The K+/H+ antiporter AhNHX1 improved tobacco tolerance to NaCl stress by enhancing K+ retention

Zhang, Weiwei; Meng, Jingjing; Xing, Jinyan; Yang, Sha; Guo, Feng; Li, Xinguo

doi:10.1007/s12374-016-0905-7

Cited by 28 publications

(9 citation statements)

References 44 publications

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“…Ionic toxicity is primarily caused by excessive accumulation of cytosolic Na + , leading to ion imbalance and perturbation of Na : K ratio (Zhu, ). Maintenance of an optimal Na : K ratio has been proposed to be instrumental in the mitigation of ionic toxicity and indispensable for sustaining normal functions of plant organelles in response to salt stress (Zhang et al ., ; Yang & Guo, ), implying that ion homeostasis is a major determinant of salt tolerance. Herein, we found that the enhanced salt tolerance of transgenic lemon is consistent with lower concentrations of Na + , but with higher K + content and reduced Na : K ratios, whereas salt hypersensitivity of the silenced line is congruent with higher concentrations of Na + , reduced K + and increased Na : K ratio.…”

Section: Discussionmentioning

confidence: 99%

The transcription factor FcWRKY40 of Fortunella crassifolia functions positively in salt tolerance through modulation of ion homeostasis and proline biosynthesis by directly regulating SOS2 and P5CS1 homologs

et al. 2018

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Although some WRKYs have been characterized, regulatory roles of most WRKYs remain poorly understood. Herein, we elucidated function of FcWRKY40 from Fortunella crassifolia in salt tolerance via overexpression and virus-induced gene silencing (VIGS) and unraveled its target genes. Overexpression of FcWRKY40 enhanced salt tolerance in transgenic tobacco and lemon, while silencing of FcWRKY40 increased salt susceptibility. Homolog genes of Salt Overly Sensitive 2 (SOS2) and Δ-1-pyrroline-5-carboxylate synthetase 1 (P5CS1) were dramatically up-regulated in transgenic lemon but down-regulated in VIGS line. Consistently, transgenic lemon displayed lower Na and higher proline concentrations, whereas the silenced line accumulated more Na but less proline. Treatment of transgenic lemon with 24-epi-brassinolide compromised salt tolerance, while supply of exogenous proline partially restored salt tolerance of the VIGS line. FcWRKY40 specifically binds to and activates promoters of FcSOS2 and FcP5CS1. FcWRKY40 was up-regulated by ABA and salt, and confirmed as a target of ABA-responsive element binding factor 2 (FcABF2). Moreover, salt treatment up-regulated FcABF2 and FcP5CS1, and elevated proline concentrations. Taken together, our findings demonstrate that FcWRKY40 participates in the ABA signaling pathway and as a positive regulator functions in salt tolerance by regulating genes involved in ion homeostasis and proline biosynthesis.

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Section: Discussionmentioning

confidence: 99%

The transcription factor FcWRKY40 of Fortunella crassifolia functions positively in salt tolerance through modulation of ion homeostasis and proline biosynthesis by directly regulating SOS2 and P5CS1 homologs

et al. 2018

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“…PDF1.5 is localized to the cell wall and may play a role in detoxifying cadmium by chelating cadmium to the cell wall. Consequently, our findings indicate that AtPDF1.5 enhances Cd tolerance by regulating the transport of this metal [ 11 , 50 , 51 ].…”

Section: Discussionmentioning

confidence: 99%

“…With respect to NO 3 − transport, nitrate transporter 1.5 (NRT1.5) is involved in xylem NO 3 − loading [ 8 ], whereas nitrate transporter 1.8 (NRT1.8) functions in xylem NO 3 − unloading [ 9 ]. Accordingly, the NRT1.5 and NRT1.8 genes play important roles in NO 3 − distribution [ 10 , 11 ].…”

Section: Introductionmentioning

confidence: 99%

PDF1.5 Enhances Adaptation to Low Nitrogen Levels and Cadmium Stress

Liu

Ning-yan

et al. 2021

IJMS

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Environmental acclimation ability plays a key role in plant growth, although the mechanism remains unclear. Here, we determined the involvement of Arabidopsis thaliana PLANT DEFENSIN 1 gene AtPDF1.5 in the adaptation to low nitrogen (LN) levels and cadmium (Cd) stress. Histochemical analysis revealed that AtPDF1.5 was mainly expressed in the nodes and carpopodium and was significantly induced in plants exposed to LN conditions and Cd stress. Subcellular localization analysis revealed that AtPDF1.5 was cell wall- and cytoplasm-localized. AtPDF1.5 overexpression significantly enhanced adaptation to LN and Cd stress and enhanced the distribution of metallic elements. The functional disruption of AtPDF1.5 reduced adaptations to LN and Cd stress and impaired metal distribution. Under LN conditions, the nitrate transporter AtNRT1.5 expression was upregulated. Nitrate transporter AtNRT1.8 expression was downregulated when AtPDF1.5 was overexpressed, resulting in enhanced transport of NO3− to shoots. In response to Cd treatment, AtPDF1.5 regulated the expression of metal transporter genes AtHMP07, AtNRAMP4, AtNRAMP1, and AtHIPP3, resulting in higher Cd accumulation in the shoots. We conclude that AtPDF1.5 is involved in the processing or transmission of signal substances and plays an important role in the remediation of Cd pollution and LN adaptation.

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“…lncRNAs are involved in tumor suppression through regulating gene expression and have received attention in accumulating research. [21] Several dysregulated lncRNAs are reported to be closely related to hematopoietic carcinogens. [22] Convincing evidence has suggested that UCA1 extensively regulates development, differentiation, proliferation, and apoptosis in cells by different mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Silencing of lncRNA UCA1 curbs proliferation and accelerates apoptosis by repressing SIRT1 signals by targeting miR‐204 in pediatric AML

Zhang

et al. 2020

J Biochem & Molecular Tox

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The long noncoding RNA urothelial carcinoma‐associated 1 (UCA1) has been reported to sustain the proliferation of acute myeloid leukemia (AML) cells through downregulating cell cycle regulators p27kip1. Yet, the foundational mechanism of UCA1 in AML pathologies remains unclear. Herein, we found an escalation of UCA1 expression and suppression of miR‐204 expression in pediatric AML patients and cells. UCA1 silencing suppressed cell proliferative abilities, promoted apoptotic rates, decreased Ki67, and increased cleaved caspase‐3 in AML cells. Moreover, UCA1 sponged miR‐204 and suppressed its expression. UCA1 overexpression inversed the miR‐204 suppressed proliferation and promoted apoptosis. UCA1 also boosted the expression of SIRT1, a miR‐204 target, via the sponging interaction. Furthermore, miR‐204 inhibited inducible nitric oxide synthase and cyclooxygenase‐2 expression, while UCA1 overexpression inversed the inhibitory effects in AML cells. Our findings concluded that UCA1 downregulation repressed cell proliferation and promoted apoptosis through inactivating SIRT1 signals by upregulating miR‐204 in pediatric AML.

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The K+/H+ antiporter AhNHX1 improved tobacco tolerance to NaCl stress by enhancing K+ retention

Cited by 28 publications

References 44 publications

The transcription factor FcWRKY40 of Fortunella crassifolia functions positively in salt tolerance through modulation of ion homeostasis and proline biosynthesis by directly regulating SOS2 and P5CS1 homologs

The transcription factor FcWRKY40 of Fortunella crassifolia functions positively in salt tolerance through modulation of ion homeostasis and proline biosynthesis by directly regulating SOS2 and P5CS1 homologs

PDF1.5 Enhances Adaptation to Low Nitrogen Levels and Cadmium Stress

Silencing of lncRNA UCA1 curbs proliferation and accelerates apoptosis by repressing SIRT1 signals by targeting miR‐204 in pediatric AML

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