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Plants cannot move, so they have evolved sophisticated strategies that integrate the external environmental cues and internal signaling networks for adaptation to dynamic circumstances. Cis-(+)-12-oxo-phytodienoic acid (OPDA) and 2,3-dinor-OPDA (dn-OPDA), the cyclopentenone-containing oxylipins, ubiquitously occur in the green lineage to orchestrate a series of growth and developmental processes as well as various stress and defense responses. OPDA/dn-OPDA are precursors of jasmonate (JA) biosynthesis in vascular plants. Dn-OPDA and its isomer also serve as bioactive JAs perceived by the coronatine insensitive 1/jasmonate ZIM-domain (COI1/JAZ) co-receptor complex in bryophytes and lycophytes. In addition, OPDA/dn-OPDA display signaling activities independent of (+)-7-iso-jasmonoyl-l-isoleucine (JA-Ile) and COI1 in both vascular and non-vascular plants. In this review, we discuss recent advances in the biosynthesis, metabolism, and signaling of OPDA/dn-OPDA, and provide an overview of the evolution of OPDA/dn-OPDA actions to obtain a deeper understanding of the pervasive role of OPDA/dn-OPDA in the plant life cycle. [ABSTRACT FROM AUTHOR]

This article, published in the New Phytologist journal, discusses the behavior and internalization of the AtRGS1 protein in response to different pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs) in Arabidopsis thaliana. The study found that AtRGS1 exhibits distinct behaviors and endocytic pathways depending on the type of PAMP/DAMP, and that its phosphorylation pattern contributes to its organization and endocytic model. The research provides insights into the mechanisms of plant immune responses. [Extracted from the article]

Background: The plasma membrane (PM) proteins function in a highly dynamic state, including protein trafficking and protein homeostasis, to regulate various biological processes. The dwell time and colocalization of PM proteins are considered to be two important dynamic features determining endocytosis and protein interactions, respectively. Dwell-time and colocalization detected using traditional fluorescence microscope techniques are often misestimated due to bulk measurement. In particular, analyzing these two features of PM proteins at the single-molecule level with spatiotemporal continuity in plant cells remains greatly challenging. Results: We developed a single molecular (SM) kymograph method, which is based on variable angle-total internal reflection fluorescence microscopy (VA-TIRFM) observation and single-particle (co-)tracking (SPT) analysis, to accurately analyze the dwell time and colocalization of PM proteins in a spatial and temporal manner. Furthermore, we selected two PM proteins with distinct dynamic behaviors, including AtRGS1 (Arabidopsis regulator of G protein signaling 1) and AtREM1.3 (Arabidopsis remorin 1.3), to analyze their dwell time and colocalization upon jasmonate (JA) treatment by SM kymography. First, we established new 3D (2D+t) images to view all trajectories of the interest protein by rotating these images, and then we chose the appropriate point without changing the trajectory for further analysis. Upon JA treatment, the path lines of AtRGS1-YFP appeared curved and short, while the horizontal lines of mCherry-AtREM1.3 demonstrated limited changes, indicating that JA might initiate the endocytosis of AtRGS1. Analysis of transgenic seedlings coexpressing AtRGS1-YFP/mCherry-AtREM1.3 revealed that JA induces a change in the trajectory of AtRGS1-YFP, which then merges into the kymography line of mCherry-AtREM1.3, implying that JA increases the colocalization degree between AtRGS1 and AtREM1.3 on the PM. These results illustrate that different types of PM proteins exhibit specific dynamic features in line with their corresponding functions. Conclusions: The SM-kymograph method provides new insight into quantitively analyzing the dwell time and correlation degree of PM proteins at the single-molecule level in living plant cells. [ABSTRACT FROM AUTHOR]

The nuclear pore complex (NPC), the sole exchange channel between the nucleus and cytoplasm, is composed of several subcomplexes, among which the central barrier determines the permeability/selectivity of the NPC to dominate the nucleocytoplasmic trafficking essential for many important signaling events in yeast and mammals. How plant NPC central barrier controls selective transport is a crucial question remaining to be elucidated. In this study, we uncovered that phase separation of the central barrier is critical for the permeability and selectivity of plant NPC in the regulation of various biotic stresses. Phenotypic assays of nup62 mutants and complementary lines showed that NUP62 positively regulates plant defense against Botrytis cinerea , one of the world's most disastrous plant pathogens. Furthermore, in vivo imaging and in vitro biochemical evidence revealed that plant NPC central barrier undergoes phase separation to regulate selective nucleocytoplasmic transport of immune regulators, as exemplified by MPK3, essential for plant resistance to B. cinerea. Moreover, genetic analysis demonstrated that NPC phase separation plays an important role in plant defense against fungal and bacterial infection as well as insect attack. These findings reveal that phase separation of the NPC central barrier serves as an important mechanism to mediate nucleocytoplasmic transport of immune regulators and activate plant defense against a broad range of biotic stresses. The plant NPC central barrier undergoes phase separation to facilitate selective nucleocytoplasmic transport of immune regulators, including MPK3, critical for plant resistance to Botrytis cinerea. Such NPC central barrier phase separation-regulated nucleocytoplasmic transport is essential for plants to defend against pathogens and insects. Phase separation of the NPC central barrier serves as an important mechanism to mediate nucleocytoplasmic transport of immune regulators and regulate plant defense against a broad range of biotic stresses. [ABSTRACT FROM AUTHOR]

The lack of United States population‐based data on Turner syndrome limits assessments of prevalence and associated characteristics for this sex chromosome abnormality. Therefore, we collated 2000–2017 data from seven birth defects surveillance programs within the National Birth Defects Prevention Network. We estimated the prevalence of karyotype‐confirmed Turner syndrome diagnosed within the first year of life. We also calculated the proportion of cases with commonly ascertained birth defects, assessed associations with maternal and infant characteristics using prevalence ratios (PR) with 95% confidence intervals (CI), and estimated survival probability. The prevalence of Turner syndrome of any pregnancy outcome was 3.2 per 10,000 female live births (95% CI = 3.0–3.3, program range: 1.0–10.4), and 1.9 for live birth and stillbirth (≥20 weeks gestation) cases (95% CI = 1.8–2.1, program range: 0.2–3.9). Prevalence was lowest among cases born to non‐Hispanic Black women compared to non‐Hispanic White women (PR = 0.5, 95% CI = 0.4–0.6). Coarctation of the aorta was the most common defect (11.6% of cases), and across the cohort, individuals without hypoplastic left heart had a five‐year survival probability of 94.6%. The findings from this population‐based study may inform surveillance practices, prenatal counseling, and diagnosis. We also identified racial and ethnic disparities in prevalence, an observation that warrants further investigation. [ABSTRACT FROM AUTHOR]

Dear Editor, The phytohormone jasmonate (JA), including jasmonic acid and its oxylipin derivatives, is essential for plant resistance against various stresses[1],[2]. Here, we identify I Jasmonate-Induced Dioxygenase1 i ( I JID1 i ) that encodes a 2OGD modifying OPDA and reducing the conversion of OPDA into jasmonic acid and JA-Ile. Interestingly, the amounts of OPDA, jasmonic acid, and JA-Ile in loss-of-function mutants I jid1-1 i and I jid1-5 i were similar to those of WT (Supplementary Figs. [Extracted from the article]

Plants and microbial pathogens often engage in a fierce war that determines their survival. Host plants have evolved sophisticated regulatory mechanisms to fine-tune defense responses to counter attacks from pathogens, while pathogens often hijack the lipid-derived phytohormone jasmonate to cause hormonal signaling imbalances for efficient infection. This review focuses on the jasmonate-based warfare between host plants and pathogenic intruders, and further discusses approaches to uncouple plant growth and defense tradeoffs in crop breeding. [ABSTRACT FROM AUTHOR]

Jasmonate (JA) is one of the key phytohormones essential for plant development and defense processes. The core JA biosynthetic and signaling pathways have been well-characterized. Notably, post-translational modifications (PTMs), which affect the protein structures and functions, have emerged as critical mechanisms to modulate JA output at different spatiotemporal levels. Disruption of PTMs in JA biosynthesis and signaling would cause the dysfunction of vital biological processes. Here, we give an overview of the PTMs that have been identified in JA biosynthetic and signaling pathways, and provide insights into the mechanisms by which PTMs define JA responses. [ABSTRACT FROM AUTHOR]

Phytohormones integrate external environmental and developmental signals with internal cellular responses for plant survival and multiplication in changing surroundings. Jasmonate (JA), which might originate from prokaryotes and benefit plant terrestrial adaptation, is a vital phytohormone that regulates diverse developmental processes and defense responses against various environmental stresses. In this review, we first provide an overview of ligand–receptor binding techniques used for the characterization of phytohormone–receptor interactions, then introduce the identification of the receptor COI1 and active JA molecules, and finally summarize recent advances on the regulation of JA perception and its evolution. Mechanisms of hormone perceptionis a topic of extraordinary significance, and perception of the hormone jasmonate (JA) is essential for plant defense and growth. This review highlights the methodology of ligand–receptor binding techniques and the interaction between bioactive JA and its receptor COI1. Recent advances on the regulation of JA perception and its evolution are also discussed. [ABSTRACT FROM AUTHOR]

Main conclusion: The N-myristoylation is required for BSK1 proper plasma membrane targeting and protein turnover. Brassinosteroid (BR) signaling kinase 1 (BSK1), with a myristoylation site at its N-terminus to anchor at plasma membrane (PM), is involved in BR-regulated plant growth and flg22-triggered immunity responses. However, little is known about the role of N-myristoylation in BSK1 protein homeostasis. Here, we revealed that N-myristoylation is critical to the PM targeting and protein stability of BSK1. The N-myristoylation-deficient mutant BSK1G2A mainly distributed in the cytoplasm and retained in the endoplasmic reticulum. We further found that the BSK1G2A proteins were unstable and degraded through ATG8e-labled autophagic pathway. This study provides a new insight into the regulation of plant protein homeostasis. [ABSTRACT FROM AUTHOR]

Background: Critical congenital heart defects (CCHDs) are one of the most common types of birth defects and can lead to significant morbidity and mortality along with surgical or catheter interventions within the first year of life. This report updates previously published estimates of CCHD prevalence with the latest population‐based surveillance data from 19 birth defect surveillance programs. Methods: The U.S. population‐based surveillance programs submitted data on identified cases of 12 CCHDs and co‐occurring cardiovascular and chromosomal birth defects from 2014 to 2018. We estimated prevalence by program type and maternal and infant characteristics. Among nine programs with active case ascertainment that collect more than live births, we estimated the percentage of co‐occurring cardiovascular and chromosomal birth defects for the 12 CCHDs. Results: We identified 18,587 cases of CCHD among all participating programs. Overall CCHD prevalence was 19.6 per 10,000 live births among all 19 programs and 20.2 per 10,000 live births among active programs. Among maternal racial/ethnic groups, infants/fetuses born to American Indian/Alaska Native mothers showed the highest overall prevalence for all CCHDs (28.3 per 10,000) along with eight of the 12 individual CCHDs. Among 7,726 infants/fetuses with CCHD from active case ascertainment programs, 15.8% had at least one co‐occurring chromosomal birth defect. Conclusion: Our study provides prevalence estimates for CCHDs by maternal and infant characteristics along with co‐occurrence with cardiovascular and chromosomal birth defects among infants/fetuses with CCHD using one of the largest and most recent cohorts since the implementation of widespread CCHD screening. These data can provide a basis for future research to better understand risk factors for these defects. [ABSTRACT FROM AUTHOR]

The bias is in the system: In Arabidopsis, the nutrient glucose and the bacterial peptide flg22 both induce the internalization of the RGS protein AtRGS1 but trigger different transcriptional responses. Watkins et al. found that the distinct changes in cellular responses were mediated by segregated signaling pathways. Glucose and flg22 induced the internalization of AtRGS1 through different forms of endocytosis and required different phosphorylation events, endocytic adaptor proteins, and G protein subunits. Because of these systemic biases, only flg22 triggered MAPK and Ca2+ signaling before changes in gene expression. Thus, AtRGS1 links the appropriate signaling outputs to the corresponding signaling inputs through differences in the architecture of the signaling pathways that originate at the plasma membrane. In animals, endocytosis of a seven-transmembrane GPCR is mediated by arrestins to propagate or arrest cytoplasmic G protein–mediated signaling, depending on the bias of the receptor or ligand, which determines how much one transduction pathway is used compared to another. In Arabidopsis thaliana, GPCRs are not required for G protein–coupled signaling because the heterotrimeric G protein complex spontaneously exchanges nucleotide. Instead, the seven-transmembrane protein AtRGS1 modulates G protein signaling through ligand-dependent endocytosis, which initiates derepression of signaling without the involvement of canonical arrestins. Here, we found that endocytosis of AtRGS1 initiated from two separate pools of plasma membrane: sterol-dependent domains and a clathrin-accessible neighborhood, each with a select set of discriminators, activators, and candidate arrestin-like adaptors. Ligand identity (either the pathogen-associated molecular pattern flg22 or the sugar glucose) determined the origin of AtRGS1 endocytosis. Different trafficking origins and trajectories led to different cellular outcomes. Thus, in this system, compartmentation with its associated signalosome architecture drives biased signaling. [ABSTRACT FROM AUTHOR]

Growth and immunity are opposing processes that compete for cellular resources, and proper resource allocation is crucial for plant survival. BSK1 plays a key role in the regulation of both growth and immunity by associating with BRI1 and FLS2, respectively. However, it remains unclear how two antagonistic signals co-opt BSK1 to induce signal-specific activation. Here we show that the dynamic spatial reorganization of BSK1 within the plasma membrane underlies the mechanism of signal-specific activation for growth or immunity. Resting BSK1 localizes to membrane rafts as complexes. Unlike BSK1-associated FLS2 and BRI1, flg22 or exogenous brassinosteroid (BR) treatment did not decrease BSK1 levels at the plasma membrane (PM) but rather induced BSK1 multimerization and dissociation from FLS2/BSK1 or BRI1/BSK1, respectively. Moreover, flg22-activated BSK1 translocated from membrane rafts to non-membrane-raft regions, whereas BR-activated BSK1 remained in membrane rafts. When applied together with flg22, BR suppressed various flg22-induced BSK1 activities such as BSK1 dissociation from FLS2/BSK1, BSK1 interaction with MAPKKK5, and BSK translocation together with MAPKKK5. Taken together, this study provides a unique insight into how the precise control of BSK1 spatiotemporal organization regulates the signaling specificity to balance plant growth and immunity. By using single-molecule techniques and biochemical approaches, this study demonstrates that the precise control of BSK1 spatiotemporal organization plays a pivotal role in fine-tuning the growth–defense trade-off between BRI1- and FLS2-mediated signaling. [ABSTRACT FROM AUTHOR]

Background: Down syndrome is the most common chromosomal disorder at birth and is often accompanied by structural birth defects. Current data on major structural defects in this population are limited. Methods: States and territorial population‐based surveillance programs submitted data on identified cases of Down syndrome and identified structural birth defects during 2013–2017. We estimated prevalence by program type and maternal and infant characteristics. Among programs with active case ascertainment, we estimated the prevalence of birth defects by organ system and for specific defects by maternal age (<35, ≥35) and infant sex. Results: We identified 13,376 cases of Down syndrome. Prevalence among all programs was 12.7 per 10,000 live births. Among these children, 75% had at least one reported co‐occurring birth defect diagnosis code. Among 6,210 cases identified by active programs, 66% had a cardiovascular defect with septal defects being the most common: atrial (32.5%), ventricular (20.6%), and atrioventricular (17.4%). Defect prevalence differed by infant sex more frequently than by maternal age. For example, atrioventricular septal defects were more common in female children (20.1% vs. 15.1%) while limb deficiencies were more prevalent in male children (0.4% vs. 0.1%). Conclusions: Our study provides updated prevalence estimates for structural defects, including rare defects, among children with Down syndrome using one of the largest and most recent cohorts to date. These data may aid clinical care and surveillance. [ABSTRACT FROM AUTHOR]

Background: The increasing number of novel approaches for large-scale, multi-dimensional imaging of cells has created an unprecedented opportunity to analyze plant morphogenesis. However, complex image processing, including identifying specific cells and quantitating parameters, and high running cost of some image analysis softwares remains challenging. Therefore, it is essential to develop an efficient method for identifying plant complex multicellularity in raw micrographs in plants. Results: Here, we developed a high-efficiency procedure to characterize, segment, and quantify plant multicellularity in various raw images using the open-source software packages ImageJ and SR-Tesseler. This procedure allows for the rapid, accurate, automatic quantification of cell patterns and organization at different scales, from large tissues down to the cellular level. We validated our method using different images captured from Arabidopsis thaliana roots and seeds and Populus tremula stems, including fluorescently labeled images, Micro-CT scans, and dyed sections. Finally, we determined the area, centroid coordinate, perimeter, and Feret's diameter of the cells and harvested the cell distribution patterns from Voronoï diagrams by setting the threshold at localization density, mean distance, or area. Conclusions: This procedure can be used to determine the character and organization of multicellular plant tissues at high efficiency, including precise parameter identification and polygon-based segmentation of plant cells. [ABSTRACT FROM AUTHOR]

Chinese fir (Cunninghamia lanceolata) cotyledons are green in darkness due to the coexistence of functional dark-operative protochlorophyllide reductase (DPOR) and light-dependent protochlorophyllide reductase (LPOR). In this study, we found that the POR gene for LPOR and the ChlB, ChlL, and ChlN genes for three DPOR subunits were strongly downregulated in dark-grown new sprouts in which chlorophyll biosynthesis was inhibited. We extracted, sequenced, and annotated the total RNA from etiolated (dark-grown) and green (light-grown) sprouts. A total of 70,499 unigenes were found, of which 47,410 were annotated. Among them, 3263 differentially expressed genes were identified between dark- and light-grown samples. According to the Kyoto Encyclopedia of Genes and Genomes databases, the five most affected metabolic pathways were flavonoid biosynthesis, photosynthesis-antenna proteins, photosynthesis, cutin, suberine and wax biosynthesis and stilbenoid, diarylheptanoid, and gingerol biosynthesis. Based on the acquired cDNA sequences, we applied quantitative PCR to further analyze the relative expression levels of 18 nuclear genes and 11 chloroplast genes related to photophosphorylation. Both transcriptomic and quantitative PCR results indicated that dark treatment can significantly block the expression of all of the identified genes related to the protein complexes of photosynthetic electron flow in new sprouts. Dark treatment of new sprouts of Chinese fir caused etiolation via blockage of the expression of DPOR- and LPOR-encoding genes. Both nuclear and plastid genomic genes related to photosynthesis were significantly downregulated in etiolated sprouts. The results provide new clues to understanding the different mechanisms of chloroplast development in different photosynthetic organs. [ABSTRACT FROM AUTHOR]

Background/Objectives: In this report, the National Birth Defects Prevention Network (NBDPN) examines and compares gastroschisis and omphalocele for a recent 5‐year birth cohort using data from 30 population‐based birth defect surveillance programs in the United States. Methods: As a special call for data for the 2019 NBDPN Annual Report, state programs reported expanded data on gastroschisis and omphalocele for birth years 2012–2016. We estimated the overall prevalence (per 10,000 live births) and 95% confidence intervals (CI) for each defect as well as by maternal race/ethnicity, maternal age, infant sex, and case ascertainment methodology utilized by the program (active vs. passive). We also compared distribution of cases by maternal and infant factors and presence/absence of other birth defects. Results: The overall prevalence estimates (per 10,000 live births) were 4.3 (95% CI: 4.1–4.4) for gastroschisis and 2.1 (95% CI: 2.0–2.2) for omphalocele. Gastroschisis was more frequent among young mothers (<25 years) and omphalocele more common among older mothers (>40 years). Mothers of infants with gastroschisis were more likely to be underweight/normal weight prior to pregnancy and mothers of infants with omphalocele more likely to be overweight/obese. Omphalocele was twice as likely as gastroschisis to co‐occur with other birth defects. Conclusions: This report highlights important differences between gastroschisis and omphalocele. These differences indicate the importance of distinguishing between these defects in epidemiologic assessments. The report also provides additional data on co‐occurrence of gastroschisis and omphalocele with other birth defects. This information can provide a basis for future research to better understand these defects. [ABSTRACT FROM AUTHOR]

Objective Despite heterogeneity among Pacific Islanders, most studies aggregate them regardless of origin. Thus, limited information is available about perinatal outcomes among various subgroups of Pacific Islanders in the United States, including immigrants from the Republic of the Marshall Islands. We sought to evaluate perinatal outcomes among Marshallese women. Methods We conducted a cross-sectional study of women with at least one singleton live birth between 1997 and 2013 in two Arkansas counties using birth certificate data from the Arkansas Department of Health. Unadjusted and adjusted prevalence ratios (PR) and 95% confidence intervals (CI) were calculated from modified Poisson regression models. Results Of the 91,662 singleton births in both counties during the study period, 2488 were to Marshallese women. In adjusted analyses, Marshallese women had higher prevalence of "other medical risk factors" (PR = 1.47; 95% CI 1.30, 1.65) than NH White women. Marshallese women had higher rates of precipitous labor and fetal distress during labor compared to NH White women (PR = 2.65; 95% CI 2.22, 3.17 and 1.89; 95% CI 1.62, 2.21, respectively). Marshallese were also more likely to have tocolysis (PR = 1.43; 95% CI 1.16, 1.76), forceps (PR = 1.68; 95% CI 1.16, 2.43) or vacuum (PR = 1.89; 95% CI 1.60, 2.22) used in delivery and cesarean section (PR = 1.13; 95% CI 1.01, 1.27). Marshallese infants had higher rates of anemia (PR = 3.10; 95% CI 2.01, 4.77), birth injury (PR = 2.13; 95% CI 1.50, 3.03), assisted ventilation < 30 min (PR = 2.11; 95% CI 1.64, 2.71), preterm birth (PR = 1.67; 95% CI 1.50, 1.83), and small-for-gestational age (PR = 1.25; 95% CI 1.12, 1.39) than NH White infants. Conclusions Marshallese women and infants had higher rates of adverse perinatal outcomes compared to their NH White counterparts. Additional studies are needed to determine if perinatal outcomes among the Marshallese differed from other Pacific Islander subgroups. [ABSTRACT FROM AUTHOR]

Background: With their unique history of exposure to extensive nuclear testing between 1946 and 1958, descendants of Marshall Island residents may have underappreciated genetic abnormalities, increasing their risk of birth defects. Methods: We conducted a retrospective cohort study of resident women with at least one singleton live birth between 1997 and 2013 in northwest Arkansas using state birth certificate data linked to data from the Arkansas Reproductive Health Monitoring System, a statewide birth defects registry. We calculated unadjusted and adjusted prevalence ratios (PR) and 95% confidence intervals (CI) from modified Poisson regression analyses for non‐Hispanic (NH) whites, NH‐blacks, Hispanics and Marshallese, using NH‐whites as the reference group. Results: Of the 91,662 singleton births during the study period, 2,488 were to Marshallese women. Due to the relatively small number of Marshallese births, we could not calculate prevalence estimates for some defects. Marshallese infants had higher rates of congenital cataracts (PR = 9.3; 95% CI: 3.1, 27.9). Although the number of defects was low, Marshallese infants also had higher rates of truncus arteriosus (PR = 44.0; 95% CI: 2.2, 896.1). Conclusions: Marshallese infants may have increased risk of specific birth defects, but estimates are unstable because of small sample size so results are inconclusive. Larger population‐based studies would allow for further investigation of this potential risk among Marshallese infants. [ABSTRACT FROM AUTHOR]

The plant cell wall is an important interface for sensing pathogen attack and activating signaling pathways that promote plant immune responses. THESEUS1 (THE1) acts as a sensor of cell wall integrity that controls cell elongation during plant growth. However, no specific role for THE1 in plant defense responses has been reported. Here, we found that THE1 interacts with GUANINE EXCHANGE FACTOR4 (GEF4) and that both proteins play regulatory roles in plant resistance to the necrotrophic fungus Botrytis cinerea. Genetic analysis showed that THE1 and GEF4 function in the same genetic pathway to mediate plant defense responses. In addition, using transcriptome analysis, we identified various genes (such as defense-related, secondary metabolite-related, and transcription factor genes) that are likely downstream targets in the THE1-GEF4 signaling pathway. Our results suggest that THE1 functions as an upstream regulator of GEF4 signaling to positively regulate defense responses against B. cinerea in Arabidopsis. [ABSTRACT FROM AUTHOR]

Biosynthesis and accumulation of jasmonate (JA) can regulate plant defense responses and organ development under insect herbivore stress conditions. One of these responses, the inhibition of root growth, is a common phenomenon. However, the physiological and molecular mechanisms of how JA affects root growth are not completely understood. In this study, the influence of MeJA treatment on auxin and proton flux rates in the root apex region of Col-0, coi1-1, pin2, and aux1-7 mutant lines was examined using a non-invasive micro-test technique. The auxin and H flux profiles taken from coi1-1 mutants suggest that the modulation of auxin and H flux by JA requires the function of COI1. The auxin and H flux in pin2 and aux1 mutants with and without JA treatment suggest that JA can affect polar auxin transport by regulating PIN-mediated auxin efflux and the AUX-mediated influx pathways. Furthermore, the expression levels of PIN1, PIN2, PIN3, PIN7, AUX1, and TIR1 genes were reduced under MeJA treatment, and expression levels of CYP79B2 and CYP79B3 were elevated. Together, these results suggest that JA signaling may modulate the auxin signaling pathways by regulating the expression of key genes. [ABSTRACT FROM AUTHOR]

Jasmonates (JAs) are a new class of plant hormone that regulate expression of diverse genes to mediate various plant responses. The Arabidopsis F-box protein COI1 is required for plant defense and male fertility in JA signal pathway. To further investigate the regulatory role of COI1 in male fertility, we compared the proteomics profiles of Arabidopsis wild type (WT) flowers with coi1-1 mutant male-sterile flowers using two-dimensional difference gel electrophoresis coupled with matrix-assisted laser desoption/ionization-time-of-flight mass spectrometry. Sixteen proteins with potential function in specific biological processes such as metabolism processes and defense/stress responses were differentially expressed in WT and coi1-1 mutant flowers. Verification on a phi class glutathione transferase AtGSTF9, one out of these 16 identified proteins, revealed that the expression of AtGSTF9 was severely downregulated in flowers of coi1-1 mutant compared with that of WT. Further function analyses of these genes would provide new insights into the molecular basis of COI1-regulated male fertility. [ABSTRACT FROM AUTHOR]

Aiming to construct a direct Z-scheme binary heterostructure for efficient degradation of the organic dye Rhodamine B (RhB), ZnWO4 nanorods decorated with SnS nanodots were rationally designed and prepared via a facile two-step route. Morphological observation and structural study showed that ultra-fine SnS nanodots were anchored on the surface of ZnWO4 nanorods to form an intimate contact between the two components. Such a special structure provided SnS/ZnWO4 nanocomposites with significantly enhanced light harvesting capacity, revealed by the results of UV-vis diffuse reflection spectroscopy (DRS). Photoluminescence (PL) analysis in combination with electrochemical measurements demonstrated that the recombination of photoactivated charge carriers was efficiently inhibited and the transfer of photoactivated charge carriers was successfully achieved due to the introduction of SnS. The degradation rate over SnS/ZnWO4 nanocomposites reached a maximum value at SnS content of 9 wt%. The significantly enhanced photoactivity of SnS/ZnWO4 nanocomposites was imputed to the synergistic effect of the promoted light absorption ability and effective photogenerated charge carriers' transfer and separation. [ABSTRACT FROM AUTHOR]

Lead is a heavy metal known to be toxic to both animals and plants. Nitric oxide (NO) was reported to participate in plant responses to different heavy metal stresses. In this study, we analyzed the function of exogenous and endogenous NO in Pb-induced toxicity in tobacco BY-2 cells, focusing on the role of NO in the generation of reactive oxygen species (ROS) as well as Pb2+ and Ca2+ fluxes using non-invasive micro-test technology (NMT). Pb treatment induced BY-2 cell death and rapid NO and ROS generation, while NO burst occurred earlier than ROS accumulation. The elimination of NO by 2-4-carboxyphenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO) resulted in a decrease of ROS, and the supplementation of NO by sodium nitroprusside (SNP) caused an increased accumulation of ROS. Furthermore, the addition of exogenous NO stimulated Pb2+ influx, thus promoting Pb uptake in cells and aggravating Pb-induced toxicity in cells, whereas the removal of endogenous NO produced the opposite effect. Moreover, we also found that both exogenous and endogenous NO enhanced Pb-induced Ca2+ effluxes and calcium homeostasis disorder. These results suggest that exogenous and endogenous NO played a critical regulatory role in BY-2 cell death induced by Pb stress by promoting Pb2+ influx and accumulation and disturbing calcium homeostasis. [ABSTRACT FROM AUTHOR]

Arabidopsis heterotrimeric G proteins regulate diverse plant growth and defense processes by coupling to 7TM AtRGS1 proteins. Although G protein mutants display alterations in response to multiple plant hormones, the underlying mechanism by which G proteins participate in the regulation of hormone responses remains elusive. Here, we show that genetic disruption of Gα and Gβ subunits results in reduced sensitivity to JA treatment. Furthermore, using confocal microscopy, VA-TIRFM, and FRET-FLIM, we provide evidence that stimulation by JA induces phosphorylation- and C-terminus-dependent endocytosis of AtRGS1, which then promotes dissociation of AtRGS1 from AtGPA1. In addition, SPT analysis reveals that JA treatment affects the diffusion dynamics of AtRGS1 and AtRGS1-ΔCt. Taken together, these findings suggest that the JA signal activates heterotrimeric G proteins through the endocytosis of AtRGS1 and dissociation of AtRGS1 from AtGPA1, thus providing valuable insight into the mechanisms of how the G protein system perceives and transduces phytohormone signals. [ABSTRACT FROM AUTHOR]