Novel solution-gated transistor sensor-based SnO2 epitaxial thin films grown by pulsed laser deposition for nitrite detection.

A solution-gate controlled thin-film transistor with SnO2 epitaxial thin films (SnO2-SGTFT) is successfully utilized for highly sensitive detection of nitrite. The SnO2 films are deposited as channel materials on a c-plane sapphire (c-Al2O3) substrate through pulsed laser deposition (PLD), with superior crystal quality and out-of-plane atomic ordering. PtAu NPs/rGO nanocomposites are electrodeposited on a gold electrode to function as a transistor gate to further enhance the nitrite catalytic performance of the device. The change in effective gate voltage due to the electrooxidation of nitrite on the gate electrode is the primary sensing mechanism of the device. Based on the inherent amplification effect of transistors, the superior electrical properties of SnO2, and the high electrocatalytic activity of PtAu NPs/rGO, the SnO2-SGTFT sensor has a low detection limit of 0.1 nM and a wide linear detection range of 0.1 nM ~ 50 mM at VGS = 1.0 V. Furthermore, the sensor has excellent characteristics such as rapid response time, selectivity, and stability. The practicability of the device has been confirmed by the quantitative detection of nitrite in natural lake water. SnO2 epitaxial films grown by PLD provide a simple and efficient way to fabricate nitrite SnO2-SGTFT sensors in environmental monitoring and food safety, among others. It also provides a reference for the construction of other high-performance thin-film transistor sensors.

GhWRKY33 negatively regulates jasmonate-mediated plant defense to Verticillium dahliae.

Verticillium wilt, caused by Verticillium dahliae, seriously restricts the yield and quality improvement of cotton. Previous studies have revealed the involvement of WRKY members in plant defense against V. dahliae, but the underlying mechanisms involved need to be further elucidated. Here, we demonstrated that Gossypium hirsutum WRKY DNA-binding protein 33 (GhWRKY33) functions as a negative regulator in plant defense against V. dahliae. GhWRKY33 expression is induced rapidly by V. dahliae and methyl jasmonate, and overexpression of GhWRKY33 reduces plant tolerance to V. dahliae in Arabidopsis. Quantitative RT-PCR analysis revealed that expression of several JA-associated genes was significantly repressed in GhWRKY33 overexpressing transgenic plants. Yeast one-hybrid analysis revealed that GhWRKY33 may repress the transcription of both AtERF1 and GhERF2 through its binding to their promoters. Protein-protein interaction analysis suggested that GhWRKY33 interacts with G. hirsutum JASMONATE ZIM-domain protein 3 (GhJAZ3). Similarly, overexpression of GhJAZ3 also decreases plant tolerance to V. dahliae. Furthermore, GhJAZ3 acts synergistically with GhWRKY33 to suppress both AtERF1 and GhERF2 expression. Our results imply that GhWRKY33 may negatively regulate plant tolerance to V. dahliae via the JA-mediated signaling pathway.

A spliceosome-associated gene signature aids in predicting prognosis and tumor microenvironment of hepatocellular carcinoma.

Splicing alterations have been shown to be key tumorigenesis drivers. In this study, we identified a novel spliceosome-related genes (SRGs) signature to predict the overall survival (OS) of patients with hepatocellular carcinoma (HCC). A total of 25 SRGs were identified from the GSE14520 dataset (training set). Univariate and least absolute shrinkage and selection operator (LASSO) regression analyses were utilized to construct the signature using genes with predictive significance. We then constructed a risk model using six SRGs (BUB3, IGF2BP3, RBM3, ILF3, ZC3H13, and CCT3). The reliability and predictive power of the gene signature were validated in two validation sets (TCGA and GSE76427 dataset). Patients in training and validation sets were divided into high and low-risk groups based on the gene signature. Patients in high-risk groups exhibited a poorer OS than in low-risk groups both in the training set and two validation sets. Next, risk score, BCLC staging, TNM staging, and multinodular were combined in a nomogram for OS prediction, and the decision curve analysis (DCA) curve exhibited the excellent prediction performance of the nomogram. The functional enrichment analyses demonstrated high-risk score patients were closely related to multiple oncology characteristics and invasive-related pathways, such as Cell cycle, DNA replication, and Spliceosome. Different compositions of the tumor microenvironment and immunocyte infiltration ratio might contribute to the prognostic difference between high and low-risk score groups. In conclusion, a spliceosome-related six-gene signature exhibited good performance for predicting the OS of patients with HCC, which may aid in clinical decision-making for individual treatment.

Bioinformatics analysis and experimental validation of a novel autophagy-related signature relevant to immune infiltration for recurrence prediction after curative hepatectomy.

Hepatocellular carcinoma (HCC) remains imposing an enormous economic and healthcare burden worldwide. In this present study, we constructed and validated a novel autophagy-related gene signature to predict the recurrence of HCC patients. A total of 29 autophagy-related differentially expressed genes were identified. A five-gene signature (CLN3, HGF, TRIM22, SNRPD1, and SNRPE) was constructed for HCC recurrence prediction. Patients in high-risk groups exhibited a significantly poor prognosis compared with low-risk patients both in the training set (GSE14520 dataset) and the validation set (TCGA and GSE76427 dataset). Multivariate cox regression analysis demonstrated that the 5-gene signature was an independent risk factor for recurrence-free survival (RFS) in HCC patients. The nomograms incorporating 5-gene signature and clinical prognostic risk factors were able to effectively predict RFS. KEGG and GSEA analysis revealed that the high-risk group was enriched with multiple oncology characteristics and invasive-related pathways. Besides, the high-risk group had a higher level of immune cells and higher levels of immune checkpoint-related gene expression in the tumor microenvironment, suggesting that they might be more likely to benefit from immunotherapy. Finally, the immunohistochemistry and cell experiments confirmed the role of SNRPE, the most significant gene in the gene signature. SNRPE was significantly overexpressed in HCC. After SNRPE knockdown, the proliferation, migration and invasion ability of the HepG2 cell line were significantly inhibited. Our study established a novel five-gene signature and nomogram to predict RFS of HCC, which may help in clinical decision-making for individual treatment.

GhWRKY33 Interacts with GhTIFY10A to Synergistically Modulate Both Ageing and JA-Mediated Leaf Senescence in Arabidopsis.

WRKY transcription factors play critical roles in the modulation of transcriptional changes during leaf senescence, but the underlying mechanisms controlled by them in this progress still remain enigmatic. In this study, Gossypium hirsutum WRKY DNA-binding protein 33 (GhWRKY33) was characterized as a negative regulator of both ageing and JA-mediated leaf senescence. The overexpression of GhWRKY33 in Arabidopsis greatly delayed leaf senescence, as determined by elevated chlorophyll content, lower H2O2 content, and reduced expression of several senescence-associated genes (SAGs). An electrophoretic mobility shift assay (EMSA) and transient dual-luciferase reporter assay revealed that GhWRKY33 could bind to the promoters of both AtSAG12 and Ghcysp and suppress their expression. Yeast two-hybrid (Y2H) and firefly luciferase complementation imaging (LUC) assays showed that GhWRKY33 could interact with GhTIFY10A. Similarly, the overexpression of GhTIFY10A in Arabidopsis also dramatically delayed leaf senescence. Furthermore, both GhWRKY33 and GhTIFY10A negatively regulate JA-mediated leaf senescence. In addition, a transientdual-luciferase reporter assay indicated that GhWRKY33 and GhTIFY10A could function synergistically to inhibit the expression of both AtSAG12 and Ghcysp. Thus, our work suggested that GhWRKY33 may function as a negative regulator to modulate both ageing and JA-mediated leaf senescence and also contributes to a basis for further functional studies on cotton leaf senescence.

Comparative physiological and metabolomic analyses reveal that Fe3O4 and ZnO nanoparticles alleviate Cd toxicity in tobacco.

BACKGROUND: Heavy metals repress tobacco growth and quality, and engineered nanomaterials have been used for sustainable agriculture. However, the underlying mechanism of nanoparticle-mediated cadmium (Cd) toxicity in tobacco remains elusive. RESULTS: Herein, we investigated the effects of Fe3O4 and ZnO nanoparticles (NPs) on Cd stress in tobacco cultivar 'Yunyan 87' (Nicotiana tabacum). Cd severely repressed tobacco growth, whereas foliar spraying with Fe3O4 and ZnO NPs promoted plant growth, as indicated by enhancing plant height, root length, shoot and root fresh weight under Cd toxicity. Moreover, Fe3O4 and ZnO NPs increased, including Zn, K and Mn contents, in the roots and/or leaves and facilitated seedling growth under Cd stress. Metabolomics analysis showed that 150 and 76 metabolites were differentially accumulated in roots and leaves under Cd stress, respectively. These metabolites were significantly enriched in the biosynthesis of amino acids, nicotinate and nicotinamide metabolism, arginine and proline metabolism, and flavone and flavonol biosynthesis. Interestingly, Fe3O4 and ZnO NPs restored 50% and 47% in the roots, while they restored 70% and 63% in the leaves to normal levels, thereby facilitating plant growth. Correlation analysis further indicated that these metabolites, including proline, 6-hydroxynicotinic acid, farrerol and quercetin-3-O-sophoroside, were significantly correlated with plant growth. CONCLUSIONS: These results collectively indicate that metal nanoparticles can serve as plant growth regulators and provide insights into using them for improving crops in heavy metal-contaminated areas.

Overexpression of chaperonin containing TCP1 subunit 7 has diagnostic and prognostic value for hepatocellular carcinoma.

Chaperonin containing TCP1 subunit 7 (CCT7) regulates the expression of many tumor-related proteins. We investigated the diagnostic and prognostic value of CCT7 expression for hepatocellular carcinoma (HCC). In datasets from The Cancer Genome Atlas and the Gene Expression Omnibus, CCT7 mRNA levels were greater in HCC tissues than adjacent normal tissues, and these results were validated using immunohistochemistry. In patients with early-stage disease and low alpha-fetoprotein expression, CCT7 expression was still higher in HCC tissues than normal tissues. Receiver operating characteristic curve analyses indicated that CCT7 expression had better diagnostic value than alpha-fetoprotein for HCC patients with early-stage disease and low alpha-fetoprotein expression. The positive predictive value of CCT7 expression was higher than that of alpha-fetoprotein expression. Higher CCT7 mRNA and protein levels were independent risk factors for poorer overall and recurrence-free survival in HCC patients. Greater methylation of the CpG site cg19515186 was associated with better overall survival in HCC patients. Genes co-expressed with CCT7 were upregulated in HCC and associated with poorer overall survival. Gene Ontology, Kyoto Encyclopedia of Genes and Genomes and Gene Set Enrichment Analyses demonstrated that CCT7 expression correlated with spliceosome signaling. These findings demonstrate that CCT7 has diagnostic and prognostic value for HCC.

Arabidopsis SIGMA FACTOR BINDING PROTEIN1 (SIB1) and SIB2 inhibit WRKY75 function in abscisic acid-mediated leaf senescence and seed germination.

The plant-specific VQ gene family participates in diverse physiological processes but little information is available on their role in leaf senescence. Here, we show that the VQ motif-containing proteins, Arabidopsis SIGMA FACTOR BINDING PROTEIN1 (SIB1) and SIB2 are negative regulators of abscisic acid (ABA)-mediated leaf senescence. Loss of SIB1 and SIB2 function resulted in increased sensitivity of ABA-induced leaf senescence. In contrast, overexpression of SIB1 significantly delayed this process. Moreover, biochemical studies revealed that SIBs interact with WRKY75 transcription factor. Loss of WRKY75 function decreased sensitivity to ABA-induced leaf senescence, while overexpression of WRKY75 significantly accelerated this process. Chromatin immunoprecipitation assays revealed that WRKY75 directly binds to the promoters of GOLDEN 2-LIKE1(GLK1) and GLK2, to repress their expression. SIBs repress the transcriptional function of WRKY75 and negatively regulate ABA-induced leaf senescence in a WRKY75-dependent manner. In contrast, WRKY75 positively modulates ABA-mediated leaf senescence in a GLK-dependent manner. In addition, SIBs inhibit WRKY75 function in ABA-mediated seed germination. These results demonstrate that SIBs can form a complex with WRKY75 to regulate ABA-mediated leaf senescence and seed germination.

MYB70 modulates seed germination and root system development in Arabidopsis.

Crosstalk among ABA, auxin, and ROS plays critical roles in modulating seed germination, root growth, and suberization. However, the underlying molecular mechanisms remain largely elusive. Here, MYB70, a R2R3-MYB transcription factor was shown to be a key component of these processes in Arabidopsis thaliana. myb70 seeds displayed decreased sensitivity, while MYB70-overexpressing OX70 seeds showed increased sensitivity in germination in response to exogenous ABA through MYB70 physical interaction with ABI5 protein, leading to enhanced stabilization of ABI5. Furthermore, MYB70 modulates root system development (RSA) which is associated with increased conjugated IAA content and H2O2/O2 ⋅- ratio but reduced root suberin deposition, consequently affecting nutrient uptake. In support of these data, MYB70 positively regulates the expression of auxin conjugation-related GH3, while negatively peroxidase-encoding and suberin biosynthesis-related genes. Our findings collectively revealed a previously uncharacterized component that modulates ABA and auxin signaling pathways, H2O2/O2 ⋅- balance, and suberization, consequently regulating RSA and seed germination.

The R2R3-MYB transcription factor AtMYB49 modulates salt tolerance in Arabidopsis by modulating the cuticle formation and antioxidant defence.

Salt stress activates defence responses in plants, including changes in leaf surface structure. Here, we showed that the transcriptional activation of cutin deposition and antioxidant defence by the R2R3-type MYB transcription factor AtMYB49 contributed to salt tolerance in Arabidopsis thaliana. Characterization of loss-of-function myb49 mutants, and chimeric AtMYB49-SRDX-overexpressing SRDX49 transcriptional repressor and AtMYB49-overexpressing (OX49) overexpressor plants demonstrated a positive role of AtMYB49 in salt tolerance. Transcriptome analysis revealed that many genes belonging to the category "cutin, suberin and wax biosyntheses" were markedly up-regulated and down-regulated in OX49 and SRDX49 plants, respectively, under normal and/or salt stress conditions. Some of these differentially expressed genes, including MYB41, ASFT, FACT and CYP86B1, were also shown to be the direct targets of AtMYB49 and activated by AtMYB49. Biochemical analysis indicated that AtMYB49 modulated cutin deposition in the leaves. Importantly, cuticular transpiration, chlorophyll leaching and toluidine blue-staining assays revealed a link between increased AtMYB49-mediated cutin deposition in leaves and enhanced salt tolerance. Additionally, increased AtMYB49 expression elevated Ca2+ level in leaves and improved antioxidant capacity by up-regulating genes encoding peroxidases and late embryogenesis abundant proteins. These results suggest that genetic manipulation of AtMYB49 may provide a novel way to improve salt tolerance in plants.

Comparative Physiological and Transcriptomic Analyses Reveal the Toxic Effects of ZnO Nanoparticles on Plant Growth.

Zinc oxide (ZnO) nanoparticles (nZnO) are among the most commonly used nanoparticles (NPs), and they have been shown to have harmful effects on plants. However, the molecular mechanisms underlying nZnO tolerance and root sensing of NP stresses have not been elucidated. Here, we compared the differential toxic effects of nZnO and Zn2+ toxicity on plants during exposure and recovery using a combination of transcriptomic and physiological analyses. Although both nZnO and Zn2+ inhibited primary root (PR) growth, nZnO had a stronger inhibitory effect on the growth of elongation zones, whereas Zn2+ toxicity had a stronger toxic effect on meristem cells. Timely recovery from stresses is critical for plant survival. Despite the stronger inhibitory effect of nZnO on PR growth, nZnO-exposed plants recovered from stress more rapidly than Zn2+-exposed plants upon transfer to normal conditions, and transcriptome data supported these results. In contrast to Zn2+ toxicity, nZnO induced endocytosis and caused microfilament rearrangement in the epidermal cells of elongation zones, thereby repressing PR growth. nZnO also repressed PR growth by disrupting cell wall organization and structure through both physical interactions and transcriptional regulation. The present study provides new insight into the comprehensive understanding and re-evaluation of NP toxicity in plants.

The R2R3-MYB Transcription Factor MYB49 Regulates Cadmium Accumulation.

Abscisic acid (ABA) reduces accumulation of potentially toxic cadmium (Cd) in plants. How the ABA signal is transmitted to modulate Cd uptake remains largely unclear. Here, we report that the basic region/Leu zipper transcription factor ABSCISIC ACID-INSENSITIVE5 (ABI5), a central ABA signaling molecule, is involved in ABA-repressed Cd accumulation in plants by physically interacting with a previously uncharacterized R2R3-type MYB transcription factor, MYB49. Overexpression of the Cd-induced MYB49 gene in Arabidopsis (Arabidopsis thaliana) resulted in a significant increase in Cd accumulation, whereas myb49 knockout plants and plants expressing chimeric repressors of MYB49:ERF-associated amphiphilic repression motif repression domain (SRDX49) exhibited reduced accumulation of Cd. Further investigations revealed that MYB49 positively regulates the expression of the basic helix-loop-helix transcription factors bHLH38 and bHLH101 by directly binding to their promoters, leading to activation of IRON-REGULATED TRANSPORTER1, which encodes a metal transporter involved in Cd uptake. MYB49 also binds to the promoter regions of the heavy metal-associated isoprenylated plant proteins (HIPP22) and HIPP44, resulting in up-regulation of their expression and subsequent Cd accumulation. On the other hand, as a feedback mechanism to control Cd uptake and accumulation in plant cells, Cd-induced ABA up-regulates the expression of ABI5, whose protein product interacts with MYB49 and prevents its binding to the promoters of downstream genes, thereby reducing Cd accumulation. Our results provide new insights into the molecular feedback mechanisms underlying ABA signaling-controlled Cd uptake and accumulation in plants.

The SNAC-A Transcription Factor ANAC032 Reprograms Metabolism in Arabidopsis.

Studies have indicated that the carbon starvation response leads to the reprogramming of the transcriptome and metabolome, and many genes, including several important regulators, such as the group S1 basic leucine zipper transcription factors (TFs) bZIP1, bZIP11 and bZIP53, the SNAC-A TF ATAF1, etc., are involved in these physiological processes. Here, we show that the SNAC-A TF ANAC032 also plays important roles in this process. The overexpression of ANAC032 inhibits photosynthesis and induces reactive oxygen species accumulation in chloroplasts, thereby reducing sugar accumulation and resulting in carbon starvation. ANAC032 reprograms carbon and nitrogen metabolism by increasing sugar and amino acid catabolism in plants. The ChIP-qPCR and transient dual-luciferase reporter assays indicated that ANAC032 regulates trehalose metabolism via the direct regulation of TRE1 expression. Taken together, these results show that ANAC032 is an important regulator of the carbon/energy status that represses photosynthesis to induce carbon starvation.

Identification of genes associated with ricinoleic acid accumulation in Hiptage benghalensis via transcriptome analysis.

BACKGROUND: Ricinoleic acid is a high-value hydroxy fatty acid with broad industrial applications. Hiptage benghalensis seed oil contains a high amount of ricinoleic acid (~ 80%) and represents an emerging source of this unusual fatty acid. However, the mechanism of ricinoleic acid accumulation in H. benghalensis is yet to be explored at the molecular level, which hampers the exploration of its potential in ricinoleic acid production. RESULTS: To explore the molecular mechanism of ricinoleic acid biosynthesis and regulation, H. benghalensis seeds were harvested at five developing stages (13, 16, 19, 22, and 25 days after pollination) for lipid analysis. The results revealed that the rapid accumulation of ricinoleic acid occurred at the early-mid-seed development stages (16-22 days after pollination). Subsequently, the gene transcription profiles of the developing seeds were characterized via a comprehensive transcriptome analysis with second-generation sequencing and single-molecule real-time sequencing. Differential expression patterns were identified in 12,555 transcripts, including 71 enzymes in lipid metabolic pathways, 246 putative transcription factors (TFs) and 124 long noncoding RNAs (lncRNAs). Twelve genes involved in diverse lipid metabolism pathways, including fatty acid biosynthesis and modification (hydroxylation), lipid traffic, triacylglycerol assembly, acyl editing and oil-body formation, displayed high expression levels and consistent expression patterns with ricinoleic acid accumulation in the developing seeds, suggesting their primary roles in ricinoleic acid production. Subsequent co-expression network analysis identified 57 TFs and 35 lncRNAs, which are putatively involved in the regulation of ricinoleic acid biosynthesis. The transcriptome data were further validated by analyzing the expression profiles of key enzyme-encoding genes, TFs and lncRNAs with quantitative real-time PCR. Finally, a network of genes associated with ricinoleic acid accumulation in H. benghalensis was established. CONCLUSIONS: This study was the first step toward the understating of the molecular mechanisms of ricinoleic acid biosynthesis and oil accumulation in H. benghalensis seeds and identified a pool of novel genes regulating ricinoleic acid accumulation. The results set a foundation for developing H. benghalensis into a novel ricinoleic acid feedstock at the transcriptomic level and provided valuable candidate genes for improving ricinoleic acid production in other plants.

Comparative physiological responses and transcriptome analysis reveal the roles of melatonin and serotonin in regulating growth and metabolism in Arabidopsis.

BACKGROUND: Melatonin and serotonin are well-known signaling molecules that mediate multiple physiological activities in plants, including stress defense, growth, development, and morphogenesis, but their underlying mechanisms have not yet been thoroughly elucidated. In this study, we investigated the roles of melatonin and serotonin in modulating plant growth and defense by integrating physiological and transcriptome analyses in Arabidopsis. RESULTS: Moderate concentrations of melatonin and serotonin did not affect primary root (PR) growth but markedly induced lateral root (LR) formation. Both melatonin and serotonin locally induced the expression of the cell-wall-remodeling-related genes LBD16 and XTR6, thereby inducing LR development. Our data support the idea that melatonin and serotonin lack any auxin-like activity. Treatment with 50 µM serotonin significantly improved PSII activity, and the transcriptome data supported this result. Melatonin and serotonin slightly affected glycolysis and the TCA cycle; however, they markedly regulated the catabolism of several key amino acids, thereby affecting carbon metabolism and energy metabolism. Melatonin and serotonin improved iron (Fe) deficiency tolerance by inducing Fe-responsive gene expression. CONCLUSIONS: Overall, our results from the physiological and transcriptome analyses reveal the roles of melatonin and serotonin in modulating plant growth and stress responses and provide insight into novel crop production strategies using these two phytoneurotransmitters.

Involvement of reactive oxygen species and auxin in serotonin-induced inhibition of primary root elongation.

The well-known neurotransmitter 5-hydroxytryptamine (serotonin) not only regulates sleep and mood in humans and animals but may also play important roles in modulating growth, development, and defense responses, such as seed germination, flowering, and abiotic stress tolerance, in plants. Serotonin inhibits primary root (PR) growth; however, the physiological and molecular mechanisms underlying serotonin-mediated PR growth inhibition remain largely unclear. Here, we investigate the effects of serotonin on root growth and development in Arabidopsis. Serotonin inhibits PR elongation by affecting both the meristem and elongation zones. In the meristem zone, serotonin represses both meristem cell division potential and stem cell niche activity. Serotonin induces H2O2 overaccumulation in the elongation zone and reduces O2- accumulation in the meristem zone by a UPB1 pathway, thereby disrupting reactive oxygen species (ROS) equilibrium in root tips, thus resulting in PR growth inhibition. Serotonin also regulates auxin distribution in root tips by decreasing auxin-related gene expression and repressing auxin transport through modulation of AUX1 and PIN2 abundances in root tips. Taken together, our data indicate that high concentrations of serotonin result in stress responses in plants by inhibiting PR elongation through the regulation of H2O2 and O2- distribution in PR tips and through an auxin pathway via the repression of auxin biosynthesis and transport.

UV-B Radiation Induces Root Bending Through the Flavonoid-Mediated Auxin Pathway in Arabidopsis.

Ultraviolet (UV)-B radiation-induced root bending has been reported; however, the underlying mechanisms largely remain unclear. Here, we investigate whether and how auxin and flavonoids are involved in UV-B radiation-induced root bending in Arabidopsis using physiological, pharmacological, and genetic approaches. UV-B radiation modulated the direction of root growth by decreasing IAA biosynthesis and affecting auxin distribution in the root tips, where reduced auxin accumulation and asymmetric auxin distribution were observed. UV-B radiation increased the distribution of auxin on the nonradiated side of the root tips, promoting growth and causing root bending. Further analysis indicated that UV-B induced an asymmetric accumulation of flavonoids; this pathway is involved in modulating the accumulation and asymmetric distribution of auxin in root tips and the subsequent redirection of root growth by altering the distribution of auxin carriers in response to UV-B radiation. Taken together, our results indicate that UV-B radiation-induced root bending occurred through a flavonoid-mediated phototropic response to UV-B radiation.

Lanthanum Inhibits Primary Root Growth by Repressing Auxin Carrier Abundances in Arabidopsis.

Lanthanum (La) is one of rare earth elements that was used as a crop growth stimulants; however, high concentration of La markedly inhibited plant growth. Our previous study indicated that, although La induced the expression of auxin biosynthesis-related genes, it markedly repressed primary root (PR) elongation by reducing auxin accumulation in PR tips. In this study, we exhibited that La reduces the abundances of auxin carriers. Treatment with La markedly inhibited the auxins IAA-, 2,4-D-, and NAA-induced elevation of DR5:GUS activity in the roots, suggesting that La inhibited auxin transport through both the influx and efflux transporters. Supplementation with auxin transport inhibitor naphthylphthalamic acid in La-treated seedlings did not further reduce PR growth compared with that of the La treatment alone, further confirmed that auxin transport is involved in La-induced inhibition of PR growth. Analysis of the protein abundances using the transgenic AUX1-YFP and PIN1/2/4/7-GFP marker lines indicated that La treatment reduced the abundances of all these auxin carriers in the PR tips. La also increased the stabilization of Aux/IAA protein AXR3. Taken together, these results indicated that La treatment inhibits PIN-mediated auxin transport and subsequently impairs auxin distribution and PR growth via reducing auxin carrier abundances.

Hydrogen sulfide toxicity inhibits primary root growth through the ROS-NO pathway.

High concentrations of hydrogen sulfide (H2S) are toxic to plants and inhibit their growth. Previous research indicated that high concentrations of H2S modulate the root system architecture (RSA) by affecting auxin transport; however, the signaling pathway underlying this process remains unclear. Here, we investigated the effects of exogenous sodium hydrosulfide (NaHS), an H2S donor, on primary root (PR) growth in Arabidopsis using pharmacological, physiological, and genetic approaches. H2S toxicity repressed PR growth by triggering a signal transduction pathway involving reactive oxygen species (ROS) accumulation, MITOGEN-ACTIVATED PROTEIN KINASE 6 (MPK6) activation, and nitric oxide (NO) production. Respiratory burst oxidase homolog mutants and an NO synthase mutant were less sensitive to NaHS, suggesting that both ROS and NO mediate the inhibitory effects of H2S on PR growth. We found that exogenous H2S-activated ROS production was required for NO generation and that MPK6 mediated H2S-induced NO production. MPK6 was shown to function downstream of ROS and upstream of NO. Finally, we demonstrated that exogenous H2S repressed the distribution of auxin and reduced the meristematic cell division potential in root tips, and NO was involved in this process.

Manganese Toxicity Inhibited Root Growth by Disrupting Auxin Biosynthesis and Transport in Arabidopsis.

Mn toxicity inhibits both primary root (PR) growth and lateral root development. However, the mechanism underlying Mn-mediated root growth inhibition remains to be further elucidated. Here, we investigated the role of auxin in Mn-mediated inhibition of PR growth in Arabidopsis using physiological and genetic approaches. Mn toxicity inhibits PR elongation by reducing meristematic cell division potential. Mn toxicity also reduced auxin levels in root tips by reducing IAA biosynthesis and down-regulating the expression of auxin efflux carriers PIN4 and PIN7. Loss of function pin4 and pin7 mutants showed less inhibition of root growth than col-0 seedlings. These results indicated that this inhibitory effect of Mn toxicity on PR growth was mediated by affecting auxin biosynthesis and the expression of auxin efflux transporters PIN4 and PIN7.