RESUMO
Biopolymer aerogel is a new type of material with potential applications in the biomedical field. Silk fibroin is of particular interest as a raw material with good biocompatibility and degradable. However, the low mechanical strength and small specific surface area of silk fibroin aerogels limit its further development. Herein, a fast water absorption, highly specific surface area and mechanically strong of aerogels were prepared using low crystal silk fibroin nanofibers (SNF), sol-gel process, solvent exchange and supercritical carbon dioxide (CO2) drying method. The resulting Aero-Sc displayed highly specific surface area (251 m2/g), porosity (97.6 %) and water absorption capacity (1200 %). Furthermore, with rapid water absorption and stronger erythrocyte adhesion, the Aero-Sc showed highly effective hemostasis in vitro. In vivo, animal experiments on rat liver hemorrhage model confirmed that SNF aerogels have a less blood loss (312 ± 29 mg) and faster hemostatic time (92 ± 13 s) than commercially gelatin sponge (p < 0.05). The unique properties of silk fibroin nanofibers aerogel developed in this study has great potential to be a safe and effective hemostatic medical device.
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In the transitional period of China's urbanization, commuting problems and demands are diversified and multi-level, so commuting research topics, viewpoints, and analysis paths should be organically combined to dynamically adapt to the complex commuting contradictions. Based on this, this paper introduces the resilience theory to improve the research paradigm of commuting behavior. Taking Nanjing, China as a case study, with the help of the survey data of commuting behavior of typical communities, this paper provides an empirical analysis of the characteristics and influencing factors of urban residents' commuting behavior from the perspective of resilience theory. The results show that: (1) in the face of commuting pressure, to a large extent, most commuters can still obtain commuting adaptability and a medium level or higher of commuting resilience; and (2) personal attributes, living and employment environment, and commuting environment all have significant heterogeneity effects on commuting pressure, commuting adaptability, and commuting resilience. From the perspective of resilience theory, the means of regulating commuting conflicts are flexible, which can not only directly reduce commuting pressure or optimize commuting adaptability, but also improve commuting resilience according to the specific commuting scenarios constructed by commuting pressure and adaptability. On the whole, the principles of comprehensive improvement, on-demand supply, and dynamic adjustment should be followed.
Assuntos
Meios de Transporte , População Urbana , Adulto , China , Emprego , Feminino , Humanos , Masculino , Pessoa de Meia-IdadeRESUMO
Light filtered through dense planting initiates the shade avoidance syndrome (SAS) in plants, which helps them compete against their neighbors. Quantitative trait loci (QTL)-based analysis identified the nighttime-expressed clock component ELF3 as a new player in the SAS, but its detailed mechanism is unclear. Here, we show that the circadian clock gates shade-induced gene expression and hypocotyl elongation at night. ELF3 is involved in nighttime suppression via interaction with and inactivation of PHYTOCHROME-INTERACTING FACTOR 7 (PIF7). Loss of function of ELF3 restores the shade induction, which is largely reduced in the absence of PIF7, indicating that ELF3 acts upstream of PIF7. Finally, we found that the repressive activity of ELF3 on the shade response is stronger under short days than under long days. Our results reveal that the interaction between ELF3 and PIF7 mediates the circadian gating of the SAS, which coordinates the daily control of physiological outputs.
RESUMO
To compete with their neighbors for light and escape shaded environments, sun-loving plants have developed the shade-avoidance syndrome (SAS), a set of responses including alteration of plant architecture and initiation of early flowering and seed set. Previous studies on SAS mainly focused on dissecting molecular basis of hypocotyl elongation in seedlings under shade light; however, the molecular mechanisms underlying shade-accelerated flowering in adult plants remain unknown. In this study, we found that CONSTANS (CO) and PHYTOCHROME-INTERACTING FACTOR 7 (PIF7) have an additive effect on shade-induced flowering, but that LONG HYPOCOTYL IN FAR-RED1 (HFR1) represses early flowering by binding to CO and PIF7 and preventing the binding of CO to the promoter of FLOWERING LOCUS T (FT) and the binding of PIF7 to the promoter of pri-MIR156E/F. Under shade, de-phosphorylated PIF7 and accumulated CO, balanced by HFR1, upregulate the expression of FT, TSF, SOC1, and SPLs to accelerate flowering. Moreover, we found that the function of PIF7 in flowering time is independent of phyA. Collectively, these regulatory interactions establish a crucial link between the light signal and genetic network that regulates flowering transition under shade.
Assuntos
Proteínas de Arabidopsis/metabolismo , Arabidopsis/crescimento & desenvolvimento , Arabidopsis/metabolismo , Proteínas de Ligação a DNA/metabolismo , Flores/crescimento & desenvolvimento , Fatores de Transcrição/metabolismo , Arabidopsis/genética , Regulação da Expressão Gênica de Plantas , MutaçãoRESUMO
Plants coordinate their growth and developmental programs with various endogenous signals and environmental challenges. Phytochrome interacting factor 4 (PIF4) plays a critical positive role in thermoresponsive gene expression and hypocotyl growth in Arabidopsis, whereas early flowering 3 (ELF3) negatively regulates the activity of PIF4 at elevated temperatures. However, it is unknown how ELF3 activity is regulated at warm temperatures. Here, we report the identification of B-box 18 (BBX18) and BBX23 as important thermomorphogenesis regulators in Arabidopsis. BBX18 and BBX23 mutations result in reduced thermoresponsive hypocotyl elongation. In contrast, BBX18 overexpression promotes hypocotyl growth at elevated temperatures, which depends on either PIF4 or constitutive photomorphogenic 1 (COP1). BBX18 and BBX23 interact with ELF3 or COP1. Knocking out BBX18 and BBX23 increases ELF3 abundance under normal and warm temperature conditions. The expression of multiple thermoresponsive genes is impaired in both a PIF4 mutant and a BBX18/BBX23 double mutant. Thus, our findings reveal an important role of B-box proteins during thermomorphogenesis and provide insights into our understanding of how warm temperature signals regulate ELF3 activity and PIF4-dependent genes.
Assuntos
Proteínas de Arabidopsis/metabolismo , Arabidopsis/crescimento & desenvolvimento , Arabidopsis/metabolismo , Proteínas de Ligação a DNA/metabolismo , Morfogênese , Temperatura , Fatores de Transcrição/metabolismo , Arabidopsis/genética , Proteínas de Arabidopsis/genética , Proteínas de Ligação a DNA/genética , Regulação da Expressão Gênica no Desenvolvimento , Regulação da Expressão Gênica de Plantas , Fatores de Transcrição/genéticaRESUMO
Shade avoidance syndrome enables shaded plants to grow and compete effectively against their neighbors. In Arabidopsis, the shade-induced de-phosphorylation of the transcription factor PIF7 (PHYTOCHROME-INTERACTING FACTOR 7) is the key event linking light perception to stem elongation. However, the mechanism through which phosphorylation regulates the activity of PIF7 is unclear. Here, we show that shade light induces the de-phosphorylation and nuclear accumulation of PIF7. Phosphorylation-resistant site mutations in PIF7 result in increased nuclear localization and shade-induced gene expression, and consequently augment hypocotyl elongation. PIF7 interacts with 14-3-3 proteins. Blocking the interaction between PIF7 and 14-3-3 proteins or reducing the expression of 14-3-3 proteins accelerates shade-induced nuclear localization and de-phosphorylation of PIF7, and enhances the shade phenotype. By contrast, the 14-3-3 overexpressing line displays an attenuated shade phenotype. These studies demonstrate a phosphorylation-dependent translocation of PIF7 when plants are in shade and a novel mechanism involving 14-3-3 proteins, mediated by the retention of PIF7 in the cytoplasm that suppresses the shade response.
Assuntos
Proteínas 14-3-3/genética , Proteínas de Arabidopsis/genética , Arabidopsis/efeitos da radiação , Proteínas de Ligação a DNA/genética , Regulação da Expressão Gênica de Plantas , Hipocótilo/efeitos da radiação , Transdução de Sinal Luminoso , Proteínas 14-3-3/metabolismo , Arabidopsis/genética , Arabidopsis/crescimento & desenvolvimento , Arabidopsis/metabolismo , Proteínas de Arabidopsis/metabolismo , Núcleo Celular/genética , Núcleo Celular/metabolismo , Proteínas de Ligação a DNA/metabolismo , Proteínas de Fluorescência Verde/genética , Proteínas de Fluorescência Verde/metabolismo , Hipocótilo/genética , Hipocótilo/crescimento & desenvolvimento , Hipocótilo/metabolismo , Luz , Fosforilação , Células Vegetais/metabolismo , Plantas Geneticamente Modificadas , Ligação Proteica , Proteínas Recombinantes de FusãoRESUMO
Leaf senescence is an integral part of plant development, and the timing and progressing rate of senescence could substantially affect the yield and quality of crops. It has been known that a circadian rhythm synchronized with external environmental cues is critical for the optimal coordination of various physiological and metabolic processes. However, the reciprocal interactions between the circadian clock and leaf senescence in plants remain unknown. Here, through measuring the physiological and molecular senescence related markers of several circadian components mutants, we found that CIRCADIAN CLOCK-ASSOCIATED 1 inhibits leaf senescence. Further molecular and genetic studies revealed that CCA1 directly activates GLK2 and suppresses ORE1 expression to counteract leaf senescence. As plants age, the expression and periodic amplitude of CCA1 declines and thus weakens the inhibition of senescence. Our findings reveal an age-dependent circadian clock component of the process of leaf senescence.
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Shade avoidance syndrome (SAS) allows a plant grown in a densely populated environment to maximize opportunities to access to sunlight. Although it is well established that SAS is accompanied by gene expression changes, the underlying molecular mechanism needs to be elucidated. Here, we identify the H3K4me3/H3K36me3-binding proteins, Morf Related Gene (MRG) group proteins MRG1 and MRG2, as positive regulators of shade-induced hypocotyl elongation in Arabidopsis (Arabidopsis thaliana). MRG2 binds PHYTOCHROME-INTERACTING FACTOR7 (PIF7) and regulates the expression of several common downstream target genes, including YUCCA8 and IAA19 involved in the auxin biosynthesis or response pathway and PRE1 involved in brassinosteroid regulation of cell elongation. In response to shade, PIF7 and MRG2 are enriched at the promoter and gene-body regions and are necessary for increase of histone H4 and H3 acetylation to promote target gene expression. Our study uncovers a mechanism in which the shade-responsive factor PIF7 recruits MRG1/MRG2 that binds H3K4me3/H3K36me3 and brings histone-acetylases to induce histone acetylations to promote expression of shade responsive genes, providing thus a molecular mechanistic link coupling the environmental light to epigenetic modification in regulation of hypocotyl elongation in plant SAS.
Assuntos
Proteínas de Arabidopsis/metabolismo , Arabidopsis/fisiologia , Proteínas Cromossômicas não Histona/metabolismo , Proteínas de Ligação a DNA/metabolismo , Histonas/metabolismo , Acetilação , Proteínas de Arabidopsis/genética , Cromatina/metabolismo , Proteínas Cromossômicas não Histona/genética , Proteínas de Ligação a DNA/genética , Regulação da Expressão Gênica de Plantas , Histonas/genética , Hipocótilo/genética , Hipocótilo/crescimento & desenvolvimento , Lisina/metabolismo , Metilação , Plantas Geneticamente ModificadasRESUMO
The reduction in the red to far-red light ratio (R/FR) and photosynthetically active radiation caused by dense planting initiates shade avoidance responses (SARs) to help plants compete against their neighbors. However, deep shade attenuates shade-induced stem elongation to suppress excessive reversion toward skotomorphogenic development, in which photoreceptor phytochrome A (PHYA) has been known to play the major role. However, the molecular mechanism underlying PHYA function in deep shade is poorly understood. Here, we report that shade-accumulated PHYA can release auxin/indole-3-acetic acid (AUX/IAA), suppressors in the auxin signaling pathway, from SCFTIR1, an auxin receptor, to weaken auxin signaling and negatively regulate shade response. Corroborating this, phyA mutants display an enhanced auxin response to deep shade and auxin treatment. Specifically, PHYA competes with TIR1 by directly binding and stabilizing AUX/IAA. Our findings illustrate a mechanistic model of how plants sense different shade levels to fine-tune auxin signaling and generate appropriate SAR.
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Proteínas de Arabidopsis/metabolismo , Arabidopsis/metabolismo , Regulação da Expressão Gênica de Plantas/efeitos dos fármacos , Ácidos Indolacéticos/farmacologia , Luz , Fitocromo A/metabolismo , Estabilidade Proteica/efeitos dos fármacos , Arabidopsis/efeitos dos fármacos , Arabidopsis/crescimento & desenvolvimento , Proteínas de Arabidopsis/genética , Mutação , Fitocromo A/genética , Reguladores de Crescimento de Plantas/farmacologia , Fenômenos Fisiológicos Vegetais , Plantas Geneticamente Modificadas/efeitos dos fármacos , Plantas Geneticamente Modificadas/crescimento & desenvolvimento , Plantas Geneticamente Modificadas/metabolismoRESUMO
Functional divergence is thought to be an important evolutionary driving force for the retention of duplicate genes. We reconstructed the evolutionary history of soybean (Glycine max) membrane-bound NAC transcription factor (NTL) genes. NTLs are thought to be components of stress signaling and unique in their requirement for proteolytic cleavage to free them from the membrane. Most of the 15 GmNTL genes appear to have evolved under strong purifying selection. By analyzing the phylogenetic tree and gene synteny, we identified seven duplicate gene pairs generated by the latest whole-genome duplication. The members of each pair were shown to have variously diverged at the transcriptional (organ specificity and responsiveness to stress), posttranscriptional (alternative splicing), and protein (proteolysis-mediated membrane release and transactivation activity) levels. The dormant (full-length protein) and active (protein without a transmembrane motif) forms of one pair of duplicated gene products (GmNTL1/GmNLT11) were each separately constitutively expressed in Arabidopsis (Arabidopsis thaliana). The heteroexpression of active but not dormant forms of these proteins caused improved tolerance to abiotic stresses, suggesting that membrane release was required for their functionality. Arabidopsis carrying the dormant form of GmNTL1 was more tolerant to hydrogen peroxide, which induces its membrane release. Tolerance was not increased in the line carrying dormant GmNTL11, which was not released by hydrogen peroxide treatment. Thus, NTL-release pattern changes may cause phenotypic divergence. It was concluded that a variety of functional divergences contributed to the retention of these GmNTL duplicates.