A fully automatic deep learning-based method for segmenting regions of interest and predicting renal function in pediatric dynamic renal scintigraphy.

OBJECTIVE: Accurate delineation of renal regions of interest (ROIs) is critical for the assessment of renal function in pediatric dynamic renal scintigraphy (DRS). The purpose of this study was to develop and evaluate a deep learning (DL) model that can fully automatically delineate renal ROIs and calculate renal function in pediatric 99mTechnetium-ethylenedicysteine (99mTc-EC) DRS. METHODS: This study retrospectively analyzed 1,283 pediatric DRS data at a single center from January to December 2018. These patients were divided into training set (n = 1027), validation set (n = 128), and testing set (n = 128). A fully automatic segmentation of ROIs (FASR) model was developed and evaluated. The pixel values of the automatically segmented ROIs were calculated to predict renal blood perfusion rate (BPR) and differential renal function (DRF). Precision, recall rate, intersection over union (IOU), and Dice similarity coefficient (DSC) were used to evaluate the performance of FASR model. Intraclass correlation (ICC) and Pearson correlation analysis were used to compare the consistency of automatic and manual method in assessing the renal function parameters in the testing set. RESULTS: The FASR model achieved a precision of 0.88, recall rate of 0.94, IOU of 0.83, and DSC of 0.91. In the testing set, the r values of BPR and DRF calculated by the two methods were 0.94 (P < 0.01) and 0.97 (P < 0.01), and the ICCs (95% confidence interval CI) were 0.94 (0.90-0.96) and 0.94 (0.91-0.96). CONCLUSION: We propose a reliable and stable DL model that can fully automatically segment ROIs and accurately predict renal function in pediatric 99mTc-EC DRS.

Drug recommendation for optimization on treatment outcome for MDR/RR-TB based on a multi-center, large scale, retrospective cohort study in China.

OBJECTIVE: With the change in drug-resistant pattern, MDR/RR-TB was faced with underlying changes in regimens. A multi-center, large-scale, retrospective study performed aims to provide a recommendation of drug selection on optimization of outcome for the patients. METHOD: The study was conducted in six TB-specialized hospitals in China. Patients were included from 2018-2021 and followed up throughout the treatment. Using a multivarariable and propensity score-matched logistic regression analysis, we evaluated associations between outcomes and drug use, as well as clinical characteritics. RESULTS: Of 3112 patients, 74.29% had treatment sucess, 14.52% lost to follow-up, 9.67% failure, and 1.51% died. Treatment success was positively associated with Bedaquiline(Bdq), Linezolid(Lzd), and Cycloserin(Cs). Capreomycin(Cm) increased the risk of unfavorable outcomes. other drugs such as Amikacin(Amk) and clofazimine had no significant effect on outcomes. If isolates were susceptible to fluoroquinolones(FQs), FQs could decrease the risk of unfavorable outcomes. CONCLUSIONS: The recommendation order for the treatment of MDR/RR-TB is Bdq, Lzd, and Cs. FQs were decreased in use intensity. Injection drugs, whether Amk or Cm, are not recommended.

Wounding induces a peroxisomal H2 O2 decrease via glycolate oxidase-catalase switch dependent on glutamate receptor-like channel-supported Ca2+ signaling in plants.

Sensing of environmental challenges, such as mechanical injury, by a single plant tissue results in the activation of systemic signaling, which attunes the plant's physiology and morphology for better survival and reproduction. As key signals, both calcium ions (Ca2+ ) and hydrogen peroxide (H2 O2 ) interplay with each other to mediate plant systemic signaling. However, the mechanisms underlying Ca2+ -H2 O2 crosstalk are not fully revealed. Our previous study showed that the interaction between glycolate oxidase and catalase, key enzymes of photorespiration, serves as a molecular switch (GC switch) to dynamically modulate photorespiratory H2 O2 fluctuations via metabolic channeling. In this study, we further demonstrate that local wounding induces a rapid shift of the GC switch to a more interactive state in systemic leaves, resulting in a sharp decrease in peroxisomal H2 O2 levels, in contrast to a simultaneous outburst of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-derived apoplastic H2 O2 . Moreover, the systemic response of the two processes depends on the transmission of Ca2+ signaling, mediated by glutamate-receptor-like Ca2+ channels 3.3 and 3.6. Mechanistically, by direct binding and/or indirect mediation by some potential biochemical sensors, peroxisomal Ca2+ regulates the GC switch states in situ, leading to changes in H2 O2 levels. Our findings provide new insights into the functions of photorespiratory H2 O2 in plant systemic acclimation and an optimized systemic H2 O2 signaling via spatiotemporal interplay between the GC switch and NADPH oxidases.

High CO2 facilitates fatty acid biosynthesis and mitigates cellular oxidative stress caused by CAC2 dysfunction in Arabidopsis.

Increasing concentration of CO2 has significant impacts on many biological processes in plants, and its impact is closely associated with changes in the ratio of photosynthesis to photorespiration. Studies have reported that high CO2 can promote carbon fixing and alleviate plant oxidative damage in response to environmental stresses. However, the effect of high CO2 on fatty acid (FA) metabolism and cellular redox balance in FA-deficient plants is rarely reported. In this study, we identified a high-CO2 -requiring mutant cac2 through forward genetic screening. CAC2 encodes biotin carboxylase, which is one of the subunits of plastid acetyl-CoA carboxylase and participates in de novo FA biosynthesis. Null mutation of CAC2 is embryonic lethal. A point mutation of CAC2 in cac2 mutants produces severe defects in chloroplast development, plant growth and photosynthetic performance. These morphological and physiological defects were largely absent under high CO2 conditions. Metabolite analyses showed that FA contents in cac2-1 leaves were decreased, while photorespiratory metabolites, such as glycine and glycolate, did not significantly change. Meanwhile, cac2 exhibited higher reactive oxygen species (ROS) levels and mRNA expression of stress-responsive genes than the wild-type, indicating that cac2 plants may suffer oxidative stress under ambient CO2 conditions. Elevated CO2 significantly increased FA contents, especially C18:3-FA, and reduced ROS accumulation in cac2-1 leaves. We propose that stress mitigation by high CO2 in cac2 could be due to increased FA levels by promoting carbon assimilation, and the prevention of over-reduction due to decreased photorespiration.

Comparisons of facial emotion recognition in different social contexts among patients with schizophrenia, major depressive disorder and bipolar disorder.

BACKGROUND: Previous studies have found that patients with schizophrenia (SCZ), major depressive disorder (MDD), and bipolar disorder (BD) all have facial emotion recognition deficits, but the differences and similarities of these deficits in the three groups of patients under different social interaction situations are not clear. The present study aims to compare the ability of facial emotion recognition in three different conversation situations from a cross-diagnostic perspective. METHODS: Thirty-three participants with SCZ, 35 participants with MDD, and 30 participants with BD were recruited, along with 31 healthy controls. A computer-based task was given to assess the ability of Facial Emotion Categorization (FEC) under three different conversational situations (praise, blame, and inquiry). RESULTS: In the "praise" situation, patients with SCZ, MDD and BD were all slower to recognize anger emotion than the healthy controls. In all three clinical groups, patients with SCZ recognized angry faces faster than those with MDD and BD on a continuum from happy faces to angry faces in the "inquiry" situation, while no significant difference was found in the latter two groups. In addition, no significant defect was found in the percentage and threshold of angry face recognition in all three patient groups. CONCLUSIONS: Our findings indicate that patients with SCZ, MDD, and BD share both common and distinct deficits in facial emotion recognition during social interactions, which may be beneficial for early screening and precise intervention for these mental disorders.

JMJ28 guides sequence-specific targeting of ATX1/2-containing COMPASS-like complex in Arabidopsis.

Despite extensive investigations in mammals and yeasts, the importance and specificity of COMPASS-like complex, which catalyzes histone 3 lysine 4 methylation (H3K4me), are not fully understood in plants. Here, we report that JMJ28, a Jumonji C domain-containing protein in Arabidopsis, recognizes specific DNA motifs through a plant-specific WRC domain and acts as an interacting factor to guide the chromatin targeting of ATX1/2-containing COMPASS-like complex. JMJ28 associates with COMPASS-like complex in vivo via direct interaction with RBL. The DNA-binding activity of JMJ28 is essential for both the targeting specificity of ATX1/2-COMPASS and the deposition of H3K4me at specific loci but exhibit functional redundancy with alternative COMPASS-like complexes at other loci. Finally, we demonstrate that JMJ28 is a negative regulator of plant immunity. In summary, our findings reveal a plant-specific recruitment mechanism of COMPASS-like complex. These findings help to gain deeper insights into the regulatory mechanism of COMPASS-like complex in plants.

The GluA1-Related BDNF Pathway Is Involved in PTSD-Induced Cognitive Flexibility Deficit in Attentional Set-Shifting Tasks of Rats.

Background: Post-Traumatic Stress Disorder (PTSD) is a severe psychological disorder characterized by intrusive thoughts, heightened arousal, avoidance, and flashbacks. Cognitive flexibility dysfunction has been linked with the emergence of PTSD, including response inhibition deficits and impaired attentional switching, which results in difficulties for PTSD patients when disengaging attention from trauma-related stimuli. However, the molecular mechanisms of cognitive flexibility deficits remain unclear. Methods: The animals were exposed to a single prolonged stress and electric foot shock (SPS&S) procedure to induce PTSD-like features. Once the model was established, the changes in cognitive flexibility were assessed using an attentional set-shifting task (ASST) in order to investigate the effects of traumatic stress on cognitive flexibility. Additionally, the molecular alterations of certain proteins (AMPA Receptor 1 (GluA1), brain-derived neurotrophic factor (BDNF), and Postsynaptic density protein 95 (PSD95) in the medial prefrontal cortex (mPFC) were measured using Western blot and immunofluorescence. Results: The SPS&S model exhibited PTSD-like behaviors and induced reversal learning and set-shifting ability deficit in the ASST. These behavioral changes are accompanied by decreased GluA1, BDNF, and PSD95 protein expression in the mPFC. Further analysis showed a correlative relationship between the behavioral and molecular alterations. Conclusions: The SPS&S model induced cognitive flexibility deficits, and the potential underlying mechanism could be mediated by GluA1-related BDNF signaling in the mPFC.

Relationship between job stress, thinking style and symptoms of post-traumatic stress disorder in mental health nurses.

Introduction: Mental health nurses are often exposed to stressful events which may lead to feeling of stress in their daily work, and this feeling has a profound impact on nurses' mental health. Aim: This study aimed to evaluate the relationship between job stress, thinking style and symptoms of post-traumatic stress disorder (PTSD) of mental health nurses, and to explore the mechanism of job stress and thinking style on symptoms of PTSD. Method: This cross-sectional study collected related data of 351 mental health nurses in China, and the data was analyzed by PROCESS macro for SPSS. Results: The results showed that 18.2% of mental health nurses had the symptoms of PTSD. Thinking style (monarchic thinking style, anarchic thinking style and external thinking style) played a moderating role in the predictive effects of job stress on the symptoms of PTSD. Discussion: The research pointed out the relationship between job stress and symptom of PTSD, and clarified the critical role of thinking style among mental health nurses. Implications for practice: It is recommended that organizations should enact effective policy and intervention programs to reduce job stress and PTSD symptoms of mental health nurses which may improve their mental health level.

The association of glutamate level in pregenual anterior cingulate, anhedonia, and emotion-behavior decoupling in patients with major depressive disorder.

Impairments of translating emotional salience into effortful behavior are core features of anhedonia in cohorts with major depressive disorder. Glutamate metabolism is considered to be involved in this process, but the empirical study is relatively few. Therefore, the present study aimed to examine the correlations between glutamate level in pregenual anterior cingulate, anhedonia, and emotion-behavior decoupling in patients with major depressive disorder. Fifteen individuals diagnosed with major depressive disorder and ten healthy individuals were recruited. All participants were asked to complete self-report instruments for anhedonia and the computerized anticipatory and consummatory pleasure task, and the in vivo glutamate levels were measured by proton magnetic resonance spectroscopy. Thus, a potential lower glutamate levels in pregenual anterior cingulate in individuals with major depressive disorder were founded to be positively correlated with the ability of pleasure experiencing. The mechanism of glutamate in pregenual anterior cingulate in anhedonia in patients with major depressive disorder may be reflected in the early pleasurable experience stage, rather than in the transformation of emotional experience to motivation or reward-seeking behavior, which may be different from that in schizophrenia.

Shared and distinct reward neural mechanisms among patients with schizophrenia, major depressive disorder, and bipolar disorder: an effort-based functional imaging study.

Unwillingness to exert effort for rewards has been found in patients with schizophrenia (SCZ), major depressive disorder (MDD), and bipolar disorder (BD), but the underlying shared and distinct reward neural mechanisms remain unclear. This study aimed to compare the neural correlates of such impairments across different diagnoses. The neural responses in an effort-expenditure for reward task (EEfRT) were assessed in 20 SCZ patients, 23 MDD patients, 17 BD patients, and 30 healthy controls (HC). The results found shared activation in the cingulate gyrus, the medial frontal gyrus, and the middle frontal gyrus during the EEfRT administration. Compared to HC, SCZ patients exhibited stronger variations of functional connectivity between the right caudate and the left amygdala, the left hippocampus and the left putamen, with increase in reward magnitude. In MDD patients, an enhanced activation compared to HC in the right superior temporal gyrus was found with the increase of reward magnitude. The variations of functional connectivity between the caudate and the right cingulate gyrus, the left postcentral gyrus and the left inferior parietal lobule with increase in reward magnitude were weaker than that found in HC. In BD patients, the degree of activation in the left precuneus was increased, but that in the left dorsolateral prefrontal cortex was decreased with increase in reward probability compared to HC. These findings demonstrate both shared and distinct reward neural mechanisms associated with EEfRT in patients with SCZ, MDD, and BD, implicating potential intervention targets to alleviate amotivation in these clinical disorders.

Entheseal involvement of the lower extremities in gout: an ultrasonographic descriptive observational study.

OBJECTIVE: The aim of this study was to explore the prevalence and distribution of lower extremity entheseal abnormities by musculoskeletal ultrasound (US) in a cohort of gout patients, taking spondyloarthritis (SpA) patients and asymptomatic hyperuricemia (HUA) patients as controls. METHOD: One hundred participants with gout, fifty patients with SpA, and twenty-nine patients with asymptomatic HUA were recruited. US was used to assess the bilateral quadriceps, patellar and Achilles tendons, and plantar fascia entheses according to the Outcome Measures in Rheumatology (OMERACT) definitions. RESULTS: The US examination revealed the presence of one or more abnormalities in at least one enthesis in 45 out of 100 subjects (45.0%) and 152 out of 1000 entheses (15.2%) in the gout patients. Among the affected entheses, the patellar insertion of the quadriceps tendon was the most commonly involved area (38.0% in the gout patients versus 48.0% in the SpA patients with at least one pathological US finding, p = 0.241). There were no significant group differences in entheseal power Doppler (PD) signals, bone erosion, or enthesophytes. The patients with lower limb entheseal involvement in the gout group had an older age, longer disease duration, higher percentage of chronic tophaceous gout, and higher levels of inflammatory biomarkers of the erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP). Multivariate logistic regression analysis revealed that age (OR = 1.052, p = 0.001) and the ESR (OR = 1.023, p = 0.028) were correlated with lower limb enthesopathy in gout patients. In the subgroup analysis of gout patients without active inflammation, age (OR = 1.119, p = 0.001) and serum uric acid (UA, OR = 1.012, p = 0.002) were correlated with lower limb enthesopathy in gout. CONCLUSION: Lower extremity entheseal involvement might be neglected but should be considered as an important element in the evaluation of gout patients. Enthesopathy most frequently involves in the patellar insertion of the quadriceps tendon and is characterized by entheseal hypoechogenicity and/or thickening. Key Points • Lower extremity enthesopathy might be neglected as an important element in gout. • Enthesopathy is most frequently involved in the patellar insertion of the quadriceps tendon in gout. • Age and ESR are correlated with lower limb enthesopathy in gout patients.

Two plastidic glycolate/glycerate translocator 1 isoforms function together to transport photorespiratory glycolate and glycerate in rice chloroplasts.

The photorespiratory pathway is highly compartmentalized. As such, metabolite shuttles between organelles are critical to ensure efficient photorespiratory carbon flux. Arabidopsis plastidic glycolate/glycerate translocator 1 (PLGG1) has been reported as a key chloroplastic glycolate/glycerate transporter. Two homologous genes, OsPLGG1a and OsPLGG1b, have been identified in the rice genome, although their distinct functions and relationships remain unknown. Herein, our analysis of exogenous expression in oocytes and yeast shows that both OsPLGG1a and OsPLGG1b have the ability to transport glycolate and glycerate. Furthermore, we demonstrate in planta that the perturbation of OsPLGG1a or OsPLGG1b expression leads to extensive accumulation of photorespiratory metabolites, especially glycolate and glycerate. Under ambient CO2 conditions, loss-of-function osplgg1a or osplgg1b mutant plants exhibited significant decreases in photosynthesis efficiency, starch accumulation, plant height, and crop productivity. These morphological defects were almost entirely recovered when the mutant plants were grown under elevated CO2 conditions. In contrast to osplgg1a, osplgg1b mutant alleles produced a mild photorespiratory phenotype and had reduced accumulation of photorespiratory metabolites. Subcellular localization analysis showed that OsPLGG1a and OsPLGG1b are located in the inner and outer membranes of the chloroplast envelope, respectively. In vitro and in vivo experiments revealed that OsPLGG1a and OsPLGG1b have a direct interaction. Our results indicate that both OsPLGG1a and OsPLGG1b are chloroplastic glycolate/glycerate transporters required for photorespiratory metabolism and plant growth, and that they may function as a singular complex.

Effects of BDNF Signaling on Anxiety-Related Behavior and Spatial Memory of Adolescent Rats in Different Length of Maternal Separation.

As an adverse form of early-life stress (ELS), maternal separation (MS) can interfere with the development of cognition and behaviors of adolescent rodents. Brain-derived neurotrophic factor (BDNF) is involved in the regulation of brain development and function, but the molecular mechanisms by which BDNF regulates brain function and behavior in MS with different stressor strengths remain unclear. This descriptive study characterized the levels of BDNF in the prefrontal cortex (PFC) and plasma corticosterone (CORT) from the offspring of rats exposed to early handling (EH, 15-min separation per day) and prolonged MS (PMS, 180-min separation per day), during postnatal days (PND) 1­21. The behavioral and biochemical analyses were performed during adolescence (PND 42­56). PMS resulted in reduced weight and decreased locomotor activity in the open field test and Y-maze task compared to control (CON) group, with EH showing an intermediate phenotype. BDNF protein levels in the PFC were lower in PMS compared to EH and further reduced in CON male rats. Plasma CORT levels were higher in PMS compared to CON with EH again showing intermediate levels. Neither PMS or EH affected spatial learning in the Y-maze task. These findings indicate that longer periods of maternal separation are necessary to increase anxiety-like behavior, elevate CORT levels, and further suppress BDNF levels in the PFC, providing a possible mechanism to explain why more severe forms of ELS lead to more significant psychiatric and medical consequences later in life.

A transdiagnostic comparison of affective decision-making in patients with schizophrenia, major depressive disorder, or bipolar disorder.

Deficit in decision-making has been found in patients with schizophrenia (SCZ), major depressive disorder (MDD), and bipolar disorder (BD), respectively, while the common and distinct characteristics of this deficit among these patients are still unclear. The present study aimed to make a transdiagnostic comparison of the affective decision-making ability in patients with SCZ, MDD, and BD. In this study, 33 patients with SCZ, 23 patients with MDD, 29 patients with BD, and 34 healthy controls (HCs) were recruited and the Iowa Gambling Task (IGT) was used to assess the affective decision-making ability. The results showed that all three diagnostic groups tended to select the disadvantageous decks but not advantageous decks compared to HCs. For patients with SCZ, an excessive preference for the disadvantageous decks with larger-magnitude less frequent punishments (deck B) may be the main reason of the deficit in affective decision-making, while that in patients with MDD was a significantly decreased ability to choose advantageous decks on the whole but with larger-magnitude less frequent punishments (deck D). As regards patients with BD, the concurrence of more choices of deck B and fewer choices of deck D was the characteristic of the deficit in affective decision-making. Our findings suggest a common affective decision-making impairment in the context of multiple choices in patients with SCZ, MDD, and BD, while the underlying mechanisms of the impairment among these patients may be slightly different.

Emotion-behavior decoupling in individuals with schizophrenia, bipolar disorder, and major depressive disorder.

Failure in translating emotional salience into effortful behavior is thought to be a core feature of anhedonia and avolition in individuals with schizophrenia (SCZ), but little is known about emotion-behavior coupling in individuals with bipolar disorder (BD) and major depressive disorder (MDD). In this study, we compared emotion-behavior correspondence in participants with SCZ, BD, and MDD. Forty-two participants with SCZ, 44 participants with MDD, 43 participants with BD, and 43 healthy controls were recruited. A computerized anticipatory and consummatory pleasure task was used to evaluate emotion-behavior correspondence. Clinical ratings of negative symptoms and self-report anhedonia questionnaires were also administered. We found that participants with SCZ, MDD, and BD exhibited different levels of negative symptoms and self-reported anhedonia, as well as emotion-behavior decoupling. In SCZ participants, both desirable and undesirable images elicited lower correspondence between self-reported liking and behavior. In MDD and BD participants, undesirable images elicited lower emotion-behavior correspondence under both direct stimulus presentation and representation conditions, whereas deficits in emotion-behavior coupling under desirable conditions were only observed when stimuli were present. Taken together, emotion-behavior decoupling showed both common and unique patterns in participants with SCZ, MDD, and BD, and showed some associations with negative symptoms and anhedonia across the combined clinical sample. This finding may be helpful for early identification and the development of novel interventions for different psychiatric diagnoses. (PsycInfo Database Record (c) 2020 APA, all rights reserved).

An Arabidopsis WD40 repeat-containing protein XIW1 promotes salt inhibition of seed germination.

WD40 repeat-containing protein (WD40 protein) acts as versatile scaffolds for protein interactions and participates in a variety of biological processes, such as plant stress and hormone responses. In a recent study, we show that XPO1-Interacting WD40 protein 1 (XIW1) is nuclear accumulated by abscisic acid (ABA), which interacts with ABA insensitive 5 (ABI5) in the nucleus and maintains its stability, thereby affecting seed germination and seedling growth. Here, we show that XIW1 promotes salt inhibition of seed germination (SSG). Mutation of XIW1 reduced the induction of ABI5 and ABA-responsive genes under salt treatment, causing mutant plants with high seed germination and suppression of SSG. In addition, we found that salt treatment facilities XIW1 accumulation in the nucleus. These findings reveal the important role of XIW1 in the regulation of SSG and provide a possible mechanism of XIW1 affecting SSG.

Mesenchymal stem cells enhance microglia M2 polarization and attenuate neuroinflammation through TSG-6.

Microglia are the primary cells that exert immune function in the central nervous system (CNS), and they play an important role in the pathogenesis and progression of neuroinflammation-related diseases. Mesenchymal stem cells (MSCs) have been demonstrated to promote functional recovery in many neurological diseases. The mechanisms underlying this may be that MSCs can reduce inflammatory responses through various soluble factors. Among these factors, tumor necrosis factor-α-induced gene/protein 6 (TSG-6) is a key factor influencing MSCs immunomodulatory properties; however, the precise mechanisms underlying the anti-inflammatory effects are not fully understood. Here, we aim to investigate the potential effects of MSCs on neuroinflammation and to reveal the underlying mechanisms. First, we confirmed that administration of MSCs could inhibit the lipopolysaccharide (LPS)-induced neuroinflammatory responses in a mouse model. Then, we found that MSCs promoted M2 polarization and inhibited M1 polarization both in vivo and in vitro. Moreover, we demonstrated that the effect of MSCs on microglial polarization was dependent on TSG-6. This study demonstrated that MSCs promoted M2 polarization of microglia via TSG-6, thus conferring anti-neuroinflammatory effects.

Nucleocytoplasmic Trafficking of the Arabidopsis WD40 Repeat Protein XIW1 Regulates ABI5 Stability and Abscisic Acid Responses.

WD40 repeat-containing proteins (WD40 proteins) serve as versatile scaffolds for protein-protein interactions, modulating a variety of cellular processes such as plant stress and hormone responses. Here we report the identification of a WD40 protein, XIW1 (for XPO1-interacting WD40 protein 1), which positively regulates the abscisic acid (ABA) response in Arabidopsis. XIW1 is located in the cytoplasm and nucleus. We found that it interacts with the nuclear transport receptor XPO1 and is exported by XPO1 from the nucleus. Mutation of XIW1 reduces the induction of ABA-responsive genes and the accumulation of ABA Insensitive 5 (ABI5), causing mutant plants with ABA-insensitive phenotypes during seed germination and seedling growth, and decreased drought stress resistance. ABA treatment upregulates the expression of XIW1, and both ABA and abiotic stresses promote XIW1 accumulation in the nucleus, where it interacts with ABI5. Loss of XIW1 function results in rapid proteasomal degradation of ABI5. Taken together, these findings suggest that XIW1 is a nucleocytoplasmic shuttling protein and plays a positive role in ABA responses by interacting with and maintaining the stability of ABI5 in the nucleus.

EXPORTIN 1A prevents transgene silencing in Arabidopsis by modulating nucleo-cytoplasmic partitioning of HDA6.

In eukaryotic cells, transport of macromolecules across the nuclear envelope is an essential process that ensures rapid exchange of cellular components, including protein and RNA molecules. Chromatin regulators involved in epigenetic control are among the molecules exported across the nuclear envelope, but the significance of this nucleo-cytoplasmic trafficking is not well understood. Here, we use a forward screen to isolate XPO1A (a nuclear export receptor in Arabidopsis) as an anti-silencing factor that protects transgenes from transcriptional silencing. Loss-of-function of XPO1A leads to locus-specific DNA hypermethylation at transgene promoters and some endogenous loci. We found that XPO1A directly interacts with histone deacetylase HDA6 in vivo and that the xpo1a mutation causes increased nuclear retention of HDA6 protein and results in reduced histone acetylation and enhanced transgene silencing. Our results reveal a new mechanism of epigenetic regulation through the modulation of XPO1A-dependent nucleo-cytoplasm partitioning of a chromatin regulator.

Impairment of FtsHi5 Function Affects Cellular Redox Balance and Photorespiratory Metabolism in Arabidopsis.

Photorespiration is an essential process for plant photosynthesis, development and growth in aerobic conditions. Recent studies have shown that photorespiration is an open system integrated with the plant primary metabolism network and intracellular redox systems, though the mechanisms of regulating photorespiration are far from clear. Through a forward genetic method, we identified a photorespiratory mutant pr1 (photorespiratory related 1), which produced a chlorotic and smaller photorespiratory growth phenotype with decreased chlorophyll content and accumulation of glycine and serine in ambient air. Morphological and physiological defects in pr1 plants can be largely abolished under elevated CO2 conditions. Genetic mapping and complementation confirmed that PR1 encodes an FtsH (Filamentation temperature-sensitive H)-like protein, FtsHi5. Reduced FtsHi5 expression in DEX-induced RNAi transgenic plants produced a similar growth phenotype with pr1 (ftsHi5-1). Transcriptome analysis suggested a changed expression pattern of redox-related genes and an increased expression of senescence-related genes in DEX: RNAi-FtsHi5 seedlings. Together with the observation that decreased accumulation of D1 and D2 proteins of photosystem II (PSII) and over-accumulation of reactive oxygen species (ROS) in ftsHi5 mutants, we hypothesize that FtsHi5 functions in maintaining the cellular redox balance and thus regulates photorespiratory metabolism.