sensitive phenotype. Interestingly, Al treatment increased the endogenous auxin and NO levels, and the auxin levels induced under Al stress further stimulated NO production. Auxin application reduced Al retention in hemicellulose and decreased the xyloglucan content, similar to the effects observed with GSNO. In yucca and aux1-7 mutants, exogenous application of NO resulted in responses similar to those of the WT, whereas exogenous auxin had little effect on the noa1 mutant under Al stress. In addition, as auxin had similar effects on the nia1nia2 mutant and the WT, exogenous auxin and NO had little effect on the xxt5 mutant under Al stress, further confirming that auxin acts upstream of NO through NOA and XXT5 pathways to regulate the binding capacity of the root cell wall to Al.

Melatonin Increases Root Cell Wall Phosphorus Reutilization via an NO Dependent Pathway in Rice (Oryza sativa).

Melatonin (MT) has been implicated in the plant response to phosphorus (P) stress; however, the precise molecular mechanisms involved remain unclear. This study investigated whether MT controls internal P distribution and root cell wall P remobilization in rice. Rice was treated with varying MT and P levels and analyzed using biochemical and molecular techniques to study phosphorus utilization. The results demonstrated that low P levels lead to a rapid increase in endogenous MT levels in rice roots. Furthermore, the exogenous application of MT significantly improved rice tolerance to P deficiency, as evidenced by the increased biomass and reduced proportion of roots to shoots under P-deficient conditions. MT application also mitigated the decrease in P content regardless in both the roots and shoots. Mechanistically, MT accelerated the reutilization of P, particularly in the root pectin fraction, leading to increased soluble P liberation. In addition, MT enhanced the expression of OsPT8, a gene involved in root-to-shoot P translocation. Furthermore, we observed that MT induced the production of nitric oxide (NO) in P-deficient rice roots and that the mitigating effect of MT on P deficiency was compromised in the presence of the NO inhibitor, c-PTIO, implying that NO is involved in the MT-facilitated mitigation of P deficiency in rice. Overall, our findings highlight the potential of MT as a promising strategy for enhancing rice tolerance to P deficiency and improving P use efficiency in agricultural practices.

Improve disaster literacy in nurses: a qualitative descriptive study.

BACKGROUND: The enhancement of nurses' disaster literacy is crucial for effective disaster emergency management, especially for clinical nurses with no prior experience in disaster rescue. This study aims to explore the perspectives of nurses who have been involved in disaster rescue operations on strategies to advance nurses' disaster literacy. METHODS: A qualitative descriptive study, which follows unified qualitative study reporting guidelines. Thirty disaster rescue nurses were recruited to participate in this study, who came from 30 third-class hospitals in China. From October to December 2021, information was acquired by conducting semi-structured telephone interviews with participants. Qualitative content analysis was used to examine the data. RESULTS: Six categories and eleven subcategories were created. Strengthening disaster education and training was the main focus, and its subcategories included continuing education, nursing curriculum development, and disaster rescue experience guide. The second focus, which included scene simulation, actual combat/military simulation, and virtual reality simulation, was strengthening disaster simulation and drill. The third focus was on providing psychosocial support, which included improving self-psychological adjustment, developing resilience, and engaging in active coping. The fourth category was to strengthen nurse/hospital managers roles and leadership, which included enhancing professional identity and policies/leadership support. The fifth category was disaster preparedness, and the sixth was enhancing knowledge transformation. CONCLUSIONS: Government agencies or healthcare organizations should actively promote the formation of nurses' disaster literacy from multiple viewpoints. Disaster education and training, simulation exercises, and psychosocial support should be prioritized.

The MYB transcription factor MYB103 acts upstream of TRICHOME BIREFRINGENCE-LIKE27 in regulating aluminum sensitivity by modulating the O-acetylation level of cell wall xyloglucan in Arabidopsis thaliana.

Modification of the O-acetylation level of xyloglucan (XyG) appears to affect aluminum (Al) sensitivity in Arabidopsis by modulating its binding capacity to Al. However, the transcriptional regulation of this process remains largely unknown. In our previous studies, we found that the expression of TRICHOME BIREFRINGENCE-LIKE27 (TBL27), which is responsible for the O-acetylation of XyG, was downregulated under Al stress. In the present study, we showed that the expression of an R2R3-type transcription factor-encoding gene, MYB103, was also inhibited by Al exposure and exhibited a co-expression pattern with TBL27 in roots and siliques, suggesting a potential link between MYB103 and TBL27. The loss of function of MYB103 resulted in increased Al sensitivity, as indicated by more inhibited root growth and elevated root Al content compared with the wild type. Moreover, we also detected increased Al accumulation in the root cell wall and the hemicellulose fraction, which was attributed to the changes in the O-acetylation level of XyG rather than the XyG content itself. In addition, further analysis revealed that MYB103 positively activated TBL27 expression by directly binding to the TBL27 promoter region, and TBL27 overexpression in the myb103 mutant rescued the Al-sensitive phenotype of the mutant to the wild-type level. Taken together, we conclude that MYB103 acts upstream of TBL27 to positively regulate Al resistance by modulating the O-acetylation of the cell wall XyG.

The NAC transcription factor ANAC017 regulates aluminum tolerance by regulating the cell wall-modifying genes.

Aluminum (Al) toxicity is one of the key factors limiting crop production in acid soils; however, little is known about its transcriptional regulation in plants. In this study, we characterized the role of a NAM, ATAF1/2, and cup-shaped cotyledon 2 (NAC) transcription factors (TFs), ANAC017, in the regulation of Al tolerance in Arabidopsis (Arabidopsis thaliana). ANAC017 was localized in the nucleus and exhibited constitutive expression in the root, stem, leaf, flower, and silique, although its expression and protein accumulation were repressed by Al stress. Loss of function of ANAC017 enhanced Al tolerance when compared with wild-type Col-0 and was accompanied by lower root and root cell wall Al content. Furthermore, both hemicellulose and xyloglucan content decreased in the anac017 mutants, indicating the possible interaction between ANAC017 and xyloglucan endotransglucosylase/hydrolase (XTH). Interestingly, the expression of XTH31, which is responsible for xyloglucan modification, was downregulated in the anac017 mutants regardless of Al supply, supporting the possible interaction between ANAC017 and XTH31. Yeast one-hybrid, dual-luciferase reporter assay, and chromatin immunoprecipitation-quantitative PCR analysis revealed that ANAC017 positively regulated the expression of XTH31 through directly binding to the XTH31 promoter region, and overexpression of XTH31 in the anac017 mutant background rescued its Al-tolerance phenotype. In conclusion, we identified that the tTF ANAC017 acts upstream of XTH31 to regulate Al tolerance in Arabidopsis.

The endo-beta mannase MAN7 contributes to cadmium tolerance by modulating root cell wall binding capacity in Arabidopsis thaliana.

The heavy metal cadmium (Cd) is detrimental to crop growth and threatens human health through the food chain. To cope with Cd toxicity, plants employ multiple strategies to decrease Cd uptake and its root-to-shoot translocation. However, genes that participate in the Cd-induced transcriptional regulatory network, including those encoding transcription factors, remain largely unidentified. In this study, we demonstrate that ENDO-BETA-MANNASE 7 (MAN7) is necessary for the response of Arabidopsis thaliana to toxic Cd levels. We show that MAN7 is responsible for mannase activity and modulates mannose content in the cell wall, which plays a role in Cd compartmentalization in the cell wall under Cd toxicity conditions. Additionally, the repression of root growth by Cd was partially reversed via exogenous application of mannose, suggesting that MAN7-mediated cell wall Cd redistribution depends on the mannose pathway. Notably, we identified a basic leucine zipper (bZIP) transcription factor, bZIP44, that acts upstream of MAN7 in response to Cd toxicity. Transient dual-luciferase assays indicated that bZIP44 directly binds to the MAN7 promoter region and activates its transcription. Loss of bZIP44 function was associated with greater sensitivity to Cd treatment and higher accumulation of the heavy metal in roots and shoots. Moreover, MAN7 overexpression relieved the inhibition of root elongation seen in the bzip44 mutant under Cd toxicity conditions. This study thus reveals a pathway showing that MAN7-associated Cd tolerance in Arabidopsis is controlled by bZIP44 upon Cd exposure.

Jasmonic acid is involved in root cell wall phosphorus remobilization through the nitric oxide dependent pathway in rice.

Jasmonic acid (JA) is involved in phosphorus (P) stress in plants, but its underlying molecular mechanisms are still elusive. In this study, we found root endogenous JA content in rice increased under P deficiency (-P), suggesting that JA might participate in P homeostasis in plants. This hypothesis was further confirmed through the addition of exogenous JA (+JA), as this could increase both the root and shoot soluble P content through regulating root cell wall P reutilization. In addition, -P+JA treatment significantly induced the expression of P transporter gene OsPT2, together with increased xylem P content, implying that JA is also important for P translocation from the root to the shoot in P-deficient rice. Furthermore, the accumulation of the molecular signal nitric oxide (NO) was enhanced under -P+JA treatment when compared with -P treatment alone, while the addition of c-PTIO, a scavenger of NO, could reverse the P-deficient phenotype alleviated by JA. Taken together, our results reveal a JA-NO-cell wall P reutilization pathway under P deficiency in rice.

Research of the Algebraic Multigrid Method for Electron Optical Simulator.

At present, electron optical simulator (EOS) takes a long time to solve linear FEM systems. The algebraic multigrid preconditioned conjugate gradient (AMGPCG) method can improve the efficiency of solving systems. This paper is focused on the implementation of the AMGPCG method in EOS. The aggregation-based scheme, which uses two passes of a pairwise matching algorithm and the K-cyle scheme, is adopted in the aggregation-based algebraic multigrid method. Numerical experiments show the advantages and disadvantages of the AMG algorithm in peak memory and solving efficiency. The AMGPCG is more efficient than the iterative methods used in the past and only needs one coarsening when EOS computes the particle motion trajectory.

Effect of glucose metabolism disorders on the short-term prognosis in neonates with asphyxia: a multicenter study in Hubei Province, China. / çª’æ¯æ–°ç”Ÿå„¿ç³–ä»£è°¢ç´Šä¹±å¯¹è¿‘æœŸé¢„åŽçš„å½±å“ï¼šä¸€é¡¹æ¹–åŒ—çœå¤šä¸­å¿ƒç ”ç©¶.

OBJECTIVES: To study the effect of glucose metabolism disorders on the short-term prognosis in neonates with asphyxia. METHODS: A retrospective analysis was performed on the medical data of the neonates with asphyxia who were admitted to 52 hospitals in Hubei Province of China from January to December, 2018 and had blood glucose data within 12 hours after birth. Their blood glucose data at 1, 2, 6, and 12 hours after birth (with an allowable time error of 0.5 hour) were recorded. According to the presence or absence of brain injury and/or death during hospitalization, the neonates were divided into a poor prognosis group with 693 neonates and a good prognosis group with 779 neonates. The two groups were compared in the incidence of glucose metabolism disorders within 12 hours after birth and short-term prognosis. RESULTS: Compared with the good prognosis group, the poor prognosis group had a significantly higher proportion of neonates from secondary hospitals (48.5% vs 42.6%, P<0.05) or with severe asphyxia (19.8% vs 8.1%, P<0.05) or hypothermia therapy (4.8% vs 1.5%, P<0.05), as well as a significantly higher incidence rate of disorder of glucose metabolism (18.8% vs 12.5%, P<0.05). Compared with the good prognosis group, the poor prognosis group had a significantly higher incidence rate of disorder of glucose metabolism at 1, 2, and 6 hours after birth (P<0.05). The multivariate logistic regression analysis showed that recurrent hyperglycemia (adjusted odds ratio=2.380, 95% confidence interval: 1.275-4.442, P<0.05) was an independent risk factor for poor prognosis in neonates with asphyxia. CONCLUSIONS: Recurrent hyperglycemia in neonates with asphyxia may suggest poor short-term prognosis, and it is necessary to strengthen the early monitoring and management of the nervous system in such neonates.

ß-Arrestin 2 mediates arginine vasopressin-induced IL-6 induction via the ERK1/2-NF-κB signal pathway in murine hearts.

Evidence to date suggests that ß-arrestins act beyond their role as adapter proteins. Arginine vasopressin (AVP) may be a factor in inflammation and fibrosis in the pathogenesis of heart failure. In the present study we investigated the effect of AVP on inflammatory cytokine IL-6 production in murine hearts and the impact of ß-arrestin 2-dependent signaling on AVP-induced IL-6 production. We found that administration of AVP (0.5 U/kg, iv) markedly increased the levels of IL-6 mRNA in rat hearts with the maximum level occurred at 6 h. In ß-arrestin 2 KO mouse hearts, deletion of ß-arrestin 2 decreased AVP-induced IL-6 mRNA expression. We then performed in vitro experiments in adult rat cardiac fibroblasts (ARCFs). We found that AVP (10-9-10-6 M) dose-dependently increased the expression of IL-6 mRNA and protein, activation of NF-κB signaling and ERK1/2 phosphorylation, whereas knockdown of ß-arrestin 2 blocked AVP-induced IL-6 increase, NF-κB activation and ERK1/2 phosphorylation. Pharmacological blockade of ERK1/2 using PD98059 diminished AVP-induced NF-κB activation and IL-6 production. The selective V1A receptor antagonist SR49059 effectively blocked AVP-induced NF-κB phosphorylation and activation as well as IL-6 expression in ARCFs. In AVP-treated mice, pre-injection of SR49059 (2 mg/kg, iv) abolished AVP-induced NF-κB activation and IL-6 production in hearts. The above results suggest that AVP induces IL-6 induction in murine hearts via the V1A receptor-mediated ß-arrestin2/ERK1/2/NF-κB pathway, thus reveal a novel mechanism of myocardial inflammation in heart failure involving the V1A/ß-arrestin 2/ERK1/2/NF-κB signaling pathway.

Jasmonic acid alleviates cadmium toxicity in Arabidopsis via suppression of cadmium uptake and translocation.

Jasmonic acid (JA) is thought to be involved in plant responses to cadmium (Cd) stress, but the underlying molecular mechanisms are poorly understood. Here, we show that Cd treatment rapidly induces the expression of genes promoting endogenous JA synthesis, and subsequently increases the JA concentration in Arabidopsis roots. Furthermore, exogenous methyl jasmonate (MeJA) alleviates Cd-generated chlorosis of new leaves by decreasing the Cd concentration in root cell sap and shoot, and decreasing the expression of the AtIRT1, AtHMA2 and AtHMA4 genes promoting Cd uptake and long-distance translocation, respectively. In contrast, mutation of a key JA synthesis gene, AtAOS, greatly enhances the expression of AtIRT1, AtHMA2 and AtHMA4, increases Cd concentration in both roots and shoots, and confers increased sensitivity to Cd. Exogenous MeJA recovers the enhanced Cd-sensitivity of the ataos mutant, but not of atcoi1, a JA receptor mutant. In addition, exogenous MeJA reduces NO levels in Cd-stressed Arabidopsis root tips. Taken together, our results suggest that Cd-induced JA acts via the JA signaling pathway and its effects on NO levels to positively restrict Cd accumulation and alleviates Cd toxicity in Arabidopsis via suppression of the expression of genes promoting Cd uptake and long-distance translocation.

AtHAP5A regulates iron translocation in iron-deficient Arabidopsis thaliana.

Iron (Fe) deficient plants employ multiple strategies to increase root uptake and root-to-shoot translocation of Fe. The identification of genes that are responsible for these processes, and a comprehensive understanding of the regulatory effects of transcriptional networks on their expression, including transcription factors (TFs), is underway in Arabidopsis thaliana. Here, we show that a Histone- or heme-associated proteins (HAP) transcription factor (TF), HAP5A, is necessary for the response to Fe deficiency in Arabidopsis. Its expression was induced under Fe deficiency, and the lack of HAP5A significantly decreased Fe translocation from the root to the shoot, resulting in substantial chlorosis of the newly expanded leaves, compared with the wild-type (WT, Col-0). Further analysis found that the expression of a gene encoding nicotianamine (NA) synthase (NAS1) was dramatically decreased in the hap5a mutant, regardless of the Fe status. Yeast-one-hybrid and ChIP analyses suggested that HAP5A directly binds to the promoter region of NAS1. Moreover, overexpression of NAS1 could rescue the chlorosis phenotype of hap5a in Fe deficient conditions. In summary, a novel pathway was elucidated, showing that NAS1-dependent translocation of Fe from the root to the shoot is controlled by HAP5A in Fe-deficient Arabidopsis thaliana.

Ammonium regulates Fe deficiency responses by enhancing nitric oxide signaling in Arabidopsis thaliana.

MAIN CONCLUSION: The accumulation of NH4+ in response to Fe deficiency plays a role not only in the remobilization of Fe from the root cell wall, but also in the transportation of Fe from root to shoot. Ammonium (NH4+) plays an important role in phosphorus-deficiency responses in rice, but its role in responses to Fe deficiency remains unknown. Here, we demonstrate that the accumulation of NH4+ plays a pivotal role when Arabidopsis thaliana plants are subject to Fe deficiency. The Arabidopsis amt1-3 mutant, which is defective in endogenous NH4+ sensing, exhibited increased sensitivity to Fe deficiency compared to WT (wild type; Col-0). In addition, exogenous application of NH4+ significantly alleviated Fe deficiency symptoms in plants. NH4+ triggers the production of nitric oxide (NO), which then induces ferric-chelate reductase (FCR) activity and accelerates the release of Fe from the cell wall, especially hemicellulose, thereby increasing the availability of soluble Fe in roots. NH4+ also increases soluble Fe levels in shoots by upregulating genes involved in Fe translocation, such as FRD3 (FERRIC REDUCTASE DEFECTIVE3) and NAS1 (NICOTIANAMINE SYNTHASE1), hence, alleviating leaf chlorosis. Overall, NH4+ plays an important role in the reutilization of Fe from the cell wall and the redistribution of Fe from root to shoot in Fe-deficient Arabidopsis, a process dependent on NO accumulation.

Nitrate inhibits the remobilization of cell wall phosphorus under phosphorus-starvation conditions in rice (Oryza sativa).

MAIN CONCLUSION: NO3- not only inhibited the reutilization of cell wall P via decreasing root cell wall pectin content and PME activity, but also hampered the P translocation from root to shoot. The rice cultivars 'Kasalath' (Kas) and 'Nipponbare' (Nip) were used to demonstrate that the nitrogen source NO3- inhibits internal phosphorus (P) reutilization in rice under P-absence conditions. Analysis using Kas showed that the expression of - P-induced marker genes OsIPS1/2 and OsSPX1/2/3/5 are significantly higher under 1 mM NO 3- - P (1N - P) treatment than 0 mM NO 3- - P (0N - P) treatment. The absence of NO3- from the nutrient solution significantly increased cell wall P release by increasing pectin synthesis and increasing the activity of pectin methylesterase (PME), and also significantly improved the translocation of soluble P from the root to the shoot by increasing xylem sap P content under P-absence conditions. The rice seedlings grown in 0 mM NO3- accumulated significantly higher nitric oxide (NO) in the roots than those grown in 1 mM NO3-. Exogenously applying the NO donor sodium nitroprusside (SNP) revealed that NO is a major contributor to differential cell wall P remobilization in rice by mediating pectin synthesis and demethylation under different NO3- concentrations (0 and 1 mM) under P-deprived conditions.

[Clinical Value of Multi-slice Spiral Enhanced CT in Diagnosing Mild Digestive Tract Hemorrhage].

Objective To investigate the clinical value of multi-slice spiral CT(MSCT) in the diagnosis of mild digestive tract hemorrhage. Methods Thirty-five patients with mild gastrointestinal hemorrhage were examined by enhanced MSCT.CT signs were observed and compared with pathologic examination findings.Results Diseases in these 35 patients included gastric and duodenal ulcer and inflammation(n=4,11.4%),esophagogastric variceal rupture(n=7,20.0%),gastric carcinoma(n=3,8.6%),gastric stromal tumor(n=3,8.6%),gastric polyp(n=1,2.9%),colonic malignancy(n=5,14.2%),small intestinal stromal tumor(n=6,17.1%),rectal cancer(n=2,5.7%),intestinal Crohn disease(n=3,8.6%),and jejunum diverticulum combined with hemorrhage(n=1,2.9%).All of them were diagnosed by endoscopy of the digestive tract and confirmed by operation and pathology.The accuracy rate of CT was 100%.The coincidence rate of CT diagnosis was 97.1%.Conclusion MSCT is a promising technique in the localization,qualitative diagnosis,and clinical treatment of mild gastrointestinal hemorrhage.

Putrescine Alleviates Iron Deficiency via NO-Dependent Reutilization of Root Cell-Wall Fe in Arabidopsis.

Plants challenged with abiotic stress show enhanced polyamines levels. Here, we show that the polyamine putrescine (Put) plays an important role to alleviate Fe deficiency. The adc2-1 mutant, which is defective in Put biosynthesis, was hypersensitive to Fe deficiency compared with wild type (Col-1 of Arabidopsis [Arabidopsis thaliana]). Exogenous Put decreased the Fe bound to root cell wall, especially to hemicellulose, and increased root and shoot soluble Fe content, thus alleviating the Fe deficiency-induced chlorosis. Intriguingly, exogenous Put induced the accumulation of nitric oxide (NO) under both Fe-sufficient (+Fe) and Fe-deficient (-Fe) conditions, although the ferric-chelate reductase (FCR) activity and the expression of genes related to Fe uptake were induced only under -Fe treatment. The alleviation of Fe deficiency by Put was diminished in the hemicellulose-level decreased mutant-xth31 and in the noa1 and nia1nia2 mutants, in which the endogenous NO levels are reduced, indicating that both NO and hemicellulose are involved in Put-mediated alleviation of Fe deficiency. However, the FCR activity and the expression of genes related to Fe uptake were still up-regulated under -Fe+Put treatment compared with -Fe treatment in xth31, and Put-induced cell wall Fe remobilization was abolished in noa1 and nia1nia2, indicating that Put-regulated cell wall Fe reutilization is dependent on NO. From our results, we conclude that Put is involved in the remobilization of Fe from root cell wall hemicellulose in a process dependent on NO accumulation under Fe-deficient condition in Arabidopsis.

The Chloroplast Protease AMOS1/EGY1 Affects Phosphate Homeostasis under Phosphate Stress.

Plastid intramembrane proteases in Arabidopsis (Arabidopsis thaliana) are involved in jasmonic acid biosynthesis, chloroplast development, and flower morphology. Here, we show that Ammonium-Overly-Sensitive1 (AMOS1), a member of the family of plastid intramembrane proteases, plays an important role in the maintenance of phosphate (P) homeostasis under P stress. Loss of function of AMOS1 revealed a striking resistance to P starvation. amos1 plants displayed retarded root growth and reduced P accumulation in the root compared to wild type (Col-0) under P-replete control conditions, but remained largely unaffected by P starvation, displaying comparable P accumulation and root and shoot growth under P-deficient conditions. Further analysis revealed that, under P-deficient conditions, the cell wall, especially the pectin fraction of amos1, released more P than that of wild type, accompanied by a reduction of the abscisic acid (ABA) level and an increase in ethylene production. By using an ABA-insensitive mutant, abi4, and applying ABA and ACC exogenously, we found that ABA inhibits cell wall P remobilization while ethylene facilitates P remobilization from the cell wall by increasing the pectin concentration, suggesting ABA can counteract the effect of ethylene. Furthermore, the elevated ABA level and the lower ethylene production also correlated well with the mimicked P deficiency in amos1 Thus, our study uncovers the role of AMOS1 in the maintenance of P homeostasis through ABA-antagonized ethylene signaling.

Differential Effects of Nitrogen Forms on Cell Wall Phosphorus Remobilization Are Mediated by Nitric Oxide, Pectin Content, and Phosphate Transporter Expression.

NH4 (+) is a major source of inorganic nitrogen for rice (Oryza sativa), and NH4 (+) is known to stimulate the uptake of phosphorus (P). However, it is unclear whether NH4 (+) can also stimulate P remobilization when rice is grown under P-deficient conditions. In this study, we use the two rice cultivars 'Nipponbare' and 'Kasalath' that differ in their cell wall P reutilization, to demonstrate that NH4 (+) positively regulates the pectin content and activity of pectin methylesterase in root cell walls under -P conditions, thereby remobilizing more P from the cell wall and increasing soluble P in roots and shoots. Interestingly, our results show that more NO (nitric oxide) was produced in the rice root when NH4 (+) was applied as the sole nitrogen source compared with the NO3 (-) The effect of NO on the reutilization of P from the cell walls was further demonstrated through the application of the NO donor SNP (sodium nitroprusside) and c-PTIO (NO scavenger 2-(4-carboxyphenyl)-4, 4, 5, 5-tetramethylimidazoline-1-oxyl-3-oxide). What's more, the P-transporter gene OsPT2 is up-regulated under NH4 (+) supplementation and is therefore involved in the stimulated P remobilization. In conclusion, our data provide novel (to our knowledge) insight into the regulatory mechanism by which NH4 (+) stimulates Pi reutilization in cell walls of rice.

PARVUS affects aluminium sensitivity by modulating the structure of glucuronoxylan in Arabidopsis thaliana.

Glucuronoxylan (GX), an important component of hemicellulose in the cell wall, appears to affect aluminium (Al) sensitivity in plants. To investigate the role of GX in cell-wall-localized xylan, we examined the Arabidopsis thaliana parvus mutant in detail. This mutant lacks α-D-glucuronic acid (GlcA) side chains in GX and has greater resistance to Al stress than wild-type (WT) plants. The parvus mutant accumulated lower levels of Al in its roots and cell walls than WT despite having cell wall pectin content and pectin methylesterase (PME) activity similar to those of WT. Our results suggest that the altered properties of hemicellulose in the mutant contribute to its decreased Al accumulation. Although we observed almost no differences in hemicellulose content between parvus and WT under control conditions, less Al was retained in parvus hemicellulose than in WT. This observation is consistent with the finding that GlcA substitutions in WT GX, but not mutant GX, were increased under Al stress. Taken together, these results suggest that the modulation of GlcA levels in GX affects Al resistance by influencing the Al binding capacity of the root cell wall in Arabidopsis.