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In tomato (Solanum lycopersicum), as in other plants, the immunity hormone jasmonate (JA) triggers genome-wide transcriptional changes in response to pathogen and insect attack. These changes are largely regulated by the basic helix-loop-helix (bHLH) transcription factor MYC2. The function of MYC2 depends on its physical interaction with the MED25 subunit of the Mediator transcriptional coactivator complex. Although much has been learned about the MYC2-dependent transcriptional activation of JA-responsive genes, relatively less studied is the termination of JA-mediated transcriptional responses and the underlying mechanisms. Here, we report an unexpected function of MYC2 in regulating the termination of JA signaling through activating a small group of JA-inducible bHLH proteins, termed MYC2-TARGETED BHLH1 (MTB1), MTB2, and MTB3. MTB proteins negatively regulate JA-mediated transcriptional responses via their antagonistic effects on the functionality of the MYC2-MED25 transcriptional activation complex. MTB proteins impair the formation of the MYC2-MED25 complex and compete with MYC2 to bind to its target gene promoters. Therefore, MYC2 and MTB proteins form an autoregulatory negative feedback circuit to terminate JA signaling in a highly organized manner. We provide examples demonstrating that gene editing tools such as CRISPR/Cas9 open up new avenues to exploit MTB genes for crop protection.

Sucrose metabolism plays a critical role in development, stress response, and yield formation of plants. Sucrose phosphate synthase (SPS) is the key rate-limiting enzyme in the sucrose synthesis pathway. To date, genome-wide survey and comprehensive analysis of the SPS gene family in soybean (Glycine max) have yet to be performed. In this study, seven genes encoding SPS were identified in soybean genome. The structural characteristics, phylogenetics, tissue expression patterns, and cold stress response of these GmSPSs were investigated. A comparative phylogenetic analysis of SPS proteins in soybean, Medicago truncatula, Medicago sativa, Lotus japonicus, Arabidopsis, and rice revealed four families. GmSPSs were clustered into three families from A to C, and have undergone five segmental duplication events under purifying selection. All GmSPS genes had various expression patterns in different tissues, and family A members GmSPS13/17 were highly expressed in nodules. Remarkably, all GmSPS promoters contain multiple low-temperature-responsive elements such as potential binding sites of inducer of CBF expression 1 (ICE1), the central regulator in cold response. qRT-PCR proved that these GmSPS genes, especially GmSPS8/18, were induced by cold treatment in soybean leaves, and the expression pattern of GmICE1 under cold treatment was similar to that of GmSPS8/18. Further transient expression analysis in Nicotiana benthamiana and electrophoretic mobility shift assay (EMSA) indicated that GmSPS8 and GmSPS18 transcriptions were directly activated by GmICE1. Taken together, our findings may aid in future efforts to clarify the potential roles of GmSPS genes in response to cold stress in soybean.

Sucrose metabolism plays a critical role in development, stress response, and yield formation of plants. Sucrose phosphate synthase (SPS) is the key rate-limiting enzyme in the sucrose synthesis pathway. To date, genome-wide survey and comprehensive analysis of the SPS gene family in soybean (Glycine max) have yet to be performed. In this study, seven genes encoding SPS were identified in soybean genome. The structural characteristics, phylogenetics, tissue expression patterns, and cold stress response of these GmSPSs were investigated. A comparative phylogenetic analysis of SPS proteins in soybean, Medicago truncatula, Medicago sativa, Lotus japonicus, Arabidopsis, and rice revealed four families. GmSPSs were clustered into three families from A to C, and have undergone five segmental duplication events under purifying selection. All GmSPS genes had various expression patterns in different tissues, and family A members GmSPS13/17 were highly expressed in nodules. Remarkably, all GmSPS promoters contain multiple low-temperature-responsive elements such as potential binding sites of inducer of CBF expression 1 (ICE1), the central regulator in cold response. qRT-PCR proved that these GmSPS genes, especially GmSPS8/18, were induced by cold treatment in soybean leaves, and the expression pattern of GmICE1 under cold treatment was similar to that of GmSPS8/18. Further transient expression analysis in Nicotiana benthamiana and electrophoretic mobility shift assay (EMSA) indicated that GmSPS8 and GmSPS18 transcriptions were directly activated by GmICE1. Taken together, our findings may aid in future efforts to clarify the potential roles of GmSPS genes in response to cold stress in soybean.

Background The excellent efficacy is mitigated by the limited safety profile of microfocused ultrasound procedures. Objective We sought to assess the safety and tightening efficacy of a novel microfocused ultrasound. Methods The randomized middle and lower face and submental region of the participants were treated with the novel device using the following transducers: M4.5, D4.5, M3.0, and D3.0. Improvement in paired comparison of pretreatment and posttreatment photographs, three-dimensional (3D) volumetric assessments, skin thickness measured by B-ultrasonography, and skin photoaging parameters were evaluated. Adverse events and patient satisfaction were also recorded. Results A total of 20 participants (20 female) were enrolled. Fourteen of 20 participants (70%) were judged to show clinically significant facial tightening during 3-month follow-up ( P  < 0.05). The mean volumetric change in the lower face, as quantitatively assessed after 3 months was −0.29 mL compared with +0.42 mL on the control side ( P  < 0.05). The VAS pain score was 3.00 ± 1.19 without any oral or intramuscular anesthesia. Conclusions A small sample size, lack of clinical scales, and impersonalized treatment parameters. The novel microfocused ultrasound appears to be a safe and effective modality for lower-face tightening. Clinical Trial Registration Number ChiCTR 2200064666.

Aberrant circular RNA (circRNA) expression is implicated in various diseases, but the regulatory mechanisms remain poorly understood. Our previous work identified circSCMH1 as a brain repair-associated circRNA, prompting investigation into its biogenesis regulation. We combined computational analysis of RNA-binding protein (RBP) binding sites in flanking intronic regions with transcriptomic sequencing to identify potential circSCMH1 regulators. Molecular biology experiments including RNA immunoprecipitation and functional assays were performed to validate the interaction between candidate RBPs and circSCMH1 precursor sequences. Polypyrimidine tract binding protein 1 (PTBP1) was identified as a key regulator binding specifically to the 800-882 segment at the 3' end of circSCMH1's flanking intron. This binding event inhibited back-splicing and reduces circSCMH1 production. Functional studies demonstrated that PTBP1-mediated suppression of circSCMH1 exacerbates post-stroke brain injury. Our study reveals a novel molecular mechanism whereby PTBP1 regulates circSCMH1 biogenesis through suppression of back-splicing. These findings advance understanding of circRNA regulatory networks and suggest potential therapeutic targets for stroke recovery.

The application of three-dimensional (3D) plasmonic nanostructures as metamaterials (MMs), nano-antennas, and other devices faces challenges in producing metallic nanostructures with easily definable orientations, sophisticated shapes, and smooth surfaces that are operational in the optical regime and beyond. Here, we demonstrate that complex 3D nanostructures can be readily achieved with focused-ion-beam irradiation-induced folding and examine the optical characteristics of plasmonic “nanograter” structures that are composed of free-standing Au films. These 3D nanostructures exhibit interesting 3D hybridization in current flows and exhibit unusual and well-scalable Fano resonances at wavelengths ranging from 1.6 to 6.4 µm. Upon the introduction of liquids of various refractive indices to the structures, a strong dependence of the Fano resonance is observed, with spectral sensitivities of 1400 nm and 2040 nm per refractive index unit under figures of merit of 35.0 and 12.5, respectively, for low-order and high-order resonance in the near-infrared region. This work indicates the exciting, increasing relevance of similarly constructed 3D free-standing nanostructures in the research and development of photonics and MMs. Plasmonic nanostructures: grater-like structures fabricated Nanostructures with grater-like structures exhibit Fano resonances with unusual properties, making them promising for plasmonic sensing. Researchers from China and the UK fabricated these structures over a large surface area by using a focused ion beam to induce nanopatterning and folding of self-supporting thin gold films. This fabrication technique can readily produce complex three-dimensional structural elements and does not require a substrate. The Fano resonances of the grater-like structures were highly sensitive to the refractive index of the surrounding medium (over 2,040 nanometres per refractive index unit in the near-infrared region), and hence the structures could potentially be used for high-performance plasmonic sensing. Furthermore, the structures may also possess novel mechanical responses and thus may find applications in optomechanics, pressure sensing and temperature monitoring on nanoscale dimensions.

The yeast Saccharomyces cerevisiae is capable of responding to various environmental stresses, such as salt stress. Such responses require a complex network and adjustment of the gene expression network. The goal of this study is to further understand the molecular mechanism of salt stress response in yeast, especially the molecular mechanism related to genes BDF1 and HAL2 . The Bromodomain Factor 1 (Bdf1p) is a transcriptional regulator, which is part of the basal transcription factor TFIID. Cells lacking Bdf1p are salt sensitive with an abnormal mitochondrial function. We previously reported that the overexpression of HAL2 or deletion of HDA1 lowers the salt sensitivity of bdf1Δ . To better understand the mechanism behind the HAL2 -related response to salt stress, we compared three global transcriptional profiles ( bdf1Δ vs WT, bdf1Δ  +  HAL2 vs bdf1Δ , and bdf1Δhda1Δ vs bdf1Δ ) in response to salt stress using DNA microarrays. Our results reveal that genes for iron acquisition and cellular and mitochondrial remodeling are induced by HAL2 . Overexpression of HAL2 decreases the concentration of nitric oxide. Mitochondrial iron–sulfur cluster (ISC) assembly also decreases in bdf1Δ  +  HAL2 . These changes are similar to the changes of transcriptional profiles induced by iron starvation. Taken together, our data suggest that mitochondrial functions and iron homeostasis play an important role in bdf1Δ -induced salt sensitivity and salt stress response in yeast.

Bromodomain-containing transcription factor, a kind of important regulating protein, can recognize and bind to acetylated histone. The homologous genes, BDF1 and BDF2 , in Saccharomyces cerevisiae , respectively, encode a bromodomain-containing transcription factor. Previously study has demonstrated that both BDF1 and BDF2 participate in yeast salt stress response. Bdf1p deletion cells are sensitive to salt stress and this phenotype is suppressed by its homologue BDF2 in a dosage-dependent manner. In this study, we show that the histone deacetylase SIR2 over-expression enhanced dosage-dependent compensation of BDF2 . SIR2 over-expression induced a global transcription change, and 1959 gene was down-regulated. We deleted some of the most significant down-regulated genes and did the spot assay. The results revealed that LSP1 , an upstream component of endocytosis pathway, and CIN5 , a transcription factor that mediates cellular resistance to stresses, can enhance salt resistance of bdf1∆ . Further analysis demonstrated that under salt stress the endocytosis is over-activated in bdf1∆ but was recovered in bdf1∆ lsp1∆ . To our best knowledge, this is the first report that the transcription factor Bdf1p regulates endocytosis under salt stress via LSP1 , a major component of eisosomes that regulate the sites of endocytosis.

Bromodomain factor 1 (Bdf1p) is a transcriptional regulator. The absence of Bdf1p causes salt sensitivity with abnormal nucleus and mitochondrial dysfunction. In this study, we reported that the salt sensitivity, mitochondrial dysfunction, and nuclear instability of bdf1Δ mutant were suppressed by HDA1 deletion or MEF1 overexpression. Hda1p overexpression inhibited the relieving effects of low‐copy overexpression of MEF1. Further analysis showed that Bdf1p regulated HDA1 transcription positively by binding to its promoter at −201 to +6 bp, whereas Hda1p modulated MEF1 expression negatively by binding to its promoter at −201 to +6 bp. These results suggested that Bdf1p likely regulated MEF1 expression negatively by regulating HDA1 positively. Mitochondrial proteomics analysis showed that the expression levels of six mitochondrial proteins were significantly changed by MEF1 overexpression. Among the six genes, over‐expression of PDB1, ILV5, or ATP2 partially recovered the salt stress sensitivity of bdf1Δ. However, none of these mitochondrial proteins could recover mitochondrial respiration indicating that the individual functional proteins could not replace Mef1p activity. It indicated that positive regulation of MEF1 was important in recovering the salt sensitivity of bdf1Δ mutant.

Abstract Bromodomain factor 1 (Bdf1p) is a transcriptional regulator. The absence of Bdf1p causes salt sensitivity with abnormal nucleus and mitochondrial dysfunction. In this study, we reported that the salt sensitivity, mitochondrial dysfunction, and nuclear instability of bdf1Δ mutant were suppressed by HDA1 deletion or MEF1 overexpression. Hda1p overexpression inhibited the relieving effects of low-copy overexpression of MEF1. Further analysis showed that Bdf1p regulated HDA1 transcription positively by binding to its promoter at −201 to +6 bp, whereas Hda1p modulated MEF1 expression negatively by binding to its promoter at −201 to +6 bp. These results suggested that Bdf1p likely regulated MEF1 expression negatively by regulating HDA1 positively. Mitochondrial proteomics analysis showed that the expression levels of six mitochondrial proteins were significantly changed by MEF1 overexpression. Among the six genes, over-expression of PDB1, ILV5, or ATP2 partially recovered the salt stress sensitivity of bdf1Δ. However, none of these mitochondrial proteins could recover mitochondrial respiration indicating that the individual functional proteins could not replace Mef1p activity. It indicated that positive regulation of MEF1 was important in recovering the salt sensitivity of bdf1Δ mutant. Overexpression of the mitochondrial elongation factor gene, MEF1, recovers the salt resistance of a Bdf1 bromodomain protein mutant; positive regulation of MEF1, via the histone deacetylase gene, HDA1 may be important for recovering the loss of respiratory function of the BDF1 deletion strain. Overexpression of the mitochondrial elongation factor gene, MEF1, recovers the salt resistance of a Bdf1 bromodomain protein mutant; positive regulation of MEF1, via the histone deacetylase gene, HDA1 may be important for recovering the loss of respiratory function of the BDF1 deletion strain.