The H3K27me3 demethylase REF6 promotes leaf senescence through directly activating major senescence regulatory and functional genes in Arabidopsis.

The roles of histone demethylation in the regulation of plant flowering, disease resistance, rhythmical response, and seed germination have been elucidated recently; however, how histone demethylation affects leaf senescence remains largely unclear. In this study, we exploited yeast one-hybrid (Y1H) to screen for the upstream regulators of NONYELLOWING1 (NYE1), and identified RELATIVE OF EARLY FLOWERING6 (REF6), a histone H3 lysine 27 tri-methylation (H3K27me3) demethylase, as a putative binding protein of NYE1 promoter. By in vivo and in vitro analyses, we demonstrated that REF6 directly binds to the motif CTCGYTY in NYE1/2 promoters through its zinc finger domain and positively regulates their expression. Loss-of-function of REF6 delayed chlorophyll (Chl) degradation, whereas overexpression of REF6 accelerated Chl degradation. Subsequently, we revealed that REF6 positively regulates the general senescence process by directly up-regulating ETHYLENE INSENSITIVE 2 (EIN2), ORESARA1 (ORE1), NAC-LIKE, ACTIVATED BY AP3/PI (NAP), PYRUVATE ORTHOPHOSPHATE DIKINASE (PPDK), PHYTOALEXIN DEFICIENT 4 (PAD4), LIPOXYGENASE 1 (LOX1), NAC DOMAIN CONTAINING PROTEIN 3 (AtNAC3), and NAC TRANSCRIPTION FACTOR-LIKE 9 (NTL9), the key regulatory and functional genes predominantly involved in the regulation of developmental leaf senescence. Importantly, loss-of-function of REF6 increased H3K27me3 levels at all the target Senescence associated genes (SAGs). We therefore conclusively demonstrate that H3K27me3 methylation represents an epigenetic mechanism prohibiting the premature transcriptional activation of key developmentally up-regulated senescence regulatory as well as functional genes in Arabidopsis.

Does travel closer to TOD have lower CO2 emissions? Evidence from ride-hailing in Chengdu, China.

Despite contributions to reducing private car dependency and carbon emissions, impacts of transit-oriented development (TOD) on ride-hailing usage are largely overlooked in existing studies. Using massive ride-hailing trips data in Chengdu, the influence of subway proximity on vehicle kilometers traveled (VKT) and corresponding CO2 emissions of ride-hailing is examined at the disaggregated level. Similarly, moderated multiple regression is adopted to investigate the interaction effects of subway proximity at pick-up and drop-off on VKT of ride-hailing. Results suggest that for each additional kilometer in subway proximity at pick-up/drop-off position, the VKT of ride-hailing trips is reduced by 0.315 km/0.273 km, resulting in the CO2 emission reduction of 0.063 kg/0.055 kg. Moreover, the influence of pick-up proximity on VKT change is negatively moderated by drop-off proximity and vice versa. Our results suggest that the carbon emission reduction can benefit from "T (Transit)" however the problem of regional imbalances in "D (Development)" needs to be addressed.

The NPR1-WRKY46-WRKY6 signaling cascade mediates probenazole/salicylic acid-elicited leaf senescence in Arabidopsis thaliana.

Endogenous salicylic acid (SA) regulates leaf senescence, but the underlying mechanism remains largely unexplored. The exogenous application of SA to living plants is not efficient for inducing leaf senescence. By taking advantage of probenazole (PBZ)-induced biosynthesis of endogenous SA, we previously established a chemical inducible leaf senescence system that depends on SA biosynthesis and its core signaling receptor NPR1 in Arabidopsis thaliana. Here, using this system, we identified WRKY46 and WRKY6 as key components of the transcriptional machinery downstream of NPR1 signaling. Upon PBZ treatment, the wrky46 mutant exhibited significantly delayed leaf senescence. We demonstrate that NPR1 is essential for PBZ/SA-induced WRKY46 activation, whereas WRKY46 in turn enhances NPR1 expression. WRKY46 interacts with NPR1 in the nucleus, binding to the W-box of the WRKY6 promoter to induce its expression in response to SA signaling. Dysfunction of WRKY6 abolished PBZ-induced leaf senescence, while overexpression of WRKY6 was sufficient to accelerate leaf senescence even under normal growth conditions, suggesting that WRKY6 may serve as an integration node of multiple leaf senescence signaling pathways. Taken together, these findings reveal that the NPR1-WRKY46-WRKY6 signaling cascade plays a critical role in PBZ/SA-mediated leaf senescence in Arabidopsis.

[Application of copy number variation sequencing combined with short tandem repeat in analysis of abortion and prenatal diagnosis].

OBJECTIVE: To explore the cause of abortion and strategy of prenatal diagnosis for pregnant women with high risk for chromosomal abnormalities by using copy number variation sequencing (CNV-seq) and short tandem repeats (STR) analysis. METHODS: A total of 36 samples were collected, including amniotic fluid, abortion tissue, whole blood, chorionic villi and umbilical cord blood. CNV-seq and STR analysis were carried out to detect microdeletions, microduplications, chromosomal aneuploidies, mosaicisms and triploidies. RESULTS: Among all samples, 1 was detected with 4p15.1p16.3 and 14q11.1q22.1 duplication, 1 was detected with 19p13.3 deletion, 8 were detected with chromosomal aneuploidies, 4 were detected with mosaicisms, two were detected with triploidies. No definite pathogenic CNVs were detected in 20 samples, which yielded a positive detection rate of 44.44%. CONCLUSION: As a high-throughput detection method, CNV-seq has the advantages of rapidity, simplicity and high accuracy. It may suit prenatal diagnosis and analysis of abortion factors in combination with STR analysis.

MKK4/MKK5-MPK1/MPK2 cascade mediates SA-activated leaf senescence via phosphorylation of NPR1 in Arabidopsis.

The mechanism by which endogenous salicylic acid (SA) regulates leaf senescence remains elusive. Here we provide direct evidence that an enhancement of endogenous SA level, via chemical-induced upregulation of ISOCHORISMATE SYNTHASE 1 (ICS1), could significantly accelerate the senescence process of old leaves through mediation of the key SA signaling component NON EXPRESSOR OF PATHOGENESIS RELATED GENES 1 (NPR1) in Arabidopsis. Importantly, by taking advantage of this chemically induced leaf senescence system, we identified a mitogen-activated protein kinase (MAPK) cascade MKK4/5-MPK1/2 that is required for the SA/NPR1-mediated leaf senescence. Both MKK4/5 and MPK1/2 exhibited SA-induced kinase activities, with MPK1/2 being the immediate targets of MKK4/5. Double mutants of mkk4 mkk5 and mpk1 mpk2 displayed delayed leaf senescence, while constitutive overexpression of the kinase genes led to premature leaf senescence. Such premature leaf senescence was suppressed when they were overexpressed in an SA synthesis defective mutant (sid2) or signaling detective mutant (npr1). We further showed that MPK1, but not MPK2, could directly phosphorylate NPR1. Meanwhile, MPK1 also mediated NPR1 monomerization. Notably, induction of disease resistance was significantly compromised in the single and double mutants of the kinase genes. Taken together, our data demonstrate that the MKK4/5-MPK1/2 cascade plays a critical role in modulating SA signaling through a complex regulatory network in Arabidopsis.

Correction to: MKK4/MKK5­MPK1/MPK2 cascade mediates SA­activated leaf senescence via phosphorylation of NPR1 in Arabidopsis.

Due to an unfortunate turn of events, the second co-corresponding author, Dr. Benke Kuai, was omitted from the original publication. The corrected authors' list and author contribution statement are published here and should be treated as definitive.

The transcription factor ZmNAC126 accelerates leaf senescence downstream of the ethylene signalling pathway in maize.

Leaf senescence is an integral part of plant development, during which, nutrients are remobilized from senescent leaves to fast-growing organs. The initiation and progression dynamics of leaf senescence is therefore vital not only to the maximal accumulation of assimilates but also to the efficient remobilization of nutrients. Senescence is a finely tuned process that involves the action of a large number of transcription factors (TFs). The NAC TFs play critical roles in regulating leaf senescence in Arabidopsis, wheat, rice and tomato. Here, we identified a NAC TF, ZmNAC126 that is responsive to leaf senescence in maize. Ectopic overexpression of ZmNAC126 in Arabidopsis and maize enhanced chlorophyll degradation and promoted leaf senescence. Electrophoretic mobility shift and chromatin immunoprecipitation assays revealed that ZmNAC126 could directly bind to the promoters of major chlorophyll catabolic genes in maize. Dual-luciferase assay in maize protoplasts indicated that ZmNAC126 positively regulates these chlorophyll catabolic genes in maize. Moreover, ZmNAC126 could be induced by ethylene, and ZmEIN3, a major TF of ethylene signalling, could bind to its promoter to transactivate its expression. Taken together, ZmNAC126 may play a pivotal role in regulating natural and ethylene-triggered leaf senescence in maize.

REF6 promotes lateral root formation through de-repression of PIN1/3/7 genes.

The H3K27 methyltransferase CLF inhibits lateral root (LR) formation through depositing the repressive H3K27me3 mark to the chromatin of PIN1, a key polar auxin transporter gene. Here, we show that the H3K27me3 demethylase REF6 promotes lateral root primordium initiation and LR emergence. REF6 directly binds to the chromatin of PIN1/3/7. Dysfunction in REF6 results in increased levels of H3K27me3 on PIN1/3/7 and suppressed expression of PIN genes. Genetic analysis of the clf ref6 double mutant revealed an antagonistic action between CLF and REF6, in terms of LR formation. Our findings indicate that H3K27 methylation and demethylation activities are likely coordinated to ensure proper LR organogenesis.

NYEs/SGRs-mediated chlorophyll degradation is critical for detoxification during seed maturation in Arabidopsis.

In the seed industry, chlorophyll (Chl) fluorescence is often used as a major non-invasive reporter of seed maturation and quality. Breakdown of Chl is a proactive process during the late stage of seed maturation, as well as during leaf senescence and fruit ripening. However, the biological significance of this process is still unclear. NYE1 and NYE2 are Mg-dechelatases, catalyzing the first rate-limiting step of Chl a degradation. Loss-of-function of both NYE1 and NYE2 not only results in a nearly complete retention of Chl during leaf senescence, but also produces green seeds in Arabidopsis. In this study, we showed that Chl retention in the nye1 nye2 double-mutant caused severe photo-damage to maturing seeds. Upon prolonged light exposure, green seeds of nye1 nye2 gradually bleached out and eventually lost their germination capacity. This organ-specific photosensitive phenotype is likely due to an over-accumulation of free Chl, which possesses photosensitizing properties and causes a burst of reactive oxygen species upon light exposure. As expected, a similar, albeit much milder, photosensitive phenotype was observed in the seeds of d1 d2, a green-seed mutant defective in NYE/SGR orthologous genes in soybean. Taken together, our data suggest that efficient NYEs-mediated Chl degradation is critical for detoxification during seed maturation.

Suppressor of Overexpression of CO 1 Negatively Regulates Dark-Induced Leaf Degreening and Senescence by Directly Repressing Pheophytinase and Other Senescence-Associated Genes in Arabidopsis.

Although the biochemical pathway of chlorophyll (Chl) degradation has been largely elucidated, how Chl is rapidly yet coordinately degraded during leaf senescence remains elusive. Pheophytinase (PPH) is the enzyme for catalyzing the removal of the phytol group from pheophytin a, and PPH expression is significantly induced during leaf senescence. To elucidate the transcriptional regulation of PPH, we used a yeast (Saccharomyces cerevisiae) one-hybrid system to screen for its trans-regulators. SUPPRESSOR OF OVEREXPRESSION OF CO 1 (SOC1), a key flowering pathway integrator, was initially identified as one of the putative trans-regulators of PPH After dark treatment, leaves of an SOC1 knockdown mutant (soc1-6) showed an accelerated yellowing phenotype, whereas those of SOC1-overexpressing lines exhibited a partial stay-green phenotype. SOC1 and PPH expression showed a negative correlation during leaf senescence. Substantially, SOC1 protein could bind specifically to the CArG box of the PPH promoter in vitro and in vivo, and overexpression of SOC1 significantly inhibited the transcriptional activity of the PPH promoter in Arabidopsis (Arabidopsis thaliana) protoplasts. Importantly, soc1-6 pph-1 (a PPH knockout mutant) double mutant displayed a stay-green phenotype similar to that of pph-1 during dark treatment. These results demonstrated that SOC1 inhibits Chl degradation via negatively regulating PPH expression. In addition, measurement of the Chl content and the maximum photochemical efficiency of photosystem II of soc1-6 and SOC1-OE leaves after dark treatment suggested that SOC1 also negatively regulates the general senescence process. Seven SENESCENCE-ASSOCIATED GENES (SAGs) were thereafter identified as its potential target genes, and NONYELLOWING1 and SAG113 were experimentally confirmed. Together, we reveal that SOC1 represses dark-induced leaf Chl degradation and senescence in general in Arabidopsis.

EIN3 and ORE1 Accelerate Degreening during Ethylene-Mediated Leaf Senescence by Directly Activating Chlorophyll Catabolic Genes in Arabidopsis.

Degreening, caused by chlorophyll degradation, is the most obvious symptom of senescing leaves. Chlorophyll degradation can be triggered by endogenous and environmental cues, and ethylene is one of the major inducers. ETHYLENE INSENSITIVE3 (EIN3) is a key transcription factor in the ethylene signaling pathway. It was previously reported that EIN3, miR164, and a NAC (NAM, ATAF, and CUC) transcription factor ORE1/NAC2 constitute a regulatory network mediating leaf senescence. However, how this network regulates chlorophyll degradation at molecular level is not yet elucidated. Here we report a feed-forward regulation of chlorophyll degradation that involves EIN3, ORE1, and chlorophyll catabolic genes (CCGs). Gene expression analysis showed that the induction of three major CCGs, NYE1, NYC1 and PAO, by ethylene was largely repressed in ein3 eil1 double mutant. Dual-luciferase assay revealed that EIN3 significantly enhanced the promoter activity of NYE1, NYC1 and PAO in Arabidopsis protoplasts. Furthermore, Electrophoretic mobility shift assay (EMSA) indicated that EIN3 could directly bind to NYE1, NYC1 and PAO promoters. These results reveal that EIN3 functions as a positive regulator of CCG expression during ethylene-mediated chlorophyll degradation. Interestingly, ORE1, a senescence regulator which is a downstream target of EIN3, could also activate the expression of NYE1, NYC1 and PAO by directly binding to their promoters in EMSA and chromatin immunoprecipitation (ChIP) assays. In addition, EIN3 and ORE1 promoted NYE1 and NYC1 transcriptions in an additive manner. These results suggest that ORE1 is also involved in the direct regulation of CCG transcription. Moreover, ORE1 activated the expression of ACS2, a major ethylene biosynthesis gene, and subsequently promoted ethylene production. Collectively, our work reveals that EIN3, ORE1 and CCGs constitute a coherent feed-forward loop involving in the robust regulation of ethylene-mediated chlorophyll degradation during leaf senescence in Arabidopsis.

Jasmonic acid promotes degreening via MYC2/3/4- and ANAC019/055/072-mediated regulation of major chlorophyll catabolic genes.

Degreening caused by rapid chlorophyll (Chl) degradation is a characteristic event during green organ senescence or maturation. Pheophorbide a oxygenase gene (PAO) encodes a key enzyme of Chl degradation, yet its transcriptional regulation remains largely unknown. Using yeast one-hybrid screening, coupled with in vitro and in vivo assays, we revealed that Arabidopsis MYC2/3/4 basic helix-loop-helix proteins directly bind to PAO promoter. Overexpression of the MYCs significantly enhanced the transcriptional activity of PAO promoter in Arabidopsis protoplasts, and methyl jasmonate (MeJA) treatment greatly induced PAO expression in wild-type Arabidopsis plants, but the induction was abolished in myc2 myc3 myc4. In addition, MYC2/3/4 proteins could promote the expression of another Chl catabolic enzyme gene, NYC1, as well as a key regulatory gene of Chl degradation, NYE1/SGR1, by directly binding to their promoters. More importantly, the myc2 myc3 myc4 triple mutant showed a severe stay-green phenotype, whereas the lines overexpressing the MYCs showed accelerated leaf yellowing upon MeJA treatment. These results suggest that MYC2/3/4 proteins may mediate jasmonic acid (JA)-induced Chl degradation by directly activating these Chl catabolic genes (CCGs). Three NAC family proteins, ANAC019/055/072, downstream from MYC2/3/4 proteins, could also directly promote the expression of a similar set of CCGs (NYE1/SGR1, NYE2/SGR2 and NYC1) during Chl degradation. In particular, anac019 anac055 anac072 triple mutant displayed a severe stay-green phenotype after MeJA treatment. Finally, we revealed that MYC2 and ANAC019 may interact with each other and synergistically enhance NYE1 expression. Together, our study reveals a hierarchical and coordinated regulatory network of JA-induced Chl degradation.

TCP transcription factors are critical for the coordinated regulation of isochorismate synthase 1 expression in Arabidopsis thaliana.

Salicylic acid (SA) plays an important role in various aspects of plant development and responses to stresses. To elucidate the sophisticated regulatory mechanism of SA synthesis and signaling, we used a yeast one-hybrid system to screen for regulators of isochorismate synthase 1 (ICS1), a gene encoding the key enzyme in SA biosynthesis in Arabidopsis thaliana. A TCP family transcription factor AtTCP8 was initially identified as a candidate regulator of ICS1. The regulation of ICS1 by TCP proteins is supported by the presence of a typical TCP binding site in the ICS1 promoter. The binding of TCP8 to this site was confirmed by in vitro and in vivo assays. Expression patterns of TCP8 and its corresponding gene TCP9 largely overlapped with ICS1 under pathogen attack. A significant reduction in the expression of ICS1 during immune responses was observed in the tcp8 tcp9 double mutant. We also detected strong interactions between TCP8 and SAR deficient 1 (SARD1), WRKY family transcription factor 28 (WRKY28), NAC (NAM/ATAF1,ATAF2/CUC2) family transcription factor 019 (NAC019), as well as among TCP8, TCP9 and TCP20, suggesting a complex coordinated regulatory mechanism underlying ICS1 expression. Our results collectively demonstrate that TCP proteins are involved in the orchestrated regulation of ICS1 expression, with TCP8 and TCP9 being verified as major representatives.

CCX1, a Putative Cation/Ca2+ Exchanger, Participates in Regulation of Reactive Oxygen Species Homeostasis and Leaf Senescence.

The major developmental significance of leaf senescence is the massive recycling of nutrients from senescing leaves to nascent organs, including seeds, to meet the requirement of their rapid development, so-called nutrient remobilization. The efficiency of nutrient remobilization is associated with the activity of diverse transporters. A large number of transporters are up-regulated during leaf senescence in Arabidopsis, many of which participate in regulating leaf senescence via different signaling pathways. Here, we report that a member of the cation/Ca2+ exchanger family, CCX1, is highly induced during leaf senescence in Arabidopsis. Although single mutation of CCX1 did not change the senescence phenotype, double mutation of CCX1 and CCX4 resulted in a subtle but significant stay-green phenotype during natural and dark-induced leaf senescence, suggesting that some members of the cation/Ca2+ exchanger family act redundantly in mediating leaf senescence. Consistently, overexpression of CCX1 accelerated leaf senescence. Moreover, the ccx1ccx4 double mutant was more tolerant to H2O2, whereas CCX1-overexpressing lines showed an elevated response to H2O2 treatment, presumably due to an overaccumulation of reactive oxygen species (ROS), indicating that CCX1 may promote leaf senescence via modulating ROS homeostasis. Notably, both ccx1-1 and ccx1ccx4 were sensitive to Ca2+ deprivation, implying that CCX1 may also be involved in modulating Ca2+ signaling and consequently affecting the initiation of leaf senescence.

The role of ANAC072 in the regulation of chlorophyll degradation during age- and dark-induced leaf senescence.

KEY MESSAGE: ANAC072 positively regulates both age- and dark-induced leaf senescence through activating the transcription of NYE1. Leaf senescence is integral to plant development, which is age-dependent and strictly regulated by internal and environmental signals. Although a number of senescence-related mutants and senescence-associated genes (SAGs) have been identified and characterized in the past decades, the general regulatory network of leaf senescence is still far from being elucidated. Here, we report the role of ANAC072, an SAG identified through bioinformatics analysis, in the regulation of chlorophyll degradation during natural and dark-induced leaf senescence. The expression of ANAC072 was increased with advancing leaf senescence in Arabidopsis. Leaf degreening was significantly delayed under normal or dark-induced conditions in anac072-1, a knockout mutant of ANAC072, with a higher chlorophyll level detected. In contrast, an overexpression mutant, anac072-2, with ANAC072 transcription markedly upregulated, showed an early leaf-yellowing phenotype. Consistently, senescent leaves of the loss-of-function mutant anac072-1 exhibited delays in the decrease of photosynthesis efficiency of photosystem II (F v/F m ratio) and the increase of plasma membrane ion leakage rate as compared with corresponding leaves of wild-type Col-0 plants, whereas the overexpression mutant anac072-2 showed opposite changes. Our data suggest that ANAC072 plays a positive role during natural and dark-induced leaf senescence. In addition, the transcript level of NYE1, a key regulatory gene in chlorophyll degradation, relied on the function of ANAC072. Combining these analyses with electrophoretic mobility shift assay and chromatin immunoprecipitation, we demonstrated that ANAC072 directly bound to the NYE1 promoter in vitro and in vivo, so ANAC072 may promote chlorophyll degradation by directly upregulating the expression of NYE1.

Genome-Wide Identification and Expression Analysis of the Cucumber FKBP Gene Family in Response to Abiotic and Biotic Stresses.

The FKBP (FK506-binding protein) gene family is an important member of the PPlase protease family and plays a vital role during the processes of plant growth and development. However, no studies of the FKBP gene family have been reported in cucumber. In this study, 19 FKBP genes were identified in cucumber, which were located on chromosomes 1, 3, 4, 6, and 7. Phylogenetic analysis divided the cucumber FKBP genes into three subgroups. The FKBP genes in the same subgroup exhibited similar structures and conserved motifs. The cis-acting elements analysis revealed that the promoters of cucumber FKBP genes contained hormone-, stress-, and development-related cis-acting elements. Synteny analysis of the FKBP genes among cucumber, Arabidopsis, and rice showed that 12 kinds of syntenic relationships were detected between cucumber and Arabidopsis FKBP genes, and 3 kinds of syntenic relationships were observed between cucumber and rice FKBP genes. The tissue-specific expression analysis showed that some FKBP genes were expressed in all tissues, while others were only highly expressed in part of the 10 types of tissues. The expression profile analysis of cucumber FKBP genes under 13 types of stresses showed that the CsaV3_1G007080 gene was differentially expressed under abiotic stresses (high temperature, NaCl, silicon, and photoperiod) and biotic stresses (downy mildew, green mottle mosaic virus, Fusarium wilt, phytophthora capsica, angular leaf spot, and root-knot nematode), which indicated that the CsaV3_1G007080 gene plays an important role in the growth and development of cucumber. The interaction protein analysis showed that most of the proteins in the FKBP gene family interacted with each other. The results of this study will lay the foundation for further research on the molecular biological functions of the cucumber FKBP gene family.

UV/Sodium percarbonate for bisphenol A treatment in water: Impact of water quality parameters on the formation of reactive radicals.

Reported herein is an investigation of the impact of water quality parameters on the formation of carbonate radical anion (CO3•-) and hydroxyl radical (HO•) in UV/sodium percarbonate (UV/SPC) system versus in UV/hydrogen peroxide (UV/H2O2) system for bisphenol A (BPA) degradation in water. Pathways of CO3•- oxidation of BPA were proposed in this study based on the evolution of direct transformation products of BPA. Observed in this study, the degradation of BPA in the UV/SPC system was slower than that in the UV/H2O2 system in the secondary effluents collected from a local wastewater treatment plant due to the significant impact of coexisting constituents in the matrices on the former system. Single water quality parameter (e.g., solution pH, common anion, or natural organic matter) affected radical formations and BPA degradation in the UV/SPC system in a way similar to that in the UV/H2O2 system. Namely, the rise of solution pH decreased the steady state concentration of HO• resulting in a decrease in the observed pseudo first-order rate constant of BPA (kobs). Chloride anion and sulfate anion played a negligible role over the examined concentrations; nitrate anion slightly suppressed the reaction at the concentration of 20 mM; bicarbonate anion decreased the steady state concentrations of both CO3•- and HO• exerting significant inhibition on BPA degradation. Different extents of HO• scavenging were observed for different types of natural organic matter in the order of fulvic acid > mixed NOM > humic acid. However, the impact was generally less pronounced on BPA degradation in the UV/SPC system than that in the UV/H2O2 system due to the existence of CO3•-. The results of this study provide new insights into the mechanism of CO3•- based oxidation and new scientific information regarding the impact of water quality parameters on BPA degradation in the sytems of UV/SPC and UV/H2O2 from the aspect of reactive radical formation, which have reference value for UV/SPC application in wastewater treatment.

Chemical induction of leaf senescence and powdery mildew resistance involves ethylene-mediated chlorophyll degradation and ROS metabolism in cucumber.

Timely initiation of leaf senescence is an integral part of plant development and, importantly, an adaptive strategy by which plants cope with various stresses, e.g. to limit the spread of pathogens. Powdery mildew is a major cucumber disease that promotes the initiation/progression of leaf senescence and reduces leaf photosynthesis, resulting in severe losses of yield and quality. However, how powdery mildew induces leaf senescence and how cucumber plants respond to enhance their resistance remain unclear. Here, with established agrochemical induction and pathogen inoculation systems, we demonstrate that both probenazole (PBZ) and powdery mildew activate ethylene (ET) biosynthesis and signal transduction, consequently promoting leaf senescence and enhancing plant resistance to powdery mildew through CsEIN3 to directly upregulate the expression of CsCCGs and CsRBOHs. Our analysis convincingly suggests that the regulation of leaf senescence and powdery mildew resistance is interconnected and mediated mainly by ET in cucumber.

Retinitis pigmentosa and molar tooth sign caused by novel AHI1 compound heterozygote pathogenic variants.

BACKGROUND: Joubert syndrome (JS) is a group of rare congenital disorders characterized by cerebellar vermis dysplasia, developmental delay, and retina dysfunctions. Herein, we reported a Chinese patient carrying a new variant in the AHI1 gene with mild JS, and the 3D structure of the affected Jouberin protein was also predicted. CASE PRESENTATION: The patient was a 31-year-old male, who presented difficulty at finding toys at the age of 2 years, night blindness from age of 5 years, intention tremor and walking imbalance from 29 years of age. Tubular visual field and retina pigmentation were observed on ophthalmology examinations, as well as molar tooth sign on brain magnetic resonance imaging (MRI). Whole exome sequence revealed two compound heterozygous variants at c.2105C>T (p.T702M) and c.1330A>T (p.I444F) in AHI1 gene. The latter one was a novel mutation. The 3D protein structure was predicted using I-TASSER and PyMOL, showing structural changes from functional ß-sheet and α-helix to non-functional D-loop, respectively. CONCLUSIONS: Mild JS due to novel variants at T702M and I444F in the AHI1 gene was reported. The 3D-structural changes in Jouberin protein might underlie the pathogenesis of JS.

Comparative toxicity reduction potential of UV/sodium percarbonate and UV/hydrogen peroxide treatments for bisphenol A in water: An integrated analysis using chemical, computational, biological, and metabolomic approaches.

Bisphenol A (BPA) is a common industrial chemical with significant adverse impacts on biological systems as an environmental contaminant. UV/hydrogen peroxide (UV/H2O2) is a well-established technology for BPA treatment in water while UV/sodium percarbonate (UV/SPC) is an emerging technology with unclear biological impacts of treated effluent. Therefore, in this study, the toxicity evaluation of BPA solution treated with UV/H2O2 and UV/SPC was preformed and compared based on transformation products (TPs) profile, quantitative structure-activity relationship (QSAR), Escherichia coli (E. coli) toxicity assays, and metabolomic analysis. TPs with hydroxylation, double-ring split, and single-ring cleavage were generated from BPA during the treatments with both technologies, but TPs with quinonation were specifically detected in UV/H2O2 treated solution at the UV dose of 1470 mJ cm-2. QSAR prediction based on TPs profile (excluding benzoquinone TPs) suggested that UV/H2O2 and UV/SPC treatments of BPA may increase matrix toxicity due to the formation of multi-hydroxylated TPs; however decreased bioaccumulation potential of all TPs may mitigate the increase of toxicity by reducing the chance of TPs to reach the concentration of toxicity threshold. In vivo assays with E. coli showed inhibited cell growth, arrested cell cycle, and increased cell death in BPA solution treated with UV/H2O2 at the UV dose of 1470 mJ cm-2. Metabolomic analysis indicated that BPA solution treated with UV/H2O2 at UV dose of 1470 mJ cm-2 impacted E. coli metabolism differently than other solutions with unique inhibition on glycerolipid metabolism. Moreover, BPA interfered in various metabolic pathways including alanine, aspartate and glutamate metabolism, starch and sucrose metabolism, pentose phosphate pathway, and lysine degradation, which were mitigated after the treatments. UV/SPC showed advantage over UV/H2O2 of attenuated impact on butanoate metabolism with UV irradiation. This study has generated valuable data for better understanding of biological impacts of BPA and its solutions treated with UV/H2O2 or UV/SPC, thus providing insights for their application prospect for water and wastewater treatment.