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Bioelectronic medicine is emerging as a powerful approach for restoring lost endogenous functions and addressing life-altering maladies such as cardiac disorders. Systems that incorporate both modulation of cellular function and recording capabilities can enhance the utility of these approaches and their customization to the needs of each patient. Here is report an integrated optogenetic and bioelectronic platform for stable and long-term stimulation and monitoring of cardiomyocyte function in vitro. Optical inputs are achieved through the expression of a photoactivatable adenylyl cyclase, that when irradiated with blue light causes a dose-dependent and time-limited increase in the secondary messenger cyclic adenosine monophosphate with subsequent rise in autonomous cardiomyocyte beating rate. Bioelectronic readouts are obtained through a multi-electrode array that measures real-time electrophysiological responses at 32 spatially-distinct locations. Irradiation at 27 µW mm-2 results in a 14% elevation of the beating rate within 20-25 min, which remains stable for at least 2 h. The beating rate can be cycled through "on" and "off" light states, and its magnitude is a monotonic function of irradiation intensity. The integrated platform can be extended to stretchable and flexible substrates, and can open new avenues in bioelectronic medicine, including closed-loop systems for cardiac regulation and intervention, for example, in the context of arrythmias.
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Recent advances in chemical proteomics have focused on developing chemical probes that react with nucleophilic amino acid residues. Although histidine is an attractive candidate due to its importance in enzymatic catalysis, metal binding and protein-protein interaction, its moderate nucleophilicity poses challenges. Its modification is frequently influenced by cysteine and lysine, which results in poor selectivity and narrow proteome coverage. Here we report a singlet oxygen and chemical probe relay labelling method that achieves high selectivity towards histidine. Libraries of small-molecule photosensitizers and chemical probes were screened to optimize histidine labelling, enabling histidine profiling in live cells with around 7,200 unique sites. Using NMR spectroscopy and X-ray crystallography, we characterized the reaction mechanism and the structures of the resulting products. We then applied this method to discover unannotated histidine sites key to enzymatic activity and metal binding in select metalloproteins. This method also revealed the accessibility change of histidine mediated by protein-protein interaction that influences select protein subcellular localization, underscoring its capability in discovering functional histidines.
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MYB transcription factors have been linked to anthocyanin synthesis and various color phenotypes in plants. In apple, MYB10 confers a red-flesh phenotype due to a minisatellite insertion in its R6 promoter, but R6:MYB10 genotypes exhibit various degrees of red pigmentation in the flesh, suggesting the involvement of other genetic factors. Here, it is shown that MdWRKY10, a transcription factor identified via DNA pull-down trapping, binds to the promoter of MdMYB10 and activates its transcription. MdWRKY10 specifically interacts with the WDR protein MdTTG1 to join the apple MYB-bHLH-WDR (MBW) complex, which significantly enhances its transcriptional activation activity. A 163-bp InDel detected in the promoter region of the alleles of MdWRKY10 in a hybrid population of identical heterozygous genotypes regarding R6 by structural variation analysis, contains a typical W-box element that MdWRKY10 binds to for transactivation. This leads to increased transcript levels of MdWRKY10 and MdMYB10 and enhanced anthocyanin synthesis in the flesh, largely accounting for the various degrees of flesh red pigmentation in the R6 background. These findings reveal a novel regulatory role of the WRKY-containing protein complex in the formation of red flesh apple phenotypes and provide broader insights into the molecular mechanism governing anthocyanin synthesis in plants.
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Regulación de la Expresión Génica de las Plantas , Malus , Fenotipo , Pigmentación , Proteínas de Plantas , Regiones Promotoras Genéticas , Factores de Transcripción , Regiones Promotoras Genéticas/genética , Pigmentación/genética , Malus/genética , Malus/metabolismo , Factores de Transcripción/genética , Factores de Transcripción/metabolismo , Regulación de la Expresión Génica de las Plantas/genética , Proteínas de Plantas/genética , Proteínas de Plantas/metabolismo , Mutación INDEL/genética , Antocianinas/genética , Antocianinas/metabolismo , Genotipo , Frutas/genética , Frutas/metabolismoRESUMEN
Rationale: Physical activity, lung function, and grip strength are associated with exacerbations, hospitalizations, and mortality in people with chronic obstructive pulmonary disease (COPD). We tested whether baseline inflammatory biomarkers were associated with longitudinal outcomes of these physiologic measurements. Methods: The COPD Activity: Serotonin Transporter, Cytokines, and Depression (CASCADE) study was a prospective observational study of individuals with COPD. A total of 14 inflammatory biomarkers were measured at baseline. Participants were followed for 2 years. We analyzed associations between baseline biomarkers and forced expiratory volume in 1 second (FEV1), physical activity, and grip strength. We used a hierarchical hypothesis testing procedure to reduce type I error. We used Pearson correlations to test associations between baseline biomarkers and longitudinal changes in the outcomes of interest. We used Fisher's linear discriminant analysis to test if linear combinations of baseline biomarkers predict rapid FEV1 decline. Finally, we used linear mixed modeling to test associations between baseline biomarkers and outcomes of interest at baseline, year 1, and year 2; models were adjusted for age, smoking status, baseline biomarkers, and FEV1. Results: A total of 302 participants (age 67.5 ± 8.5 years, 19.5% female, 28.5% currently smoking) were included. Baseline biomarkers were not associated with longitudinal changes in grip strength, physical activity, or rapid FEV1 decline. Higher interleukin-6 and C-reactive protein were associated with lower physical activity at baseline and these relationships persisted at year 1 and year 2. Conclusion: Baseline inflammatory biomarkers did not predict changes in lung function or physical activity, but higher inflammatory biomarkers were associated with persistently low levels of physical activity.
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Deinococcus radiodurans, with its high homologous recombination (HR) efficiency of double-stranded DNA breaks (DSBs), is a model organism for studying genome stability maintenance and an attractive microbe for industrial applications. Here, we developed an efficient CRISPR/Cpf1 genome editing system in D. radiodurans by evaluating and optimizing double-plasmid strategies and four Cas effector proteins from various organisms, which can precisely introduce different types of template-dependent mutagenesis without off-target toxicity. Furthermore, the role of DNA repair genes in determining editing efficiency in D. radiodurans was evaluated by introducing the CRISPR/Cpf1 system into 13 mutant strains lacking various DNA damage response and repair factors. In addition to the crucial role of RecA-dependent HR required for CRISPR/Cpf1 editing, D. radiodurans showed higher editing efficiency when lacking DdrB, the single-stranded DNA annealing (SSA) protein involved in the RecA-independent DSB repair pathway. This suggests a possible competition between HR and SSA pathways in the CRISPR editing of D. radiodurans. Moreover, off-target effects were observed during the genome editing of the pprI knockout strain, a master DNA damage response gene in Deinococcus species, which suggested that precise regulation of DNA damage response is critical for a high-fidelity genome editing system.
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Sistemas CRISPR-Cas , Reparación del ADN , Deinococcus , Edición Génica , Deinococcus/genética , Edición Génica/métodos , Reparación del ADN/genética , Genoma Bacteriano , Roturas del ADN de Doble Cadena , Recombinación Homóloga , Proteínas Bacterianas/genética , Proteínas Bacterianas/metabolismo , Plásmidos/genética , Mutagénesis , Inestabilidad Genómica , Repeticiones Palindrómicas Cortas Agrupadas y Regularmente Espaciadas , Rec A Recombinasas/genética , Rec A Recombinasas/metabolismo , Daño del ADNRESUMEN
Proteotoxic stress drives numerous degenerative diseases. Cells initially adapt to misfolded proteins by activating the unfolded protein response (UPR), including endoplasmic-reticulum-associated protein degradation (ERAD). However, persistent stress triggers apoptosis. Enhancing ERAD is a promising therapeutic approach for protein misfolding diseases. The ER-localized Zn2+ transporter ZIP7 is conserved from plants to humans and required for intestinal self-renewal, Notch signaling, cell motility, and survival. However, a unifying mechanism underlying these diverse phenotypes was unknown. In studying Drosophila border cell migration, we discovered that ZIP7-mediated Zn2+ transport enhances the obligatory deubiquitination of proteins by the Rpn11 Zn2+ metalloproteinase in the proteasome lid. In human cells, ZIP7 and Zn2+ are limiting for deubiquitination. In a Drosophila model of neurodegeneration caused by misfolded rhodopsin (Rh1), ZIP7 overexpression degrades misfolded Rh1 and rescues photoreceptor viability and fly vision. Thus, ZIP7-mediated Zn2+ transport is a previously unknown, rate-limiting step for ERAD in vivo with therapeutic potential in protein misfolding diseases.
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Proteínas de Transporte de Catión , Proteínas de Drosophila , Degradación Asociada con el Retículo Endoplásmico , Retículo Endoplásmico , Zinc , Animales , Proteínas de Transporte de Catión/metabolismo , Proteínas de Transporte de Catión/genética , Zinc/metabolismo , Proteínas de Drosophila/metabolismo , Proteínas de Drosophila/genética , Humanos , Retículo Endoplásmico/metabolismo , Complejo de la Endopetidasa Proteasomal/metabolismo , Proteolisis , Drosophila melanogaster/metabolismo , Respuesta de Proteína Desplegada , Ubiquitinación , Movimiento Celular , Drosophila/metabolismoRESUMEN
In addition to long-range periodicity, local disorder, with local structures deviating from the average lattice structure, dominates the physical properties of phonons, electrons, and spin subsystems in crystalline functional materials. Experimentally characterizing the 3D atomic configuration of such a local disorder and correlating it with advanced functions remains challenging. Using a combination of femtosecond electron diffraction, structure factor calculations, and time-dependent density functional theory molecular dynamics simulations, the static local disorder and its local anharmonicity in thermoelectric SnSe are identified exclusively. The ultrafast structural dynamics reveal that the crystalline SnSe is composed of multiple locally correlated configurations dominated by the static off-symmetry displacements of Sn (≈0.4 Å) and such a set of locally correlated structures is termed local disorder. Moreover, the anharmonicity of this local disorder induces an ultrafast atomic displacement within 100 fs, indicating the signature of probable THz Einstein oscillators. The identified local disorder and local anharmonicity suggest a glass-like thermal transport channel, which updates the fundamental insight into the long-debated ultralow thermal conductivity of SnSe. The method of revealing the 3D local disorder and the locally correlated interactions by ultrafast structural dynamics will inspire broad interest in the construction of structure-property relationships in material science.
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Bacteria have evolved various response systems to adapt to environmental stress. A protease-based derepression mechanism in response to DNA damage was characterized in Deinococcus, which is controlled by the specific cleavage of repressor DdrO by metallopeptidase PprI (also called IrrE). Despite the efforts to document the biochemical, physiological, and downstream regulation of PprI-DdrO, the upstream regulatory signal activating this system remains unclear. Here, we show that single-stranded DNA physically interacts with PprI protease, which enhances the PprI-DdrO interactions as well as the DdrO cleavage in a length-dependent manner both in vivo and in vitro. Structures of PprI, in its apo and complexed forms with single-stranded DNA, reveal two DNA-binding interfaces shaping the cleavage site. Moreover, we show that the dynamic monomer-dimer equilibrium of PprI is also important for its cleavage activity. Our data provide evidence that single-stranded DNA could serve as the signal for DNA damage sensing in the metalloprotease/repressor system in bacteria. These results also shed light on the survival and acquired drug resistance of certain bacteria under antimicrobial stress through a SOS-independent pathway.
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Deinococcus , Péptido Hidrolasas , Péptido Hidrolasas/genética , Péptido Hidrolasas/metabolismo , Deinococcus/genética , Deinococcus/metabolismo , ADN de Cadena Simple/metabolismo , Daño del ADN , Metaloproteasas/química , Endopeptidasas/metabolismo , Proteínas Bacterianas/genética , Proteínas Bacterianas/metabolismoRESUMEN
Interface passivation through Lewis acid-base coordinate chemistry in perovskite solar cells (PSCs) is a universal strategy to reduce interface defects and hinder ion migration. However, the formation of coordinate covalent bonding demands strict directional alignment of coordinating atoms. Undoubtedly, this limits the selected range of the interface passivation molecules, because a successful molecular bridge between charge transport layer and perovskite bottom interface needs a well-placed molecular orientation. In this study, it is discovered that potassium ions can migrate to the hollow sites of multiple iodine ions from perovskite to form K-Ix ionic bonding, and the ionic bonds without directionality can support molecular backbone rotation to facilitate polar sites (carboxyl groups) chelating Pb at the bottom perovskite interface, finally forming a closed-loop bonding structure. The synergy of coordinate and ionic bonding significantly reduces interface defects, changes electric field distribution, and immobilizes iodine at the perovskite bottom interface, resulting in eliminating the hysteresis effect and enhancing the performance of PSCs. As a result, the corresponding devices achieve a high efficiency exceeding 24.5% (0.09 cm2), and a mini-module with 21% efficiency (12.4 cm2). These findings provide guidelines for designing molecular bridging strategies at the buried interface of PSCs.
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Enhancement of glucose-stimulated insulin secretion (GSIS) in exogenously delivered pancreatic ß-cells is desirable, for example, to overcome the insulin resistance manifested in type 2 diabetes or to reduce the number of ß-cells for supporting homeostasis of blood sugar in type 1 diabetes. Optogenetically engineered cells can potentiate their function with exposure to light. Given that cyclic adenosine monophosphate (cAMP) mediates GSIS, we surmised that optoamplification of GSIS is feasible in human ß-cells carrying a photoactivatable adenylyl cyclase (PAC). To this end, human EndoC-ßH3 cells were engineered to express a blue-light-activated PAC, and a workflow was established combining the scalable manufacturing of pseudoislets (PIs) with efficient adenoviral transduction, resulting in over 80% of cells carrying PAC. Changes in intracellular cAMP and GSIS were determined with the photoactivation of PAC in vitro as well as after encapsulation and implantation in mice with streptozotocin-induced diabetes. cAMP rapidly rose in ß-cells expressing PAC with illumination and quickly declined upon its termination. Light-induced amplification in cAMP was concomitant with a greater than 2-fold GSIS vs ß-cells without PAC in elevated glucose. The enhanced GSIS retained its biphasic pattern, and the rate of oxygen consumption remained unchanged. Diabetic mice receiving the engineered ß-cell PIs exhibited improved glucose tolerance upon illumination compared to those kept in the dark or not receiving cells. The findings support the use of optogenetics for molecular customization of the ß-cells toward better treatments for diabetes without the adverse effects of pharmacological approaches.
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Diabetes Mellitus Experimental , Diabetes Mellitus Tipo 2 , Humanos , Ratones , Animales , Insulina , Línea Celular , Glucosa/farmacología , AMP Cíclico , Adenilil Ciclasas/genéticaRESUMEN
Blue light using flavin (BLUF) photoreceptors respond to light via one of nature's smallest photo-switching domains. Upon photo-activation, the flavin cofactor in the BLUF domain exhibits multi-phasic dynamics, quenched by a proton-coupled electron transfer reaction involving the conserved Tyr and Gln. The dynamic behavior varies drastically across different species, the origin of which remains controversial. Here, we incorporate site-specific fluorinated Trp into three BLUF proteins, i.e., AppA, OaPAC and SyPixD, and characterize the percentages for the Wout, WinNHin and WinNHout conformations using 19F nuclear magnetic resonance spectroscopy. Using femtosecond spectroscopy, we identify that one key WinNHin conformation can introduce a branching one-step proton transfer in AppA and a two-step proton transfer in OaPAC and SyPixD. Correlating the flavin quenching dynamics with the active-site structural heterogeneity, we conclude that the quenching rate is determined by the percentage of WinNHin, which encodes a Tyr-Gln configuration that is not conducive to proton transfer.
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Luz , Protones , Transporte de Electrón , Conformación Molecular , Flavinas/química , Proteínas Bacterianas/metabolismoRESUMEN
Interrogating plasma cell-free DNA (cfDNA) to detect cancer offers promise; however, no current tests scan structural variants (SVs) throughout the genome. Here, we report a simple molecular workflow to enrich a tumorigenic SV (DNA palindromes/fold-back inversions) that often demarcates genomic amplification and its feasibility for cancer detection by combining low-throughput next-generation sequencing with automated machine learning (Genome-wide Analysis of Palindrome Formation, GAPF-seq). Tumor DNA signal manifested as skewed chromosomal distributions of high-coverage 1-kb bins (HCBs), differentiating 39 matched breast tumor DNA from normal DNA with an average AUC of 0.9819. In a proof-of-concept liquid biopsy study, cfDNA from 0.5 mL plasma from prostate cancer patients was sufficient for binary classification against matched buffy coat DNA with an average AUC of 0.965. HCBs on the X chromosome emerged as a determinant feature and were associated with AR amplification. GAPF-seq could generate unique cancer-specific SV profiles in an agnostic liquid biopsy setting.
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Ginger is cultivated in tropical and subtropical regions and is one of the most crucial spices worldwide owing to its special taste and scent. Here, we present a high-quality genome assembly for 'Small Laiwu Ginger', a famous cultivated ginger in northern China. The ginger genome was phased into two haplotypes, haplotype A (1.55Gb), and haplotype B (1.44Gb). Analysis of Ty1/Copia and Ty3/Gypsy LTR retrotransposon families revealed that both have undergone multiple retrotransposon bursts about 0-1 million years ago. In addition to a recent whole-genome duplication event, there has been a lineage-specific expansion of genes involved in stilbenoid, diarylheptanoid, and gingerol biosynthesis, thereby enhancing 6-gingerol biosynthesis. Furthermore, we focused on the biosynthesis of 6-gingerol, the most important gingerol, and screened key transcription factors ZoMYB106 and ZobHLH148 that regulate 6-gingerol synthesis by transcriptomic and metabolomic analysis in the ginger rhizome at four growth stages. The results of yeast one-hybrid, electrophoretic mobility shift, and dual-luciferase reporter gene assays showed that both ZoMYB106 and ZobHLH148 bind to the promoters of the key rate-limiting enzyme genes ZoCCOMT1 and ZoCCOMT2 in the 6-gingerol synthesis pathway and promote their transcriptional activities. The reference genome, transcriptome, and metabolome data pave the way for further research on the molecular mechanism underlying the biosynthesis of 6-gingerol. Furthermore, it provides precious new resources for the study on the biology and molecular breeding of ginger.
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Catecoles , Alcoholes Grasos , Genoma de Planta , Zingiber officinale , Zingiber officinale/genética , Zingiber officinale/metabolismo , Alcoholes Grasos/metabolismo , Catecoles/metabolismo , Genoma de Planta/genética , Evolución Molecular , Retroelementos/genética , Haplotipos , Rizoma/genética , Rizoma/metabolismo , Factores de Transcripción/genética , Factores de Transcripción/metabolismo , Proteínas de Plantas/genética , Proteínas de Plantas/metabolismo , Filogenia , Regulación de la Expresión Génica de las PlantasRESUMEN
Plasma cell-free DNA (cfDNA) is a promising source of gene mutations for cancer detection by liquid biopsy. However, no current tests interrogate chromosomal structural variants (SVs) genome-wide. Here, we report a simple molecular and sequencing workflow called Genome-wide Analysis of Palindrome Formation (GAPF-seq) to probe DNA palindromes, a type of SV that often demarcates gene amplification. With low-throughput next-generation sequencing and automated machine learning, tumor DNA showed skewed chromosomal distributions of high-coverage 1-kb bins (HCBs), which differentiated 39 breast tumors from matched normal DNA with an average Area Under the Curve (AUC) of 0.9819. A proof-of-concept liquid biopsy study using cfDNA from prostate cancer patients and healthy individuals yielded an average AUC of 0.965. HCBs on the X chromosome emerged as a determinant feature and were associated with androgen receptor gene amplification. As a novel agnostic liquid biopsy approach, GAPF-seq could fill the technological gap offering unique cancer-specific SV profiles.
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Induction of ferroptosis emerges as an effective method for cancer treatment. With massive efforts to elucidate the ferroptosis mechanism, the development of new ferroptosis inducers proceeds rather slowly, with only a few small molecules identified. Herein, we report our discovery of marine alkaloid lepadins E and H as a new class of ferroptosis inducers. Our in vitro studies show that lepadins E and H exhibit significant cytotoxicity, promote p53 expression, increase ROS production and lipid peroxides, reduce SLC7A11 and GPX4 levels, and upregulate ACSL4 expression, all of which consistently support induction of ferroptosis through the classical p53-SLC7A11-GPX4 pathway. Our animal model study of lepadin H confirms its in vivo antitumor efficacy with negligible toxicity to normal organs. This work elucidates the mode of action of lepadins (E and H) and verifies their in vivo efficacy as a new class of ferroptosis inducers for anticancer therapy with translational potential.
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Alcaloides , Antineoplásicos , Ferroptosis , Neoplasias , Animales , Alcaloides/farmacología , Alcaloides/uso terapéutico , Antineoplásicos/farmacología , Antineoplásicos/uso terapéutico , Proteína p53 Supresora de TumorRESUMEN
In the present study, a global presence/absence dataset including 2486 scale insect species in 157 countries was extracted to assess the establishment risk of potential invasive species based on a self-organizing map (SOM). According to the similarities in species assemblages, a risk list of scale insects for each country was generated. Meanwhile, all countries in the dataset were divided into five clusters, each of which has high similarities of species assemblages. For those countries in the same neuron of the SOM output, they may pose the greatest threats to each other as the sources of potential invasive scale insect species, and therefore, require more attention from quarantine departments. In addition, normalized ζi values were used to measure the uncertainty of the SOM output. In total, 9 out of 63 neurons obtained high uncertainty with very low species counts, indicating that more investigation of scale insects should be undertaken in some parts of Africa, Asia and Northern Europe.
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Proteotoxic stress drives numerous degenerative diseases. In response to misfolded proteins, cells adapt by activating the unfolded protein response (UPR), including endoplasmic reticulum-associated protein degradation (ERAD). However persistent stress triggers apoptosis. Enhancing ERAD is a promising therapeutic approach for protein misfolding diseases. From plants to humans, loss of the Zn2+ transporter ZIP7 causes ER stress, however the mechanism is unknown. Here we show that ZIP7 enhances ERAD and that cytosolic Zn2+ is limiting for deubiquitination of client proteins by the Rpn11 Zn2+ metalloproteinase as they enter the proteasome in Drosophila and human cells. ZIP7 overexpression rescues defective vision caused by misfolded rhodopsin in Drosophila. Thus ZIP7 overexpression may prevent diseases caused by proteotoxic stress, and existing ZIP inhibitors may be effective against proteasome-dependent cancers.
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INTRODUCTION: Tobacco contains carcinogens called tobacco-specific nitrosamines. Among the tobacco-specific nitrosamines, is nicotine-derived nitrosamine ketone (NNK) which produces the metabolite 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL). We aimed to examine the association between urinary tobacco-specific NNAL and cognitive functioning among older adults. METHODS: A total of 1673 older adults aged ≥60 years from the National Health and Nutrition Examination Survey 2013-2014 were included. Urinary tobacco-specific NNAL was analyzed in the laboratory. Cognitive functioning was measured using the Consortium to Establish a Registry for Alzheimer's Disease Word Learning subtest (CERAD-WL) immediate and delayed memory tests, the Animal Fluency test (AFT), and the Digit Symbol Substitution Test (DSST). Test-specific and global cognition z-scores were calculated based on means and standard deviations of the cognitive test scores. Multivariable linear regression models were constructed to examine the independent association between quartiles of urinary tobacco-specific NNAL and cognitive test-specific and global cognition z-scores controlling for age, sex, race/ethnicity, education level, depressive symptoms, body mass index, systolic blood pressure, urinary creatinine, hypertension, diabetes, alcohol use, and smoking status. RESULTS: About half of the participants (mean age 69.8 years) were female (52.1%), non-Hispanic White (48.3%), and completed some college and above (49.7%). Multivariable linear regression results showed that participants in the 4th quartile (highest quartile) of urinary NNAL, compared with those in the 1st quartile (lowest quartile), had lower DSST z-scores (ß= -0.19; 95% CI: -0.34 - -0.04). CONCLUSIONS: Tobacco-specific NNAL was negatively associated with processing speed, sustained attention, and working memory in older adults.
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We used 'Shannong No.1' experimental material to simulate higher salt concentration in ginger and analyzed the physiological responses of different parts of ginger seedlings under salt stress. The results showed that salt stress led to a significant decrease in fresh and dry weight of ginger, lipid membrane peroxidation, increased sodium ion content and enhanced activity of antioxidant enzymes. Compared with the control, the overall plant dry weight of ginger under salt stress decreased by about 60%, and the MDA content in roots, stems, leaves, and rhizomes increased by 372.27%, 184.88%, 291.5%, and 171.13%, respectively, and the APX content increased by 188.85%, 165.56%, 195.38%, and 40.08%, respectively. After analysis of the physiological indicators, it was found that the roots and leaves of ginger were the most significantly changed parts. We analyzed the transcriptional differences between ginger roots and leaves by RNA-seq and found that they jointly initiated MAPK signaling pathways in response to salt stress. By combining physiological and molecular indicators, we elucidated the response of different tissues and parts of ginger to salt stress during the seedling stage.
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Vanadium dioxide (VO2) exhibits an insulator-to-metal transition accompanied by a structural transition near room temperature. This transition can be triggered by an ultrafast laser pulse. Exotic transient states, such as a metallic state without structural transition, were also proposed. These unique characteristics let VO2 have great potential in thermal switchable devices and photonic applications. Although great efforts have been made, the atomic pathway during the photoinduced phase transition is still not clear. Here, we synthesize freestanding quasi-single-crystal VO2 films and examine their photoinduced structural phase transition with mega-electron-volt ultrafast electron diffraction. Leveraging the high signal-to-noise ratio and high temporal resolution, we observe that the disappearance of vanadium dimers and zigzag chains does not coincide with the transformation of crystal symmetry. After photoexcitation, the initial structure is strongly modified within 200 femtoseconds, resulting in a transient monoclinic structure without vanadium dimers and zigzag chains. Then, it continues to evolve to the final tetragonal structure in approximately 5 picoseconds. In addition, only one laser fluence threshold instead of two thresholds suggested in polycrystalline samples is observed in our quasi-single-crystal samples. Our findings provide essential information for a comprehensive understanding of the photoinduced ultrafast phase transition in VO2.