T cell-intrinsic ASC critically promotes T(H)17-mediated experimental autoimmune encephalomyelitis.

Interleukin 1ß (IL-1ß) is critical for the in vivo survival, expansion and effector function of IL-17-producing helper T (T(H)17) cells during autoimmune responses, including experimental autoimmune encephalomyelitis (EAE). However, the spatiotemporal role and cellular source of IL-1ß during EAE pathogenesis are poorly defined. In the present study, we uncovered a T cell-intrinsic inflammasome that drives IL-1ß production during T(H)17-mediated EAE pathogenesis. Activation of T cell antigen receptors induced expression of pro-IL-1ß, whereas ATP stimulation triggered T cell production of IL-1ß via ASC-NLRP3-dependent caspase-8 activation. IL-1R was detected on T(H)17 cells but not on type 1 helper T (T(H)1) cells, and ATP-treated T(H)17 cells showed enhanced survival compared with ATP-treated T(H)1 cells, suggesting autocrine action of T(H)17-derived IL-1ß. Together these data reveal a critical role for IL-1ß produced by a T(H)17 cell-intrinsic ASC-NLRP3-caspase-8 inflammasome during inflammation of the central nervous system.

Noncanonical contribution of microglial transcription factor NR4A1 to post-stroke recovery through TNF mRNA destabilization.

Microglia-mediated neuroinflammation is involved in various neurological diseases, including ischemic stroke, but the endogenous mechanisms preventing unstrained inflammation is still unclear. The anti-inflammatory role of transcription factor nuclear receptor subfamily 4 group A member 1 (NR4A1) in macrophages and microglia has previously been identified. However, the endogenous mechanisms that how NR4A1 restricts unstrained inflammation remain elusive. Here, we observed that NR4A1 is up-regulated in the cytoplasm of activated microglia and localizes to processing bodies (P-bodies). In addition, we found that cytoplasmic NR4A1 functions as an RNA-binding protein (RBP) that directly binds and destabilizes Tnf mRNA in an N6-methyladenosine (m6A)-dependent manner. Remarkably, conditional microglial deletion of Nr4a1 elevates Tnf expression and worsens outcomes in a mouse model of ischemic stroke, in which case NR4A1 expression is significantly induced in the cytoplasm of microglia. Thus, our study illustrates a novel mechanism that NR4A1 posttranscriptionally regulates Tnf expression in microglia and determines stroke outcomes.

BTNL2 promotes colitis-associated tumorigenesis in mice by regulating IL-22 production.

Interleukin 22 (IL-22) has an important role in colorectal tumorigenesis and many colorectal diseases such as inflammatory bowel disease and certain infections. However, the regulation of IL-22 production in the intestinal system is still unclear. Here, we present evidence that butyrophilin-like protein 2 (BTNL2) is required for colorectal IL-22 production, and BTNL2 knockout mice show decreased colonic tumorigenesis and more severe colitis phenotypes than control mice due to defective production of IL-22. Mechanistically, BTNL2 acts on group 3 innate lymphoid cells (ILC3s), CD4+ T cells, and γδ T cells to promote the production of IL-22. Importantly, we find that a monoclonal antibody against BTNL2 attenuates colorectal tumorigenesis in mice and that the mBTNL2-Fc recombinant protein has a therapeutic effect in a dextran sulfate sodium (DSS)-induced colitis model. This study not only identifies a regulatory mechanism of IL-22 production in the colorectal system but also provides a potential therapeutic target for the treatment of human colorectal cancer and inflammatory bowel diseases.

Exercise accelerates recruitment of CD8+ T cell to promotes anti-tumor immunity in lung cancer via epinephrine.

BACKGROUND AND PURPOSE: In recent years, there has been extensive research on the role of exercise as an adjunctive therapy for cancer. However, the potential mechanisms underlying the anti-tumor therapy of exercise in lung cancer remain to be fully elucidated. As such, our study aims to confirm whether exercise-induced elevation of epinephrine can accelerate CD8+ T cell recruitment through modulation of chemokines and thus ultimately inhibit tumor progression. METHOD: C57BL/6 mice were subcutaneously inoculated with Lewis lung cancer cells (LLCs) to establish a subcutaneous tumor model. The tumor mice were randomly divided into different groups to performed a moderate-intensity exercise program on a treadmill for 5 consecutive days a week, 45 min a day. The blood samples and tumor tissues were collected after exercise for IHC, RT-qPCR, ELISA and Western blot. In addition, another group of mice received daily epinephrine treatment for two weeks (0.05 mg/mL, 200 µL i.p.) (EPI, n = 8) to replicate the effects of exercise on tumors in vivo. Lewis lung cancer cells were treated with different concentrations of epinephrine (0, 5, 10, 20 µM) to detect the effect of epinephrine on chemokine levels via ELISA and RT-qPCR. RESULTS: This study reveals that both pre- and post-cancer exercise effectively impede the tumor progression. Exercise led to an increase in EPI levels and the infiltration of CD8+ T cell into the lung tumor. Exercise-induced elevation of EPI is involved in the regulation of Ccl5 and Cxcl10 levels further leading to enhanced CD8+ T cell infiltration and ultimately inhibiting tumor progression. CONCLUSION: Exercise training enhance the anti-tumor immunity of lung cancer individuals. These findings will provide valuable insights for the future application of exercise therapy in clinical practice.

The association of prealbumin, transferrin, and albumin with immunosenescence among elderly males.

OBJECTIVE: As people get older, the innate and acquired immunity of the elderly are affected, resulting in immunosenescence. Prealbumin (PAB), transferrin (TRF), and albumin (ALB) are commonly used markers to monitor protein energy malnutrition (PEM). However, their relationship with the immune system has not been fully explored. METHODS: In our study, a total of 93 subjects (≥65 years) were recruited from Tongji Hospital between January 2015 and February 2017. According to the serum levels of these proteins (PAB, TRF, and ALB), we divided the patients into the high serum protein group and the low serum protein group. Then, we compared the percent expression of lymphocyte subsets between two groups. RESULTS: All the low serum protein groups (PAB, TRF, and ALB) had significant decreases in the percentage of CD4+ cells, CD3+CD28+ cells, CD4+CD28+ cells and significant increases in the percentage of CD8+ cells, CD8+CD28- cells. PAB, TRF, and ALB levels revealed positive correlations with CD4/CD8 ratio, proportions of CD4+ cells, CD3+CD28+ cells, CD4+CD28+ cells, and negative correlation with proportions of CD8+ cells, CD8+CD28- cells. CONCLUSIONS: This study suggested PAB, TRF, and ALB could be used as immunosenescence indicators. PEM might accelerate the process of immunosenescence in elderly males.

Identification of a Small Molecule with Strong Anti-Inflammatory Activity in Experimental Autoimmune Encephalomyelitis and Sepsis through Blocking Gasdermin D Activation.

Pyroptosis is a key inflammatory form of cell death participating in the progression of many inflammatory diseases, such as experimental autoimmune encephalomyelitis (EAE) and sepsis. Identification of small molecules to inhibit pyroptosis is emerging as an attractive strategy. In this study, we performed a screening based on in silico docking of compounds on the reported Gasdermin D (GSDMD) three-dimensional structure and found C202-2729 demonstrated strong anti-inflammatory effects in both endotoxin shock and EAE mouse models. Oral administration of C202-2729 was capable of attenuating EAE disease severity significantly and has the comparable effects to teriflunomide, the first-line clinical drug of multiple sclerosis. We found C202-2729 remarkably suppressed macrophage and T cell-associated immune inflammation. Mechanistically, C202-2729 neither impact GSDMD cleavage nor the upstream inflammasome activation in mouse immortalized bone marrow-derived macrophages. However, C202-2729 exposure significantly repressed the IL-1ß secretion and cell pyroptosis. We found C202-2729 directly bonds to the N terminus of GSDMD and blocks the migration of the N-terminal GSDMD fragment to cell membrane, restraining the pore-forming and mature IL-1ß release. Collectively, our findings provide a new molecule with the potential for translational application in GSDMD-associated inflammatory diseases.

Angiotensin II type-2 receptor signaling facilitates liver injury repair and regeneration via inactivation of Hippo pathway.

The angiotensin II type 2 receptor (AT2R) is a well-established component of the renin-angiotensin system and is known to counteract classical activation of this system and protect against organ damage. Pharmacological activation of the AT2R has significant therapeutic benefits, including vasodilation, natriuresis, anti-inflammatory activity, and improved insulin sensitivity. However, the precise biological functions of the AT2R in maintaining homeostasis in liver tissue remain largely unexplored. In this study, we found that the AT2R facilitates liver repair and regeneration following acute injury by deactivating Hippo signaling and that interleukin-6 transcriptionally upregulates expression of the AT2R in hepatocytes through STAT3 acting as a transcription activator binding to promoter regions of the AT2R. Subsequently, elevated AT2R levels activate downstream signaling via heterotrimeric G protein Gα12/13-coupled signals to induce Yap activity, thereby contributing to repair and regeneration processes in the liver. Conversely, a deficiency in the AT2R attenuates regeneration of the liver while increasing susceptibility to acetaminophen-induced liver injury. Administration of an AT2R agonist significantly enhances the repair and regeneration capacity of injured liver tissue. Our findings suggest that the AT2R acts as an upstream regulator in the Hippo pathway and is a potential target in the treatment of liver damage.

Genetic mechanisms underlying gray matter volume changes in patients with drug-naive first-episode schizophrenia.

Brain structural damage is a typical feature of schizophrenia. Investigating such disease phenotype in patients with drug-naive first-episode schizophrenia (DFSZ) may exclude the confounds of antipsychotics and illness chronicity. However, small sample sizes and marked clinical heterogeneity have precluded definitive identification of gray matter volume (GMV) changes in DFSZ as well as their underlying genetic mechanisms. Here, GMV changes in DFSZ were assessed using a neuroimaging meta-analysis of 19 original studies, including 605 patients and 637 controls. Gene expression data were derived from the Allen Human Brain Atlas and processed with a newly proposed standardized pipeline. Then, we used transcriptome-neuroimaging spatial correlations to identify genes associated with GMV changes in DFSZ, followed by a set of gene functional feature analyses. Meta-analysis revealed consistent GMV reduction in the right superior temporal gyrus, right insula and left inferior temporal gyrus in DFSZ. Moreover, we found that these GMV changes were spatially correlated with expression levels of 1,201 genes, which exhibited a wide range of functional features. Our findings may provide important insights into the genetic mechanisms underlying brain morphological abnormality in schizophrenia.

MYO1F regulates antifungal immunity by regulating acetylation of microtubules.

Opportunistic fungal infections have become one of the leading causes of death among immunocompromised patients, resulting in an estimated 1.5 million deaths each year worldwide. The molecular mechanisms that promote host defense against fungal infections remain elusive. Here, we find that Myosin IF (MYO1F), an unconventional myosin, promotes the expression of genes that are critical for antifungal innate immune signaling and proinflammatory responses. Mechanistically, MYO1F is required for dectin-induced α-tubulin acetylation, acting as an adaptor that recruits both the adaptor AP2A1 and α-tubulin N-acetyltransferase 1 to α-tubulin; in turn, these events control the membrane-to-cytoplasm trafficking of spleen tyrosine kinase and caspase recruitment domain-containing protein 9 Myo1f-deficient mice are more susceptible than their wild-type counterparts to the lethal sequelae of systemic infection with Candida albicans Notably, administration of Sirt2 deacetylase inhibitors, namely AGK2, AK-1, or AK-7, significantly increases the dectin-induced expression of proinflammatory genes in mouse bone marrow-derived macrophages and microglia, thereby protecting mice from both systemic and central nervous system C. albicans infections. AGK2 also promotes proinflammatory gene expression in human peripheral blood mononuclear cells after Dectin stimulation. Taken together, our findings describe a key role for MYO1F in promoting antifungal immunity by regulating the acetylation of α-tubulin and microtubules, and our findings suggest that Sirt2 deacetylase inhibitors may be developed as potential drugs for the treatment of fungal infections.

N-acetyltransferase 10 promotes the progression of oral squamous cell carcinoma through N4-acetylcytidine RNA acetylation of MMP1 mRNA.

The pathogenesis of oral squamous cell carcinoma (OSCC) remains unclear. Therefore, clarifying its pathogenesis and molecular-level development mechanism has become the focus of OSCC research. N-acetyltransferase 10 (NAT10) is a crucial enzyme involved in mRNA acetylation, regulating target gene expression and biological functions of various diseases through mediating N4-acetylcytidine (ac4C) acetylation. However, its role in OSCC progression is not well understood. In this study, we showed that NAT10 was significantly upregulated in OSCC tissues compared to normal oral tissues. Moreover, lentivirus-mediated NAT10 knockdown markedly suppressed cell proliferation, migration, and invasion in two OSCC cell lines (SCC-9 and SCC-15). Interestingly, MMP1 was found to be significantly upregulated in OSCC tissues and was a potential target of NAT10. N-acetyltransferase 10 knockdown significantly reduced both the total and ac4C acetylated levels of MMP1 mRNA and decreased its mRNA stability. Xenograft experiments further confirmed the inhibitory effect of NAT10 knockdown on the tumorigenesis and metastasis ability of OSCC cells and decreased MMP1 expression in vivo. Additionally, NAT10 knockdown impaired the proliferation, migration, and invasion abilities in OSCC cell lines in an MMP1-dependent manner. Our results suggest that NAT10 acts as an oncogene in OSCC, and targeting ac4C acetylation could be a promising therapeutic strategy for OSCC treatment.

Brain function mediates the association between low vitamin D and neurocognitive status in female patients with major depressive disorder.

BACKGROUND: Vitamin D is engaged in various neural processes, with low vitamin D linked to depression and cognitive dysfunction. There are gender differences in depression and vitamin D level. However, the relationship between depression, gender, vitamin D, cognition, and brain function has yet to be determined. METHODS: One hundred and twenty-two patients with major depressive disorder (MDD) and 119 healthy controls underwent resting-state functional MRI and fractional amplitude of low-frequency fluctuations (fALFF) was calculated to assess brain function. Serum concentration of vitamin D (SCVD) and cognition (i.e. prospective memory and sustained attention) were also measured. RESULTS: We found a significant group-by-gender interaction effect on SCVD whereby MDD patients showed a reduction in SCVD relative to controls in females but not males. Concurrently, there was a female-specific association of SCVD with cognition and MDD-related fALFF alterations in widespread brain regions. Remarkably, MDD- and SCVD-related fALFF changes mediated the relation between SCVD and cognition in females. CONCLUSION: Apart from providing insights into the neural mechanisms by which low vitamin D contributes to cognitive impairment in MDD in a gender-dependent manner, these findings might have clinical implications for assignment of female patients with MDD and cognitive dysfunction to adjuvant vitamin D supplementation therapy, which may ultimately advance a precision approach to personalized antidepressant choice.

Fracture strength and failure mechanism of graphene-containing grain boundaries and pores.

Grain boundaries and pores commonly manifest in graphene sheets during experimental preparation. Additionally, pores have been intentionally incorporated into graphene to fulfill specific functions for various applications. However, how does the simultaneous presence of pores and grain boundaries impact the mechanical properties of graphene? This paper establishes uniaxial tension models of single-layer graphene-containing pores and three types of experimentally observed. The effect of interaction between pores and grain boundaries on the fracture strength of graphene was studied respectively for three types of grain boundaries by employing molecular dynamics simulations and considering factors such as pore size, the distance between pores and grain boundaries, and loading angle. A competitive mechanism between the intrinsic strength of pristine graphene with grain boundaries (referred to as pristine GGBs), which varies with the loading angle and the fracture strength of graphene sheets with pores that changes with the size of the pores, governs the fracture strength and failure modes of GGBs with pores. When the former exceeds the latter, the fracture strength of GGBs with pores primarily depends on the size of the pores, and fractures occur at the edges of the pores. Conversely, when the former is lower, the fracture strength of GGBs with pores relies on the loading angle and the distance between pores and grain boundaries, leading to grain boundary rupture. If the two strengths are comparable, the failure modes are influenced by the distance between pores and grain boundaries as well as the loading angle. The findings further elucidate the impact of coexisting grain boundaries and pores on the fracture behavior of graphene, providing valuable guidance for the precise design of graphene-based devices in the future.

Identification of a Long Noncoding RNA TRAF3IP2-AS1 as Key Regulator of IL-17 Signaling through the SRSF10-IRF1-Act1 Axis in Autoimmune Diseases.

IL-17A plays an essential role in the pathogenesis of many autoimmune diseases, including psoriasis and multiple sclerosis. Act1 is a critical adaptor in the IL-17A signaling pathway. In this study, we report that an anti-sense long noncoding RNA, TRAF3IP2-AS1, regulates Act1 expression and IL-17A signaling by recruiting SRSF10, which downregulates the expression of IRF1, a transcriptional factor of Act1. Interestingly, we found that a psoriasis-susceptible variant of TRAF3IP2-AS1 A4165G (rs13210247) is a gain-of-function mutant. Furthermore, we identified a mouse gene E130307A14-Rik that is homologous to TRAF3IP2-AS1 and has a similar ability to regulate Act1 expression and IL-17A signaling. Importantly, treatment with lentiviruses expressing E130307A14-Rik or SRSF10 yielded therapeutic effects in mouse models of psoriasis and experimental autoimmune encephalomyelitis. These findings suggest that TRAF3IP2-AS1 and/or SRSF10 may represent attractive therapeutic targets in the treatment of IL-17-related autoimmune diseases, such as psoriasis and multiple sclerosis.

Frequency-dependent genetic modulation of neuronal oscillations: a combined transcriptome and resting-state functional MRI study.

Neuronal oscillations within certain frequency bands are assumed to associate with specific neural processes and cognitive functions. To examine this hypothesis, transcriptome-neuroimaging spatial correlation analysis was applied to resting-state functional magnetic resonance imaging data from 793 healthy individuals and gene expression data from the Allen Human Brain Atlas. We found that expression measures of 336 genes were correlated with fractional amplitude of low-frequency fluctuations (fALFF) in the slow-4 band (0.027-0.073 Hz), whereas there were no expression-fALFF correlations for the other frequency bands. Furthermore, functional enrichment analyses showed that these slow-4 fALFF-related genes were mainly enriched for ion channel, synaptic function, and neuronal system as well as many neuropsychiatric disorders. Specific expression analyses demonstrated that these genes were specifically expressed in brain tissue, in neurons, and during the late stage of cortical development. Concurrently, the fALFF-related genes were linked to multiple behavioral domains, including dementia, attention, and emotion. In addition, these genes could construct a protein-protein interaction network supported by 30 hub genes. Our findings of a frequency-dependent genetic modulation of spontaneous neuronal activity may support the concept that neuronal oscillations within different frequency bands capture distinct neurobiological processes from the perspective of underlying molecular mechanisms.

Genetic Architecture Underlying Differential Resting-state Functional Connectivity of Subregions Within the Human Visual Cortex.

The human visual cortex is a heterogeneous entity that has multiple subregions showing substantial variability in their functions and connections. We aimed to identify genes associated with resting-state functional connectivity (rsFC) of visual subregions using transcriptome-neuroimaging spatial correlations in discovery and validation datasets. Results showed that rsFC of eight visual subregions were associated with expression measures of eight gene sets, which were specifically expressed in brain tissue and showed the strongest correlations with visual behavioral processes. Moreover, there was a significant divergence in these gene sets and their functional features between medial and lateral visual subregions. Relative to those associated with lateral subregions, more genes associated with medial subregions were found to be enriched for neuropsychiatric diseases and more diverse biological functions and pathways, and to be specifically expressed in multiple types of neurons and immune cells and during the middle and late stages of cortical development. In addition to shared behavioral processes, lateral subregion associated genes were uniquely correlated with high-order cognition. These findings of commonalities and differences in the identified rsFC-related genes and their functional features across visual subregions may improve our understanding of the functional heterogeneity of the visual cortex from the perspective of underlying genetic architecture.

[Rapid identification of components in Wuzhuyu Decoction using UHPLC Q-Exactive Orbitrap MS~n and molecular network technology].

Wuzhuyu Decoction, the classical formula recorded in the Treatise on Febrile Diseases(Shang Han Lun), has been included in the Catalogue of Ancient Classic Prescriptions(the First Batch). Consisting of Euodiae Fructus, Ginseng Radix et Rhizoma, Zingiberis Rhizoma Recens, and Jujubae Fructus, it is effective in warming the middle, tonifying deficiency, dispelling cold, and descending adverse Qi, and is widely applied clinically with remarkable efficacies. For a classical formula, the chemical composition is the material basis and an important premise for quantity value transfer. This study aimed to establish a rapid identification method of chemical components in Wuzhuyu Decoction by high-resolution mass spectrometry(HR-MS) and molecular network. AQUITY UPLC BEH C_(18) column(2.1 mm×100 mm, 1.7 µm) was used for sample separation, and acetonitrile-0.1% formic acid in water was used as mobile phases for gradient elution. Q-Exactive Orbitrap MS data were collected in positive and negative ion modes, and GNPS molecular network was plotted according to the similarity of MS/MS fragmentation modes. Cytoscape 3.6.1 was used to screen molecular clusters with similar structures. Finally, the chemical components of Wuzhuyu Decoction were rapidly identified according to the controls, as well as the information of retention time, accurate relative molecular weight of HR-MS, and MS/MS multistage fragments. A total of 105 chemical components were identified in Wuzhuyu Decoction. This study can provide data for the follow-up quality control, standard substance research, and pharmacodynamic material research on Wuzhuyu Decoction, as well as references for the rapid qualitative analysis of the chemical components of Chinese medicine.

Transcriptional substrates underlying functional connectivity profiles of subregions within the human sensorimotor cortex.

The human sensorimotor cortex has multiple subregions showing functional commonalities and differences, likely attributable to their connectivity profiles. However, the molecular substrates underlying such connectivity profiles are unclear. Here, transcriptome-neuroimaging spatial correlation analyses were performed between transcriptomic data from the Allen human brain atlas and resting-state functional connectivity (rsFC) of 24 fine-grained sensorimotor subregions from 793 healthy subjects. Results showed that rsFC of six sensorimotor subregions were associated with expression measures of six gene sets that were specifically expressed in brain tissue. These sensorimotor subregions could be classified into the polygenic- and oligogenic-modulated subregions, whose rsFC were related to gene sets diverging on their numbers (hundreds vs. dozens) and functional characteristics. First, the former were specifically expressed in multiple types of neurons and immune cells, yet the latter were not specifically expressed in any cortical cell types. Second, the former were preferentially expressed during the middle and late stages of cortical development, while the latter showed no preferential expression during any stages. Third, the former were prone to be enriched for general biological functions and pathways, but the latter for specialized biological functions and pathways. Fourth, the former were enriched for neuropsychiatric disorders, whereas this enrichment was absent for the latter. Finally, although the identified genes were commonly associated with sensorimotor behavioral processes, the polygenic-modulated subregions associated genes were additionally related to vision and dementia. These findings may advance our understanding of the functional homogeneity and heterogeneity of the human sensorimotor cortex from the perspective of underlying genetic architecture.

Functional connectivity of the central autonomic and default mode networks represent neural correlates and predictors of individual personality.

There is solid evidence for the prominent involvement of the central autonomic and default mode systems in shaping personality. However, whether functional connectivity of these systems can represent neural correlates and predictors of individual variation in personality traits is largely unknown. Resting-state functional magnetic resonance imaging data of 215 healthy young adults were used to construct the sympathetic (SN), parasympathetic (PN), and default mode (DMN) networks, with intra- and internetwork functional connectivity measured. Personality factors were assessed using the five-factor model. We examined the associations between personality factors and functional network connectivity, followed by performance of personality prediction based on functional connectivity using connectome-based predictive modeling (CPM), a recently developed machine learning approach. All personality factors (neuroticism, extraversion, conscientiousness, and agreeableness) other than openness were significantly correlated with intra- and internetwork functional connectivity of the SN, PN, and DMN. Moreover, the CPM models successfully predicted conscientiousness and agreeableness at the individual level using functional network connectivity. Our findings may expand existing knowledge regarding the neural substrates underlying personality.

The SNF5-type protein BUSHY regulates seed germination via the gibberellin pathway and is dependent on HUB1 in Arabidopsis.

MAIN CONCLUSION: The SNF5-type protein BUSHY plays a role in the regulation of seed germination via the gibberellin pathway dependent on HUB1 in Arabidopsis thaliana. SWITCH/SUCROSE NONFERMENTING (SWI/SNF) complexes play diverse roles in plant development. Some components have roles in embryo development and seed maturation, however, whether the SNF5-type protein BUSHY (BSH), one of the components, plays a role in Arabidopsis seed related traits is presently unclear. In our study, we show that a loss-of-function mutation in BSH causes increased seed germination in Arabidopsis. BSH transcription was induced by the gibberellin (GA) inhibitor paclobutrazol (PAC) in the seed, and BSH regulates the expression of GA pathway genes, such as Gibberellin 3-Oxidase 1 (GA3OX1), Gibberellic Acid-Stimulated Arabidopsis 4 (GASA4), and GASA6 during seed germination. A genetic analysis showed that seed germination was distinctly improved in the bshga3ox1ga3ox2 triple mutant, indicating that BSH acts partially downstream of GA3OX1 and GA3OX2. Moreover, the regulation of seed germination by BSH in response to PAC is dependent on HUB1. These results provide new insights and clues to understand the mechanisms of phytohormones in the regulation of seed germination.

Highly sensitive detection of broadband terahertz waves using aqueous salt solutions.

Water-based coherent detection of broadband terahertz (THz) wave has been recently proposed with superior performances, which can alleviate the limited detection bandwidth and high probe laser energy requirement in the solid- and air-based detection schemes, respectively. Here, we demonstrate that the water-based detection method can be extended to the aqueous salt solutions and the sensitivity can be significantly enhanced. The THz coherent detection signal intensity scales linearly with the third-order nonlinear susceptibility χ(3) or quadratically with the linear refractive index η0 of the aqueous salt solutions, while the incoherent detection signal intensity scales quadratically with χ(3) or quartically with η0, proving the underlying mechanism is the four-wave mixing. Both the coherent and incoherent detection signal intensities appear positive correlation with the solution concentration. These results imply that the liquid-based THz detection scheme could provide a new technique to measure χ(3) and further investigate the physicochemical properties in the THz band for various liquids.