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Background: Opioid-free anesthesia (OFA) is increasing being explored due to increased awareness of opioid related adverse events and the national opioid crisis. The objective of this study was to examine the feasibility of Dexmedetomidine-Esketamine-Lidocaine OFA technique for patients diagnosed with breast begin mass underwent Lumpectomy, especially paying attention to its impact on postoperative pain, intraoperative hemodynamic parameters, recovery quality, and adverse events. Methods: In this prospective, randomized study, sixty patients who aged from 20 to 60 years, graded with American Society of Anesthesiologists physical status I or II, diagnosed with breast begin mass and scheduled to undergo Lumpectomy were enrolled. These patients were randomized to receive either OFA (OFA group) or opioid-based (OA group) anesthesia. Dexmedetomidine-Esketamine-Lidocaine or Sufentanil-Remifentanil was administered for induction and maintenance in OFA group or OA group, respectively. Postoperative visual analog scale (VAS) pain score at 2 h, 12 h, and 24 h after extubation was recorded. Intraoperative hemodynamic parameters were recorded at the following time points: entering operating room (T0), immediately after induction of anesthesia (T1), immediately after intubation (T2), 1 minute after surgical incision (T3), 5 minutes after surgical incision (T4), and 10 minutes after surgical incision (T5). Number of rescue analgesics used, rescue vasoactive drugs required, awakening time and recovery time of orientation, and incidence of adverse events were recorded as well. Results: The VAS score at 2, 12, and 24 h after extubation and number of rescue hydromorphone required (0 of 30 [0%] versus 0 of 30 [0%]) had no statistically significant difference between the two groups. The mean arterial pressure and heart rate at T1, T2, T3, T4, T5 were significantly lower in OA group than that in OFA group. The number of rescue ephedrine (1 of 30 [3.3%] versus 12 of 30 [40%], P=0.001) and rescue atropine (2 of 30 [6.7%] versus 6 of 30 [20%], P=0.038) were significantly lower in OFA group compared with OA group. Postoperative nausea and vomiting (3 of 30 [10%] versus 16 of 30 [53%], P=0.001) and application of rescue ondansetron (1 of 30 [3.3%] versus 10 of 30 [33%], P=0.003) were both less in the OFA group compared to those in OA group. However, compared with OA group, patients in OFA group had a longer awakening time ([7.27±2.85] min versus [4.47±1.11] min, P=0.000), longer recovery time of orientation ([11.97±3.19] min versus [6.93±1.17] min, P=0.000), higher analgesia-related drug cost ([$23.89±4.20] versus [ $21.31±3.94], P=0.017). Conclusions: The combination of Dexmedetomidine-Esketamine-Lidocaine OFA technique may be an alternative anesthesia for lumpectomy as better hemodynamic stability, lower incidence of postoperative nausea and vomiting, and adequate postoperative analgesia compared with OBA. But the traditional OA technique has shorter awakening time, shorter recovery time of orientation and lower analgesia-related cost.

Salicylic acid (SA) acts antagonistically to jasmonic acid (JA) in plant immunity. We previously reported that CATALASE2 (CAT2) promotes JA‐biosynthetic acyl‐CoA oxidase (ACX) activity to enhance plant resistance to necrotrophic Botrytis cinerea, and SA represses JA biosynthesis through inhibiting CAT2 activity, while the underlying mechanism remains to be further elucidated. Here, we report that the truncated CAT2 N‐terminus (CAT2‐N) interacts with and promotes ACX2/3, and CAT2‐N‐overexpressing plants have increased JA accumulation and enhanced resistance to B. cinerea B05.10, but compromised antagonism of SA on JA. Catalase inhibitor treatment or mutating CAT2 active amino acids abolished CAT2 H2O2‐decomposing activity but did not affect its promotion of ACX2/3 activity via interaction. CAT2‐N, a truncated protein with no catalase activity, interacted with and promoted ACX2/3. Overexpressing CAT2‐N in Arabidopsis plants resulted in increased ACX activity, higher JA accumulation, and stronger resistance to B. cinerea B05.10 infection. Additionally, SA dramatically repressed JA biosynthesis and resistance to B. cinerea in the wild type but not in the CAT2‐N‐overexpressing plants. Together, our study reveals that CAT2‐N can be utilized as an accelerator for JA biosynthesis during plant resistance to B. cinerea B05.10, and this truncated protein partly relieves SA repression of JA biosynthesis in plant defence responses., N‐terminal fragment of CATALASE2 interacts with and promotes acyl‐CoA oxidases implicated in JA biosynthesis and enhances plant resistance to Botrytis cinerea, thus CATALASE2‐N could be a genetic tool conferring plant resistance.

The inhibitory ability of Fokienia hodginsii heartwood (FHH) extracts on Trametes versicolor (TV) and Gloeophyllum trabeum (GT) as well as the toxic effect of its heartwood extracts on GT were studied. The growth inhibition ability of the samples was analyzed using the growth rate method. The results showed that in the experiment of inhibiting TV, extracts using hot water had little effect, acetone extracts had the best inhibiting effect, and the lowest value of acetone EC50 was 0.409 g/L. The parameter EC50 is the concentration of the corresponding agent that inhibits the growth of 50% fungi. In the antifungal experiment of GT, methanol extract had the best inhibition effect, and the lowest EC50 value was 0.283 g/L. The antifungal effect of five solvent extracts of FHH was good when the concentration was 10% (w/w), and at this time, the mass loss rate of the test pieces was below 11%, all of them were Class I, indicating a strong antifungal level. After observing the samples of GT with SEM, it was found that the structure of methanol extract treatment was more complete and the antiseptic effect was better than that of the hot water extract treatment.

Transthoracic echocardiographic evaluation of the right ventricle is more difficult than the left ventricle and has not been well characterised in the parturient during delivery. As a preliminary investigation, our goal was to use bedside transthoracic echocardiography to evaluate right ventricular myocardial function before and after caesarean delivery. Term parturients undergoing caesarean delivery under spinal anaesthesia were enrolled. Echocardiography was performed pre- and postoperatively. Assessment of myocardial function included longitudinal myocardial strain using 2D-speckle tracking for both ventricles, and fractional area change for the right ventricle. Troponin-T, creatine kinase-muscle/brain and brain natriuretic peptide were measured pre- and postoperatively. One hundred patients were enrolled; 98 completed the study. Adequate images from both timepoints (pre- and postoperatively) were obtained in 85 patients for left ventricle assessment, and 66 for the right ventricle. Right ventricular fractional area change (mean (standard deviation)) (24.9% (8.9%) to 24.9% (9.2%); P = 0.99) and strain (−19.7% (6.8%) to −18.1% (6.5%); P = 0.08) measurements suggested mild baseline dysfunction and did not change after delivery. Left ventricular strain values were normal and unchanged after delivery (−23.8% (7.4%) to −24.3% (6.7%); P = 0.51). One patient had elevated troponin-T and demonstrated worse biventricular function. Elevation of brain natriuretic peptide ( n=7) was associated with mildly decreased left ventricular strain, but creatine kinase-muscle/brain ( n=4) was not associated with consistent changes in cardiac function. Further investigations into peripartum right ventricular function are required to validate the findings in this preliminary study. Findings of baseline mild right ventricular dysfunction and functional changes associated with troponin-T and brain natriuretic peptide warrant rigorous investigation.

H

Magnesium (Mg) is an essential metal for chlorophyll biosynthesis and other metabolic processes in plant cells. Mg is largely stored in the vacuole of various cell types and remobilized to meet cytoplasmic demand. However, the transport proteins responsible for mobilizing vacuolar Mg2+ remain unknown. Here, we identified two Arabidopsis (Arabidopsis thaliana) Mg2+ transporters (MAGNESIUM TRANSPORTER 1 and 2; MGT1 and MGT2) that facilitate Mg2+ mobilization from the vacuole, especially when external Mg supply is limited. In addition to a high degree of sequence similarity, MGT1 and MGT2 exhibited overlapping expression patterns in Arabidopsis tissues, implying functional redundancy. Indeed, the mgt1 mgt2 double mutant, but not mgt1 and mgt2 single mutants, showed exaggerated growth defects as compared to the wild type under low-Mg conditions, in accord with higher expression levels of Mg-starvation gene markers in the double mutant. However, overall Mg level was also higher in mgt1 mgt2, suggesting a defect in Mg2+ remobilization in response to Mg deficiency. Consistently, MGT1 and MGT2 localized to the tonoplast and rescued the yeast (Saccharomyces cerevisiae) mnr2Δ (manganese resistance 2) mutant strain lacking the vacuolar Mg2+ efflux transporter. In addition, disruption of MGT1 and MGT2 suppressed high-Mg sensitivity of calcineurin B-like 2 and 3 (cbl2 cbl3), a mutant defective in vacuolar Mg2+ sequestration, suggesting that vacuolar Mg2+ influx and efflux processes are antagonistic in a physiological context. We further crossed mgt1 mgt2 with mgt6, which lacks a plasma membrane MGT member involved in Mg2+ uptake, and found that the triple mutant was more sensitive to low-Mg conditions than either mgt1 mgt2 or mgt6. Hence, Mg2+ uptake (via MGT6) and vacuolar remobilization (through MGT1 and MGT2) work synergistically to achieve Mg2+ homeostasis in plants, especially under low-Mg supply in the environment.

Low temperature is a key factor limiting the rubber plantation extending to high latitude area. Previous work has shown that cold-induced DNA demethylation was coordinated with the expression of cold-responsive (

Low temperature remarkably limits rubber tree (Hevea brasiliensis Muell. Arg.) growth, latex production, and geographical distribution, but the underlying mechanisms of Hevea brasiliensis cold stress response remain elusive. Here, we identified HbSnRK2.6 as a key component in ABA signaling functions in phytohormone abscisic acid (ABA)-regulated cold stress response in Hevea brasiliensis. Exogenous application of ABA enhances Hevea brasiliensis cold tolerance. Cold-regulated (COR) genes in the CBF pathway are upregulated by ABA. Transcript levels of all five HbSnRK2.6 members are significantly induced by cold, while HbSnRK2.6A, HbSnRK2.6B, and HbSnRK2.6C can be further activated by ABA under cold conditions. Additionally, HbSnRK2.6s are localized in the cytoplasm and nucleus, and can physically interact with HbICE2, a crucial positive regulator in the cold signaling pathway. Overexpression of HbSnRK2.6A or HbSnRK2.6B in Arabidopsis extensively enhances plant responses to ABA and expression of COR genes, leading to increased cold stress tolerance. Furthermore, HbSnRK2.6A and HbSnRK2.6B can promote transcriptional activity of HbICE2, thus, increasing the expression of HbCBF1. Taken together, we demonstrate that HbSnRK2.6s are involved in ABA-regulated cold stress response in Hevea brasiliensis by regulating transcriptional activity of HbICE2.

An ICE-like transcription factor mediates jasmonate-regulated cold tolerance in the rubber tree (Hevea brasiliensis), and confers cold tolerance in transgenic Arabidopsis. The rubber tree (Hevea brasiliensis) is susceptible to low temperatures, and understanding the mechanisms regulating cold stress is of great potential value for enhancing tolerance to this environmental variable. In this study, we find that treatment with exogenous methyl jasmonate (MeJA) could significantly enhance Hevea brasiliensis cold tolerance. In addition, yeast two-hybrid and bimolecular fluorescence complementation (BiFC) experiments show that JASMONATE ZIM-DOMAIN(JAZ) proteins, HbJAZ1 and HbJAZ12, key repressors of JA signaling pathway, interact with HbICE2, a novel ICE (Inducer of CBF Expression)-like protein. HbICE2 was nuclear-localised and bound to the MYC recognition (MYCR) sequence. The transcriptional activation activity of HbICE2 in yeast cells was dependent on the N-terminus, and overexpression of HbICE2 in Arabidopsis resulted in elevated tolerance to chilling stress. Furthermore, dual-luciferase transient assay reveals that HbJAZ1 and HbJAZ12 proteins inhibit the transcriptional function of HbICE2. The expression of C-repeat-binding factor (CBF) signalling pathway genes including HbCBF1, HbCBF2 and HbCOR47 were up-regulated by MeJA. Taken together, our data suggest that the new ICE-like transcription factor HbICE2 is involved in jasmonate-regulated cold tolerance in Hevea brasiliensis.

Maternal immune activation (MIA) during pregnancy is considered a risk factor for neurodevelopment in the offspring, resulting in behavioral abnormalities. Furthermore, adolescence is a vulnerable period for developing different psycho-cognitive deficits. Here, we aimed to observe the cognitive consequences of prenatal MIA exposure in adolescents and explored the underlying mechanisms. We divided dams into CON and MIA groups after inducing a mouse model of MIA using lipopolysaccharide (120 μg/kg) on gestational day 15. Open field (OF), elevated plus maze (EPM), and novel object recognition (NOR) tests were performed on postnatal day (PD) 35-37. The expression of hippocampal Wisteria floribunda agglutinin (WFA)

Systemic inflammation induces cognitive impairment, yet the mechanism involved in this process is unclear. Neurotrophin receptor p75 (p75NTR) signaling is a key pathological factor contributing to neurobehavioral abnormalities in many neurodegenerative diseases. However, the role of p75NTR signaling in the regulation of sepsis-induced cognitive impairment remains largely to be elucidated. In this study, systemic inflammation was induced by cecal ligation and puncture (CLP). Neurobehavioral performances were evaluated by open field, novel object recognition, and fear conditioning tests. The expressions of proinflammatory cytokines (tumor necrosis factor (TNF-α), interleukin-1β (IL-1β), IL-6, IL-10), apoptosis marker cleaved caspase-3, ionized calcium binding adaptor molecule 1 (IBA1), proBDNF, p75NTR, c-Jun N-terminal kinase (JNK), and pJNK in the hippocampus were determined by enzyme-linked immunosorbent assay, western blot analysis, and immunofluorescence. The synaptic marker in the CA1 region of the hippocampus was assessed by Golgi staining. In the present study, we showed that systemic inflammation induced cognitive impairment, which was accompanied by increased expressions of hippocampcal proBDNF and p75NTR. Of note, we found that LM11A-31, an orally available, blood-brain barrier-permeant small-molecule p75NTR signaling modulator significantly reversed the sepsis-induced cognitive impairment and restored most of the abnormal biochemical parameters. Taken together, our study suggests that proBDNF/p75NTR signaling pathway might play a key role in the development of sepsis-induced cognitive impairment, whereas specific p75NTR inhibitor may provide a novel therapeutic approach for this disorder and possible other neurodegenerative diseases.

Increased fatty acid β-oxidation is essential for early postgerminative growth in seedlings, but high levels of H2 O2 produced by β-oxidation can induce oxidative stress. Whether and how catalase (CAT) functions in fine-tuning H2 O2 homeostasis during seedling growth remain unclear. Here, we report that CAT2 functions in early seedling growth. Compared to the wild type, the cat2-1 mutant, with elevated H2 O2 levels, exhibited reduced root elongation on sucrose (Suc)-free medium, mimicking soils without exogenous sugar supply. Treatment with the H2 O2 scavenger potassium iodide rescued the mutant phenotype of cat2-1. In contrast to the wild type, the cat2-1 mutant was insensitive to the CAT inhibitor 3-amino-1,2,4-triazole in terms of root elongation when grown on Suc-free medium, suggesting that CAT2 modulates early seedling growth by altering H2 O2 accumulation. Furthermore, like cat2-1, the acyl-CoA oxidase (ACX) double mutant acx2-1 acx3-6 showed repressed root elongation, suggesting that CAT2 functions in early seedling growth by regulating ACX activity, as this activity was inhibited in cat2-1. Indeed, decreased ACX activity and short root of cat2-1 seedlings grown on Suc-free medium were rescued by overexpressing ACX3. Together, these findings suggest that CAT2 functions in early seedling growth by scavenging H2 O2 and stimulating ACX2/3 activity.

// Mu-Huo Ji 1, * , Hui Tang 2, * , Dan Luo 1 , Li-Li Qiu 1 , Min Jia 2 , Hong-Mei Yuan 3 , Shan-Wu Feng 3 and Jian-Jun Yang 1 1 Department of Anesthesiology, Zhongda Hospital, Medical School, Southeast University, Nanjing, China 2 Department of Anesthesiology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, China 3 Department of Anesthesiology, Obstetrics and Gynecology Hospital Affiliated to Nanjing Medical University, Nanjing, China * These authors have contributed equally to this work Correspondence to: Shan-Wu Feng, email: shanwufeng@163.com Jian-Jun Yang, email: yjyangjj@126.com Keywords: sepsis, environmental conditions, neuroplasticity, cognitive function Received: February 24, 2017 Accepted: June 18, 2017 Published: July 26, 2017 ABSTRACT Brain dysfunction remains a common complication after sepsis development and is an independent risk factor for a poorer prognosis and an increased mortality. Here we tested the hypothesis that the behavioral outcomes after lipopolysaccharides (LPS) administration are exacerbated by an impoverished environment (IE) and alleviated by an enriched environment (EE), respectively. Mice were randomly allocated in a standard environment (SE), an EE, or an IE for 4 weeks after LPS or normal saline (NS) administration. Neurobehavioral alternations were assessed by the open field, novel objective recognition, and fear conditioning tests. The expressions of proinflammatory cytokines (tumor necrosis factor (TNF-α), interleukin-1β (IL-1β), IL-6, IL-10), ionized calcium-binding adaptor molecule-1 (IBA1)-positive cells as well as glial fibrillary acidic protein (GFAP)-positive cells, brain derived neurotrophic factor (BDNF), 5-bromo-2-deoxyuridine-labeled cells in the dentate gyrus of the hippocampus, and the number of dendritic spines in the hippocampal CA1 were determined. Our results showed that the some of the neurocognitive abnormalities induced by LPS administration can be aggravated by stressful conditions such as IE but alleviated by EE. These neurocognitive alternations were accompanied by significant changes in biomarkers of immune response and hippocampal synaptic plasticity. In summary, our study confirmed the negative impact of IE and the positive effects of EE on the cognitive function after LPS administration, with potential implications to the basis of sepsis-related cognitive impairments in the critically ill patients.

Sepsis-associated encephalopathy (SAE) is a potentially irreversible acute cognitive dysfunction with unclear mechanism. Striatal-enriched protein tyrosine phosphatase (STEP) is a brain-specific phosphatase which normally opposes synaptic strengthening by regulating key signaling molecules involved in synaptic plasticity and neuronal function. Thus, we hypothesized that abnormal STEP signaling pathway was involved in sepsis-induced cognitive impairment evoked by lipopolysaccharides (LPS) injection. The levels of STEP, phosphorylation of GluN2B (pGluN2B), the kinases extracellular signal-regulated kinase 1/2 (pERK), cAMP-response element binding protein (CREB), synaptophysin, brain derived neurotrophic factor (BDNF), and post-synaptic density protein 95 (PSD95) in the hippocampus, prefrontal cortex, and striatum were determined at the indicated time points. In the present study, we found that STEP levels were significantly increased in the hippocampus, prefrontal cortex, and striatum following LPS injection, which might resulted from the disruption of the ubiquitin-proteasome system. Notably, a STEP inhibitor TC-2153 treatment alleviated sepsis-induced memory impairment by increasing phosphorylation of GluN2B and ERK1/2, CREB/BDNF, and PSD95. In summary, our results support the key role of STEP in sepsis-induced memory impairment in a mouse model of SAE, whereas inhibition of STEP may provide a novel therapeutic approach for this disorder and possible other neurodegenerative diseases.

To improve the reuse rate of bamboo materials, laminated bamboo lumber (LBL) with high bond strength has been developed for structural use using bamboo residues (BRs). The laminated structure design is an important factor affecting LBL performance, and thus, it is essential to study various LBL blank structures. The major direction is parallel to the panel length, and the minor direction is perpendicular to the panel length. In this study, BRs were cut into A and B units along the major and minor directions, respectively. The LBL with good performance was selected by different forming methods and modified by O2 plasma. It was found that 1) the volume utilization rate of BRs in LBL is above 85%; 2) the wet bonding strength of LBL products is increased by 58.58% compared to ordinary plywood, when the O2 plasma modification time is 6 min and 12 min respectively, the wet bonding strength is increased by 75.69% and 76.27% compared to ordinary plywood; 3) when bamboo pieces are arranged in parallel, the modulus of rupture in the major direction is ~ 2 times greater than in the minor direction, while a staggered arrangement can effectively reduce the bamboo anisotropic effect; 4) the destruction of LBL mainly occurs at the joints; 5) after O2 plasma modification, the wettability of green bamboo and yellow bamboo was significantly improved, followed by bamboo flesh.

Nitric oxide (NO) generation by NO synthase (NOS) in guard cells plays a vital role in stomatal closure for adaptive plant response to drought stress. However, the mechanism underlying the regulation of NOS activity in plants is unclear. Here, by screening yeast deletion mutants with decreased NO accumulation and NOS-like activity when subjected to H2 O2 stress, we identified TUP1 as a novel regulator of NOS-like activity in yeast. Arabidopsis WD40-REPEAT 5a (WDR5a), a homolog of yeast TUP1, complemented H2 O2 -induced NO accumulation of a yeast mutant Δtup1, suggesting the conserved role of WDR5a in regulating NO accumulation and NOS-like activity. This note was further confirmed by using an Arabidopsis RNAi line wdr5a-1 and two T-DNA insertion mutants of WDR5a with reduced WDR5a expression, in which both H2 O2 -induced NO accumulation and stomatal closure were repressed. This was because H2 O2 -induced NOS-like activity was inhibited in the mutants compared with that of the wild type. Furthermore, these wdr5a mutants were more sensitive to drought stress as they had reduced stomatal closure and decreased expression of drought-related genes. Together, our results revealed that WDR5a functions as a novel factor to modulate NOS-like activity for changes of NO accumulation and stomatal closure in drought stress tolerance.

Post-traumatic stress disorder (PTSD) is a common psychiatric disease following exposure to a severe traumatic event or physiological stress, yet the precise mechanisms underlying PTSD remains largely to be determined. Using an animal model of PTSD induced by a single prolonged stress (SPS), we assessed the role of hippocampal nicotinamide adenosine dinucleotide phosphate (NADPH) oxidase 2 (NOX2) and parvalbumin (PV) interneurons in the development of PTSD symptoms. In the present study, behavioral tests were performed by the open field (day 13 after SPS) and fear conditioning tests (days 13 and 14 after SPS). For the interventional study, rats were chronically treated with a NADPH oxidase inhibitor apocynin either by early or delayed administration. The levels of tumor necrosis factor-alpha, interleukin (IL)-1β, IL-6, IL-10, malondialdehyde, superoxide dismutase, NOX2, 4-hydroxynonenal, and PV in the hippocampus were measured at the indicated time points. In the present study, we showed that SPS rats displayed anxiety-like and enhanced fear learning behavior, which was accompanied by the increased expressions of malondialdehyde, IL-6, NOX2, 4-hydroxynonenal, and decreased PV expression. Notably, early but not delayed treatment with apocynin reversed all these abnormalities after SPS. In conclusion, our results provided evidence that NOX2 activation in the hippocampus, at least in part, contributes to oxidative stress and neuroinflammation, which further results in PV interneuron loss and consequent PTSD symptoms in a rat model of PTSD induced by SPS.

The root is the first plant organ to get in contact with the toxin cadmium (Cd), which is a widespread soil contaminant. Cd inhibits the growth of the primary root, but the mechanisms underlying this inhibition remain elusive. In this study, we used physiological, pharmacological and genetic approaches to investigate the roles of nitric oxide (NO) and auxin in Cd-mediated inhibition of Arabidopsis thaliana root meristem growth. Our study demonstrated that in the first 12 h of exposure, Cd inhibits primary root elongation through a decrease in the sizes of both the elongation and meristematic zones. Following Cd exposure, a decrease in auxin levels is associated with reduced PIN1/3/7 protein accumulation, but not with reduced PIN1/3/7 transcript levels. Additionally, Cd stabilized AXR3/IAA17 protein to repress auxin signalling in this Cd-mediated process. Furthermore, decreasing Cd-induced NO accumulation with either NO-specific scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO) or NO synthase inhibitor Nω-nitro-l-Arg-methylester (l-NAME) compromised the Cd-mediated inhibition of root meristem development, reduction in auxin and PIN1/3/7 accumulation, as well as stabilization of AXR3/IAA17, indicating that NO participates in Cd-mediated inhibition of root meristem growth. Taken together, our data suggest that Cd inhibits root meristem growth by NO-mediated repression of auxin accumulation and signalling in Arabidopsis.

Rubber trees (Hevea brasiliensis) were successfully introduced to south China in the 1950s on a large-scale; however, due to the climate, are prone to cold injury during the winter season. Increased cold tolerance is therefore an important goal, yet the mechanism underlying rubber tree responses to cold stress remains unclear. This study carried out functional characterization of HbICE1 (Inducer of CBF Expression 1) from H. brasiliensis. A nucleic protein with typical features of ICEs, HbICE1 was able to bind to MYC recognition sites and had strong transactivation activity. HbICE1 was constitutively expressed in all tested tissues, with highest levels in the bark, and was up-regulated when subjected to various stresses including cold, dehydration, salinity and wounding. When overexpressed in Arabidopsis, 35S::HbICE1 plants showed enhanced cold resistance with increased proline content, reduced malondialdehyde (MDA) metabolism and electrolyte leakage, and decreased reactive oxygen species (ROS) accumulation. Expression of the cold responsive genes (COR15A, COR47, RD29A, and KIN1) was also significantly promoted in 35S::HbICE1 compared to wild-type plants under cold stress. Differentially expressed genes (DEGs) analysis showed that cold treatment changed genes expression profiles involved in many biological processes and phytohormones perception and transduction. Ethylene, JA, ABA, as well as ICE-CBF signaling pathways might work synergistically to cope with cold tolerance in rubber tree. Taken together, these findings suggest that HbICE1 is a member of the ICE gene family and a positive regulator of cold tolerance in H. brasiliensis.

Plants defend against pathogen attack by modulating auxin signaling and activating the salicylic acid (SA) and jasmonic acid (JA) signaling pathways. SA and JA act antagonistically in resistance to specific pathogen types, yet how plants coordinate these phytohormones remains elusive. Here we report that biotrophic-pathogen-induced SA accumulation dampens both auxin and JA synthesis by inhibiting CATALASE2 (CAT2) activity in the model plant Arabidopsis. SA suppression of CAT2 results in increased H2O2 levels and subsequent sulfenylation of tryptophan synthetase β subunit 1, thus depleting the auxin biosynthetic precursor tryptophan. In addition, we find that CAT2 promotes JA biosynthesis by facilitating direct interaction of the JA biosynthetic enzymes ACX2 and ACX3, and thus SA repression of CAT2 inhibits JA accumulation. As such, the cat2-1 mutant exhibits increased resistance to biotrophic pathogens and increased susceptibility to necrotrophic pathogens. Our study illustrates how CAT2 coordinates SA repression of auxin accumulation and JA biosynthesis in plant defense.

Reason for Corrigendum: There was a mistake in the color of the arrow of Figure 1A as published. Red arrows should be white and white arrows should be red in Figure 1A. The corrected Figure ​Figure11 is below. The authors apologize for the mistake. This error does not change the scientific conclusions of the article in any way. Figure 1 Cytological observation of P. simonii × P. nigra PG and PTG. (A) DAPI fluorescence image of two-celled and three-celled pollen. (B,B′) Bright-field and DAPI fluorescence images of the two and three nuclei states in the tube; red arrows ...

Pollen tubes are an ideal model for the study of cell growth and morphogenesis because of their extreme elongation without cell division; however, the genetic basis of pollen germination and tube growth remains largely unknown. Using the Illumina/Solexa digital gene expression system, we identified 13,017 genes (representing 28.3% of the unigenes on the reference genes) at three stages, including mature pollen, hydrated pollen, and pollen tubes of Populus simonii × P. nigra. Comprehensive analysis of P. simonii × P. nigra pollen revealed dynamic changes in the transcriptome during pollen germination and pollen tube growth (PTG). Gene ontology analysis of differentially expressed genes showed that genes involved in functional categories such as catalytic activity, binding, transporter activity, and enzyme regulator activity were overrepresented during pollen germination and PTG. Some highly dynamic genes involved in pollen germination and PTG were detected by clustering analysis. Genes related to some key pathways such as the mitogen-activated protein kinase signaling pathway, regulation of the actin cytoskeleton, calcium signaling, and ubiquitin-mediated proteolysis were significantly changed during pollen germination and PTG. These data provide comprehensive molecular information toward further understanding molecular mechanisms underlying pollen germination and PTG.

Nitric oxide (NO) plays key roles in yeast responses to various environmental factors, such as H2O2 and high temperature. However, the gene encoding NO synthase (NOS) in yeast has not yet been identified, and the mechanism underlying the regulation of NOS-like activity is poorly understood. Here, we report on the involvement of CKA2 in H2O2-induced yeast apoptosis and yeast high-temperature stress tolerance. Our results showed that although Δcka2 mutant had reduced NO accumulation with decreased apoptosis after H2O2 exposure, treatment with a NO donor, sodium nitroprusside, resulted in similar survival rate of Δcka2 mutant compared to that of wild-type yeast when subjected to H2O2 stress. This finding occurred because H2O2-enhanced NOS-like activity in wild-type yeast was significantly repressed in Δcka2. Our additional experiments indicated that both high-temperature-enhanced NO accumulation and NOS-like activity were also suppressed in Δcka2, leading to the hypersensitivity of the mutant to high temperature in terms of changes in survival rate. Thus, our results showed that CKA2 functioned in H2O2-induced apoptosis and high-temperature stress tolerance by regulating NOS-like-dependent NO accumulation in yeast.