Improvement of Torenia fournieri salinity tolerance by expression of Arabidopsis AtNHX5

2008 ◽  
Vol 35 (3) ◽  
pp. 185 ◽  
Author(s):  
Le-Yi Shi ◽  
Hong-Qing Li ◽  
Xiao-Ping Pan ◽  
Guo-Jiang Wu ◽  
Mei-Ru Li
Keyword(s):  
Salt Stress ◽  
Salt Tolerance ◽  
Potential Role ◽  
Ion Homeostasis ◽  
Leaf Explants ◽  
Wild Type ◽  
Torenia Fournieri ◽  
Regenerated Plants ◽  
Plant Salt Tolerance

In this paper, transgenic torenia plants expressing the AtNHX5 gene from Arabidopsis in sense and antisense orientations were produced to examine the potential role of AtNHX5 in plant salt tolerance and development. We found that torenia plants overexpressing AtNHX5 showed markedly enhanced tolerance to salt stress compared with both wild-type and antisense AtNHX5 transgenic plants upon salt stress. Measurements of ion levels indicated that Na+ and K+ contents were all higher in AtNHX5 overexpressing shoots than in those of both wild-type and antisense AtNHX5 shoots treated with 50 mm NaCl. This indicated that overexpression of AtNHX5 could improve the salt tolerance of transgenic torenia via accumulation of both Na+ and K+ in shoots, in which overall ion homeostasis and osmotic adjustment was changed to sustain the increase in shoot salt tolerance. Further, we found that overexpression of AtNHX5 in torenia significantly improved the shoot regeneration frequency in leaf explants and increased the plantlet survival rate when transferring the regenerated plants to soil. In addition, the AtNHX5 expressing plants produced flowers earlier than both wild-type and the antisense AtNHX5 plants. Taken together, the results indicated that AtNHX5 functions not only in plant salt tolerance but also in plant growth and development.

scholarly journals The RNA-seq transcriptomic analysis reveals genes mediating salt tolerance through rapid triggering of ion transporters in a mutant barley

2019 ◽  
Author(s):  
Sareh Yousefirad ◽  
Hassan Soltanloo ◽  
Sayad Sanaz Ramezanpour ◽  
Khalil Zaynalinezhad ◽  
Vahid Shariati
Keyword(s):  
Salt Stress ◽  
Salt Tolerance ◽  
Ion Homeostasis ◽  
High Ratio ◽  
Rna Seq ◽  
Ion Transporters ◽  
Wild Type ◽  
Specific Expression ◽  
Mutant Genotype ◽  
In The Wild

Abstract Regarding the complexity of the mechanisms of salinity tolerance, the use of isogenic lines or mutants that have the same genetic background but show different tolerance to salinity is a suitable method to reduce the analytical complexity to study these mechanisms. In the current study, whole transcriptome analysis was evaluated using RNA-seq method between a salt-tolerant mutant line “73-M4-30” and its wild-type “Zarjou” cultivar at a seedling stage after six hours of exposure to salt stress (300 mM NaCl). Transcriptome sequencing yielded 20 million reads for each genotype. A total number of 7116 transcripts with differential expression were identified, 1586 and 1479 of which were obtained with significantly increased expression in the mutant and the wild-type, respectively. In addition, the families of WRKY, ERF, AP2/EREBP, NAC, CTR/DRE, AP2/ERF, MAD, MIKC, HSF, and bZIP were identified as the important transcription factors with specific expression in the mutant genotype. The RNA-seq results were confirmed in several time points using qRT-PCR of some important salt-responsive genes. In general, the results revealed that the mutant compared to its wild-type via fast stomach closure and consequently transpiration reduction under the salt stress, saved more sodium ion in the root and decreased its transfer to the shoot, and increased the amount of potassium ion leading to the maintenance a high ratio [K+]/­[Na+] in the shoot. Moreover, it caused a reduction in photosynthesis and respiration, resulting in the use of the stored energy and the carbon for maintaining the plant tissues, which is a mechanism of salt tolerance in plants. Up-regulation of catalase, peroxidase, and ascorbate peroxidase genes, which was probably due to the more accumulation of H2O2 in the wild-type compared to the mutant. Therefore, the wild-type initiated rapid ROS signals lead to less oxidative scavenging than the mutant. The mutant increased expression in the ion transporters and the channels related to the salinity to retain the ion homeostasis. Totally, the results demonstrated that the mutant responded better to the salt stress under both the osmotic and the ionic stress phases. Less damage was observed in the mutant compared to its wild-type under the salt stress.

Reduced expression of a vesicle trafficking-related ATPase SKD1 decreases salt tolerance in Arabidopsis

2010 ◽  
Vol 37 (10) ◽  
pp. 962 ◽  
Author(s):  
Li-Wei Ho ◽  
Ting-Ting Yang ◽  
Shyan-Shu Shieh ◽  
Gerald E. Edwards ◽  
Hungchen E. Yen
Keyword(s):  
Salt Stress ◽  
Salt Tolerance ◽  
Higher Plants ◽  
Lateral Roots ◽  
Ion Homeostasis ◽  
Normal Activity ◽  
Growth Defect ◽  
Naphthaleneacetic Acid ◽  
Wild Type ◽  
Salinity Response

In this study we present the functional characterisation of SKD1 (suppressor of K+ transport growth defect) in salt tolerance of higher plants. SKD1 participates in endosome-mediated protein sorting and expression of SKD1 is salt-induced in Na+ storage cells of halophyte ice plant. Transgenic Arabidopsis with reduced SKD1 expression were generated by expressing AtSKD1 in antisense orientation. Relative root growth rate of antisense seedlings was slower than that of wild-type seedlings under salt treatment. The Na+/K+ ratio doubled in the antisense seedlings compared with the wild-type seedlings indicating a loss in Na+/K+ homeostasis. The PSII activity dropped following one week of salt-stress in antisense plants whereas wild-type plants maintained normal activity. Upon germination, transgenic seedlings developed multiple roots where each root had lower density of lateral roots. Application of 1-naphthaleneacetic acid restored the ability of transgenic seedlings to form lateral roots. Expression profiling analyses revealed that expressions of one stress-related kinase, several salt-induced transcription factors and one auxin efflux transporter were altered in antisense seedlings. With decreased expression of SKD1, plants experience a reduced salinity response and altered root development indicating the importance of intracellular vesicular trafficking in both auxin-mediated plant growth and in maintaining ion homeostasis under salt stress.

scholarly journals PLATZ2 negatively regulates salt tolerance in Arabidopsis seedlings by directly suppressing the expression of the CBL4/SOS3 and CBL10/SCaBP8 genes

2020 ◽  
Vol 71 (18) ◽  
pp. 5589-5602
Author(s):  
Shasha Liu ◽  
Rui Yang ◽  
Miao Liu ◽  
Shizhong Zhang ◽  
Kang Yan ◽  
...  
Keyword(s):  
Salt Stress ◽  
Salt Tolerance ◽  
Transgenic Plants ◽  
Loss Of Function ◽  
Wild Type ◽  
Salt Stress Response ◽  
In The Wild ◽  
Plant Salt Tolerance

Abstract Although the salt overly sensitive (SOS) pathway plays essential roles in conferring salt tolerance in Arabidopsis thaliana, the regulatory mechanism underlying SOS gene expression remains largely unclear. In this study, AtPLATZ2 was found to function as a direct transcriptional suppressor of CBL4/SOS3 and CBL10/SCaBP8 in the Arabidopsis salt stress response. Compared with wild-type plants, transgenic plants constitutively overexpressing AtPLATZ2 exhibited increased sensitivity to salt stress. Loss of function of PLATZ2 had no observed salt stress phenotype in Arabidopsis, while the double mutant of PLATZ2 and PLATZ7 led to weaker salt stress tolerance than wild-type plants. Overexpression of AtPLATZ2 in transgenic plants decreased the expression of CBL4/SOS3 and CBL10/SCaBP8 under both normal and saline conditions. AtPLATZ2 directly bound to A/T-rich sequences in the CBL4/SOS3 and CBL10/SCaBP8 promoters in vitro and in vivo, and inhibited CBL4/SOS3 promoter activity in the plant leaves. The salt sensitivity of #11 plants constitutively overexpressing AtPLATZ2 was restored by the overexpression of CBL4/SOS3 and CBL10/SCaBP8. Salt stress-induced Na+ accumulation in both the shoots and roots was more exaggerated in AtPLATZ2-overexpressing plants than in the wild type. The salt stress-induced Na+ accumulation in #11 seedlings was also rescued by the overexpression of CBL4/SOS3 and CBL10/SCaBP8. Furthermore, the transcription of AtPLATZ2 was induced in response to salt stress. Collectively, these results suggest that AtPLATZ2 suppresses plant salt tolerance by directly inhibiting CBL4/SOS3 and CBL10/SCaBP8, and functions redundantly with PLATZ7.

scholarly journals Isocitrate lyase plays important roles in plant salt tolerance

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Worawat Yuenyong ◽  
Supaart Sirikantaramas ◽  
Li-Jia Qu ◽  
Teerapong Buaboocha
Keyword(s):  
Salt Stress ◽  
Salt Tolerance ◽  
Transgenic Arabidopsis ◽  
Isocitrate Lyase ◽  
Glyoxylate Cycle ◽  
Knockout Mutant ◽  
Encoding Gene ◽  
Plant Salt Tolerance ◽  
The Glyoxylate Cycle

Abstract Background Isocitrate lyase (ICL) is a key enzyme in the glyoxylate cycle. In a previous study in rice, the expression of the ICL-encoding gene (OsICL) was highly induced by salt stress and its expression was enhanced in transgenic rice lines overexpressing OsCam1–1, a calmodulin (CaM)-encoding gene. CaM has been implicated in salt tolerance mechanisms in plants; however, the cellular mechanisms mediated by CaM are not clearly understood. In this study, the role of OsICL in plant salt tolerance mechanisms and the possible involvement of CaM were investigated using transgenic plants expressing OsICL or OsCam1–1. Results OsICL was highly expressed in senesced leaf and significantly induced by salt stress in three OsCam1–1 overexpressing transgenic rice lines as well as in wild type (WT). In WT young leaf, although OsICL expression was not affected by salt stress, all three transgenic lines exhibited highly induced expression levels. In Arabidopsis, salt stress had negative effects on germination and seedling growth of the AtICL knockout mutant (Aticl mutant). To examine the roles of OsICL we generated the following transgenic Arabidopsis lines: the Aticl mutant expressing OsICL driven by the native AtICL promoter, the Aticl mutant overexpressing OsICL driven by the 35SCaMV promoter, and WT overexpressing OsICL driven by the 35SCaMV promoter. Under salt stress, the germination rate and seedling fresh and dry weights of the OsICL-expressing lines were higher than those of the Aticl mutant, and the two lines with the icl mutant background were similar to the WT. The Fv/Fm and temperature of rosette leaves in the OsICL-expressing lines were less affected by salt stress than they were in the Aticl mutant. Finally, glucose and fructose contents of the Aticl mutant under salt stress were highest, whereas those of OsICL-expressing lines were similar to or lower than those of the WT. Conclusions OsICL, a salt-responsive gene, was characterized in the transgenic Arabidopsis lines, revealing that OsICL expression could revert the salt sensitivity phenotypes of the Aticl knockout mutant. This work provides novel evidence that supports the role of ICL in plant salt tolerance through the glyoxylate cycle and the possible involvement of OsCam1–1 in regulating its transcription.

scholarly journals 14-3-3 Proteins and Other Candidates form Protein-Protein Interactions with the Cytosolic C-terminal End of SOS1 Affecting Its Transport Activity

2020 ◽  
Vol 21 (9) ◽  
pp. 3334 ◽  
Author(s):  
Kerstin Duscha ◽  
Cristina Martins Rodrigues ◽  
Maria Müller ◽  
Ruth Wartenberg ◽  
Larry Fliegel ◽  
...  
Keyword(s):  
Salt Stress ◽  
Salt Tolerance ◽  
Protein Interactions ◽  
Soluble Sugar ◽  
Underlying Mechanism ◽  
Transport Activity ◽  
Wild Type ◽  
Protein Protein Interactions ◽  
Cell Extracts ◽  
Plant Salt Tolerance

The plasma membrane transporter SOS1 (SALT-OVERLY SENSITIVE1) is vital for plant survival under salt stress. SOS1 activity is tightly regulated, but little is known about the underlying mechanism. SOS1 contains a cytosolic, autoinhibitory C-terminal tail (abbreviated as SOS1 C-term), which is targeted by the protein kinase SOS2 to trigger its transport activity. Here, to identify additional binding proteins that regulate SOS1 activity, we synthesized the SOS1 C-term domain and used it as bait to probe Arabidopsis thaliana cell extracts. Several 14-3-3 proteins, which function in plant salt tolerance, specifically bound to and interacted with the SOS1 C-term. Compared to wild-type plants, when exposed to salt stress, Arabidopsis plants overexpressing SOS1 C-term showed improved salt tolerance, significantly reduced Na+ accumulation in leaves, reduced induction of the salt-responsive gene WRKY25, decreased soluble sugar, starch, and proline levels, less impaired inflorescence formation and increased biomass. It appears that overexpressing SOS1 C-term leads to the sequestration of inhibitory 14-3-3 proteins, allowing SOS1 to be more readily activated and leading to increased salt tolerance. We propose that the SOS1 C-term binds to previously unknown proteins such as 14-3-3 isoforms, thereby regulating salt tolerance. This finding uncovers another regulatory layer of the plant salt tolerance program.

scholarly journals NMR and LC-MS-Based Metabolomics to Study Osmotic Stress in Lignan-Deficient Flax

Molecules ◽  
2021 ◽  
Vol 26 (3) ◽  
pp. 767
Author(s):  
Kamar Hamade ◽  
Ophélie Fliniaux ◽  
Jean-Xavier Fontaine ◽  
Roland Molinié ◽  
Elvis Otogo Nnang ◽  
...  
Keyword(s):  
Stress Response ◽  
Osmotic Stress ◽  
Biosynthetic Pathway ◽  
Potential Role ◽  
Plant Secondary Metabolites ◽  
Wild Type ◽  
Osmotic Stress Response ◽  
Transgenic Flax ◽  
Insight Into

Lignans, phenolic plant secondary metabolites, are derived from the phenylpropanoid biosynthetic pathway. Although, being investigated for their health benefits in terms of antioxidant, antitumor, anti-inflammatory and antiviral properties, the role of these molecules in plants remains incompletely elucidated; a potential role in stress response mechanisms has been, however, proposed. In this study, a non-targeted metabolomic analysis of the roots, stems, and leaves of wild-type and PLR1-RNAi transgenic flax, devoid of (+) secoisolariciresinol diglucoside ((+) SDG)—the main flaxseed lignan, was performed using 1H-NMR and LC-MS, in order to obtain further insight into the involvement of lignan in the response of plant to osmotic stress. Results showed that wild-type and lignan-deficient flax plants have different metabolic responses after being exposed to osmotic stress conditions, but they both showed the capacity to induce an adaptive response to osmotic stress. These findings suggest the indirect involvement of lignans in osmotic stress response.

A Functional Alternative Oxidase Modulates Plant Salt Tolerance in Physcomitrella patens

2019 ◽  
Vol 60 (8) ◽  
pp. 1829-1841 ◽  
Author(s):  
Guochun Wu ◽  
Sha Li ◽  
Xiaochuan Li ◽  
Yunhong Liu ◽  
Shuangshuang Zhao ◽  
...  
Keyword(s):  
Salt Stress ◽  
Salt Tolerance ◽  
Stress Responses ◽  
Alternative Oxidase ◽  
Physcomitrella Patens ◽  
Redox Homeostasis ◽  
Respiratory Pathway ◽  
Functional Link ◽  
Salt Stress Condition ◽  
Plant Salt Tolerance

Abstract Alternative oxidase (AOX) has been reported to be involved in mitochondrial function and redox homeostasis, thus playing an essential role in plant growth as well as stress responses. However, its biological functions in nonseed plants have not been well characterized. Here, we report that AOX participates in plant salt tolerance regulation in moss Physcomitrella patens (P. patens). AOX is highly conserved and localizes to mitochondria in P. patens. We observed that PpAOX rescued the impaired cyanide (CN)-resistant alternative (Alt) respiratory pathway in Arabidopsis thaliana (Arabidopsis) aox1a mutant. PpAOX transcription and Alt respiration were induced upon salt stress in P. patens. Using homologous recombination, we generated PpAOX-overexpressing lines (PpAOX OX). PpAOX OX plants exhibited higher Alt respiration and lower total reactive oxygen species accumulation under salt stress condition. Strikingly, we observed that PpAOX OX plants displayed decreased salt tolerance. Overexpression of PpAOX disturbed redox homeostasis in chloroplasts. Meanwhile, chloroplast structure was adversely affected in PpAOX OX plants in contrast to wild-type (WT) P. patens. We found that photosynthetic activity in PpAOX OX plants was also lower compared with that in WT. Together, our work revealed that AOX participates in plant salt tolerance in P. patens and there is a functional link between mitochondria and chloroplast under challenging conditions.

Abstract 450: The Role of CD38 as a Therapeutic Target for Protection Against Doxorubicin-induced Cardiotoxicity Through Nad+ Boosting

2020 ◽  
Vol 127 (Suppl_1) ◽  
Author(s):  
Thais R Peclat ◽  
Guillermo Agorrody ◽  
Lilian S Gomez ◽  
Eduardo N Chini
Keyword(s):  
Single Dose ◽  
Therapeutic Target ◽  
Potential Role ◽  
Damage Mechanism ◽  
Treated Group ◽  
Wild Type ◽  
Chemotherapeutic Treatment ◽  
Positive Effect ◽  
Dose Injection

Background: Doxorubicin is a chemotherapy medication used to treat several types of cancer. Its major adverse effect is cardiotoxicity, which may limit its use. Doxorubicin-induced cardiotoxicity (DIC), once developed, carries a poor prognosis. Therefore strategies to prevent or treat DIC are of paramount importance but have not yet been fully developed. Being NAD + a critical nucleotide which is involved in oxy-reduction reactions and CD38 the main NAD + -consuming enzyme responsible for NAD levels regulation and homeostasis, we aim to investigate the link of CD38 and NAD + metabolism in DIC and its potential role as a therapeutic target. Methods: We compared Wild-type (WT) control mice with WT mice treated with a single dose injection of 15 mg/kg of doxorubicin who received vehicle or an antibody that blocksCD38 ecto-enzymatic activity. We also compared genetically CD38 catalytic inactive (CI) mice treated or not with the same single dose injection. Results: Doxorubicin caused a decrease in Ejection Fraction (EF) in WT mice. We also observed that CD38 CI mice treated with doxorubicin did not have changes in EF compared to their control. When compared to WT receiving just doxorubicin, WT mice treated also with the antibody had a trend to improve EF. As for exercise performance, our results show a decrease in exercise capacity induced by doxorubicin that was reversed in the antibody group and did not happen in the CD38 CI mice treated with doxorubicin. Doxorubicin caused a decrease in heart rate variability (HRV) which was improved in the antibody treated group. Moreover, our results show a survival rate that is similar to what has been previously shown, with 50% mortality associated with doxorubicin. Blockage of CD38 activity with antibody reduced mortality in this model to approximately 20%. Mechanistically, we did not observe decreases in NAD+ levels induced by Doxorubicin. However, boost of NAD induced by blocking CD38 was related to protection against DIC. Conclusion: Our results indicate that the damage mechanism of DIC may not be related directly with NAD decrease, but NAD boosting induced by CD38 blockage seems to have a positive effect in protection against cardiac dysfunction related to this chemotherapeutic treatment.

scholarly journals Manganese promotes the aggregation and prion-like cell-to-cell exosomal transmission of α-synuclein

2019 ◽  
Vol 12 (572) ◽  
pp. eaau4543 ◽  
Author(s):  
Dilshan S. Harischandra ◽  
Dharmin Rokad ◽  
Matthew L. Neal ◽  
Shivani Ghaisas ◽  
Sireesha Manne ◽  
...  
Keyword(s):  
Potential Role ◽  
Neuronal Model ◽  
Experimental Models ◽  
Bimolecular Fluorescence Complementation ◽  
Wild Type ◽  
Biological Mechanisms ◽  
Extracellular Medium ◽  
Cell To Cell Transfer ◽  
Serum Exosomes

The aggregation of α-synuclein (αSyn) is considered a key pathophysiological feature of certain neurodegenerative disorders, collectively termed synucleinopathies. Given that a prion-like, cell-to-cell transfer of misfolded αSyn has been recognized in the spreading of αSyn pathology in synucleinopathies, we investigated the biological mechanisms underlying the propagation of the disease with respect to environmental neurotoxic stress. Considering the potential role of the divalent metal manganese (Mn2+) in protein aggregation, we characterized its effect on αSyn misfolding and transmission in experimental models of Parkinson’s disease. In cultured dopaminergic neuronal cells stably expressing wild-type human αSyn, misfolded αSyn was secreted through exosomes into the extracellular medium upon Mn2+ exposure. These exosomes were endocytosed through caveolae into primary microglial cells, thereby mounting neuroinflammatory responses. Furthermore, Mn2+-elicited exosomes exerted a neurotoxic effect in a human dopaminergic neuronal model (LUHMES cells). Moreover, bimolecular fluorescence complementation (BiFC) analysis revealed that Mn2+ accelerated the cell-to-cell transmission of αSyn, resulting in dopaminergic neurotoxicity in a mouse model of Mn2+ exposure. Welders exposed to Mn2+ had increased misfolded αSyn content in their serum exosomes. Stereotaxically delivering αSyn-containing exosomes, isolated from Mn2+-treated αSyn-expressing cells, into the striatum initiated Parkinsonian-like pathological features in mice. Together, these results indicate that Mn2+ exposure promotes αSyn secretion in exosomal vesicles, which subsequently evokes proinflammatory and neurodegenerative responses in both cell culture and animal models.

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