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Petroleum-derived single-use plastics have dominated a range of material applications, including packaging and service ware (e.g., water bottles, food containers, and drinking straws). However, despite their short-lived service life, the inherent durability, and stability of these plastics have resulted in significant environmental accumulation and spill, contaminating both aquatic and land ecosystems. Consequently, there is a surging interest in the development of bioplastics as a sustainable alternative to petrochemical derived plastics that align with circular economy principles. Among potential materials, cellulose acetate (CA) showcases impressive mechanical properties, optical characteristics, melt processability, and compostability. However, due to its hygroscopic behavior, inferior barrier properties, and lack of dimensional stability, CA applications in the packaging industry are minimal. In this research, the acetylation of lignin and its use as a functional filler for CA matrix was studied. The impact of varying lignin loadings (up to 30 wt.%) on the tensile, morphological, barrier, and viscoelastic properties of the resulting materials was investigated. A thorough characterization of the compression-molded acetylated lignin-CA films revealed a reduction in water uptake (by 59% over baseline), up to a 41.5% reduction in water vapor permeability, and enhanced tensile properties with melt flowability. In summary, the examined films displayed favorable characteristics for use in food and other packaging applications. Consequently, they serve as low carbon footprint, and eco-friendly substitutes for conventional petrochemical-based packaging materials. [ABSTRACT FROM AUTHOR]

Efficient DNA double strand break (DSB) repair is necessary for genomic stability and determines efficacy of DNA damaging cancer therapeutics. Spatiotemporal dynamics and post-translational modifications of repair proteins at DSBs dictate repair efficacy. Here, we identified a non-canonical function of GCN5 in regulating both HR and NHEJ repair post genotoxic stress. Mechanistically, genotoxic stress induced GCN5 recruitment to DSBs. GCN5 PARylation by PARP1 was essential for its recruitment, acetyltransferase activity and DSB repair function. Liquid chromatography-mass spectrometry (LC–MS) identified DNA-PKcs as part of GCN5 interactome. In-vitro acetyltransferase assays revealed that GCN5 acetylates DNA-PKcs at K3241 residue, a prerequisite for DNA-PKcs S2056 phosphorylation and DSB recruitment. Alongside, ChIP-qPCR revealed GCN5 mediates transcription of PRKDC via H3K27Ac acetylation in its promoter region (− 710 to − 554). Genetic perturbation of GCN5 also decreased CHEK1, NBN1, TP53BP1, POL-L transcription and abrogated ATM, BRCA1 activation. Accordingly, GCN5 loss led to persistent ɣ-H2AX foci formation, compromised in-vivo HR-NHEJ and caused GBM radio-sensitization. Importantly, PARP1 inhibition phenocopied GCN5 loss. Together, this study identifies an untraversed DSB repair function of GCN5 and provides mechanistic insights into transcriptional as well as post-translational regulation of pivotal HR-NHEJ factors. Alongside, it highlights the translational importance of PARP1-GCN5 axis in mediating GBM radio-resistance. [ABSTRACT FROM AUTHOR]

Cervical cancer, CC, is one of the malignant cancers in women worldwide. Many studies about the genesis and progression of CC have been done at genomic, transcriptional, translational, and epigenetic levels. However, much less is done at post-translational modification (PTM) level. We first used pan-PTM antibodies to compare the pan PTM levels between clinical normal cervical tissues and CC tissues; we then sent the selected samples for label-free identification of acetylation sites. Next, we employed WT or K119A mutant PARP1-EGFP-STREPII plasmid transfection in Hela cells and examined various indexes including colony formation, wound healing, ROS generation, early apoptosis, and immunofluorescence and quantification of proliferation markers (Ki67, PCNA, and p-P53). Last, we examined the levels of multiple important kinases regulating cervical cancer progression. We found that pan-acetylation was the most downregulated in clinical CC samples, whereas the acetylation of PARP1, Poly(ADP-ribose) polymerase-1, was upregulated at K119. Next, we showed that PARP1-WT overexpression significantly suppressed the proliferation and progression in CC cell line Hela, while K119A overexpression didn't show any impact. Finally, PARP1-WT overexpression significantly decreased p-ERK1/2 while didn't affect the phosphorylation levels of other important kinases such as AKT, MTOR, and RPS6. This study discovered a new type of PTM of PARP1 in CC, and showed that PARP1 acetylation at K119 is essential in regulating the proliferation and progression of CC through ERK1/2. Further studies are required to investigate how PARP1 acetylation impact its function. [ABSTRACT FROM AUTHOR]

Sirtuin 7 (SIRT7) is a member of the sirtuin family and has emerged as a key player in numerous cellular processes. It exhibits various enzymatic activities and is predominantly localized in the nucleolus, playing a role in ribosomal RNA expression, DNA damage repair, stress response and chromatin compaction. Recent studies have revealed its involvement in diseases such as cancer, cardiovascular and bone diseases, and obesity. In cancer, SIRT7 has been found to be overexpressed in multiple types of cancer, including breast cancer, clear cell renal cell carcinoma, lung adenocarcinoma, prostate adenocarcinoma, hepatocellular carcinoma, and gastric cancer, among others. In general, cancer cells exploit SIRT7 to enhance cell growth and metabolism through ribosome biogenesis, adapt to stress conditions and exert epigenetic control over cancer-related genes. The aim of this review is to provide an in-depth understanding of the role of SIRT7 in cancer carcinogenesis, evolution and progression by elucidating the underlying molecular mechanisms. Emphasis is placed on unveiling the intricate molecular pathways through which SIRT7 exerts its effects on cancer cells. In addition, this review discusses the feasibility and challenges associated with the development of drugs that can modulate SIRT7 activity. [ABSTRACT FROM AUTHOR]

Zinc plays a pivotal role in tissue regeneration and maintenance being as a central cofactor in a plethora of enzymatic activities. Hypozincemia is commonly seen with chronic liver disease and is associated with an increased risk of liver fibrosis development and hepatocellular carcinoma. Previously favorable effects of zinc supplementation on liver fibrosis have been shown. However, the underlying mechanism of this effect is not elucidated. Liver fibrosis was induced in mice by using CCl4 injection, followed by treatment with zinc chloride (ZnCl2) both at fibrotic and sham groups, and their hepatocytes were isolated. Our results showed that the administration of ZnCl2 restored the depleted cytosolic zinc levels in the hepatocytes isolated from the fibrotic group. Also, alpha-smooth muscle actin (αSMA) expression in hepatocytes was decreased, indicating a reversal of the fibrotic process. Notably, ZIP14 expression significantly increased in the fibrotic group following ZnCl2 treatment, whereas in the sham group ZIP14 expression decreased. Chromatin immunoprecipitation (ChIP) experiments revealed an increased binding percentage of Metal-regulatory transcription factor 1 (MTF1) on ZIP14 promoter in the hepatocytes isolated from fibrotic mice compared to the sham group after ZnCl2 administration. In the same group, the binding percentage of the histone deacetylase HDAC4 on ZIP14 promoter decreased. Our results suggest that the ZnCl2 treatment ameliorates liver fibrosis by elevating intracellular zinc levels through MTF1-mediated regulation of ZIP14 expression and the reduction of ZIP14 deacetylation via HDAC4. The restoration of intracellular zinc concentrations and the modulation of ZIP14 expression by zinc orchestrated through MTF1 and HDAC4, appear to be essential determinants of the therapeutic response in hepatic fibrosis. These findings pave the way for potential novel interventions targeting zinc-related pathways for the treatment of liver fibrosis and associated conditions. [ABSTRACT FROM AUTHOR]

A mild strategy was developed for efficient preparation of acetylsalicylic acid (ASA) from the acetylation of salicylic acid (SA) and acetic anhydride (AA) assisted ultrasonic over Y-immobilized cation exchange resin (Y-CER). With this strategy, an ASA yield of 95.2% was obtained. The results showed that the increased yield was due to Lewis acidic sites (LAS) combined with ultrasonic assistance. The process reduced the AA reagent feed while lowering the reaction temperature. The characterization results showed that metal Y species were dispersedly anchored on the CER surface through S-O-Y triple-dentate bonds, resulting in abundant LAS and stable catalytic activity. Comparative experiments revealed that LAS was more favorable for the formation of ASA than Bronsted acidic sites (BAS). Furthermore, a plausible mechanism for the acetylation of SA and AA by Y-CER has been proposed. This work provided a practical protocol for improving ASA yield and reducing acid wastewater discharge, with potential application prospects. [ABSTRACT FROM AUTHOR]

Main conclusion: This review focuses on HATs and HDACs that modify non-histone proteins, summarizes functional mechanisms of non-histone acetylation as well as the roles of HATs and HDACs in rice and Arabidopsis. The growth and development of plants, as well as their responses to biotic and abiotic stresses, are governed by intricate gene and protein regulatory networks, in which epigenetic modifying enzymes play a crucial role. Histone lysine acetylation levels, modulated by histone acetyltransferases (HATs) and histone deacetylases (HDACs), are well-studied in the realm of transcriptional regulation. However, the advent of advanced proteomics has unveiled that non-histone proteins also undergo acetylation, with its underlying mechanisms now being clarified. Indeed, non-histone acetylation influences protein functionality through diverse pathways, such as modulating protein stability, adjusting enzymatic activity, steering subcellular localization, influencing interactions with other post-translational modifications, and managing protein–protein and protein–DNA interactions. This review delves into the recent insights into the functional mechanisms of non-histone acetylation in plants. We also provide a summary of the roles of HATs and HDACs in rice and Arabidopsis, and explore their potential involvement in the regulation of non-histone proteins. [ABSTRACT FROM AUTHOR]

This work aimed to isolate cellulose nanofibers (CNF) from sisal fibers and to impart hydrophobic characteristics through acetylation with acetic anhydride. The sisal fibers were pre-treated using alkaline hydrogen peroxide (AHP) followed by acetylation using acetic anhydride. Acetylated and non-acetylated CNF were then isolated by mechanical defibrillation of pre-treated fibers using a high-speed blender. Both resulting CNF were evaluated using attenuated total reflection Fourier transform infrared spectroscopy (ATR-FTIR), X-ray diffraction (XRD), transmissions electron microscopy (TEM), thermogravimetric analysis (TGA), and water contact angle measurement. ATR-FTIR results revealed the substitution of hydroxyl groups by some acetyl groups as indicated by the presence of carbonyl and methyl groups for the acetylated CNF (ACNF). The yield of ACNF and CNF obtained in this work was 90% and 86%, respectively. The dispersion studies exhibited that ACNF formed a more stable suspension and dispersed better in acetone than CNF. XRD analysis indicated that the acetylation process decreased the crystallinity index of CNF from 79 to 66%. The average diameter distribution of ACNF and CNF was 5.59 ± 1.45 nm and 6.22 ± 1.97, respectively. Furthermore, without lowering the thermal stability of CNF, ACNF exhibited higher hydrophobicity as high as 87° compared with that of CNF with a 12° contact angle. The resulting ACNF extracted from sisal fibers had great potential application as reinforcement for nanocomposites with a nonpolar polymer matrix. [ABSTRACT FROM AUTHOR]

METTL3 methylates RNA and regulates the fate of mRNA through its methyltransferase activity. METTL3 enhances RNA translation independently of its catalytic activity. However, the underlying mechanism is still elusive. Here, we report that METTL3 is both interacted with and acetylated at lysine 177 by the acetyltransferase PCAF and deacetylated by SIRT3. Neither the methyltransferase activity nor the stability of METTL3 is affected by its acetylation at K177. Importantly, acetylation of METTL3 blocks its interaction with EIF3H, a subunit of the translation initiation factor, thereby reducing mRNA translation efficiency. Interestingly, acetylation of METTL3 responds to oxidative stress. Mechanistically, oxidative stress enhances the interaction of PCAF with METTL3, increases METTL3 acetylation, and suppresses the interaction of METTL3 with EIF3H, thereby decreasing the translation efficiency of ribosomes and inhibiting cell proliferation. Altogether, we suggest a mechanism by which oxidative stress regulates RNA translation efficiency by the modulation of METTL3 acetylation mediated by PCAF. [ABSTRACT FROM AUTHOR]

Nascent chains undergo co-translational enzymatic processing as soon as their N-terminus becomes accessible at the ribosomal polypeptide tunnel exit (PTE). In eukaryotes, N-terminal methionine excision (NME) by Methionine Aminopeptidases (MAP1 and MAP2), and N-terminal acetylation (NTA) by N-Acetyl-Transferase A (NatA), is the most common combination of subsequent modifications carried out on the 80S ribosome. How these enzymatic processes are coordinated in the context of a rapidly translating ribosome has remained elusive. Here, we report two cryo-EM structures of multi-enzyme complexes assembled on vacant human 80S ribosomes, indicating two routes for NME-NTA. Both assemblies form on the 80S independent of nascent chain substrates. Irrespective of the route, NatA occupies a non-intrusive 'distal' binding site on the ribosome which does not interfere with MAP1 or MAP2 binding nor with most other ribosome-associated factors (RAFs). NatA can partake in a coordinated, dynamic assembly with MAP1 through the hydra-like chaperoning function of the abundant Nascent Polypeptide-Associated Complex (NAC). In contrast to MAP1, MAP2 completely covers the PTE and is thus incompatible with NAC and MAP1 recruitment. Together, our data provide the structural framework for the coordinated orchestration of NME and NTA in protein biogenesis. How methionine excision and acetylation are co-translationally coordinated at the ribosome has remained elusive. Here, the authors report cryo-EM structures of two different multi-protein assemblies capable of both successive enzymatic functions. [ABSTRACT FROM AUTHOR]

The aim of the current study is to modify water hyacinth fibre (WHF), which are then used to produce novel oil sorption polymers. Two synthetic materials were derived from acetylation by acetic anhydride using N-bromosuccinimide (NBS) as a catalyst and the graft co-polymerisation of butyl acrylate (BA) using 2,2′-azobisisobutyronitrile (AIBN) as an initiator. Physicochemical properties were comprehensively characterised by Fourier transform infrared spectroscopy, scanning electron microscopy, X-ray diffraction, contact angle, and thermogravimetric analysis. In the seawater/crude oil system, the best oil sorption capacity values of the raw WHFs and their acetylated-WHF and graft co-polymer WHF-g-BA were 7.46 g/g, 20.16 g/g, and 25.47 g/g, respectively. The sorption kinetic and isotherm studies exhibited that the oil sorption of the co-polymer WHF-g-BA is ruled by pseudo-second-order kinetic and Freundlich isotherm models. The reusability of the WHFs and their synthetic materials has reached 6 cycles of sorption/desorption, and this property of the co-polymer is always better than that of acetylated and original fibres. [ABSTRACT FROM AUTHOR]

Proper function of the centromeres ensures correct attachment of kinetochores to spindle microtubules and faithful chromosome segregation in mitosis. Defects in the integrity and function of centromeres can result in chromosome missegregation and genomic instability. Bub1 is essential for the mitotic centromere dynamics, yet the underlying molecular mechanisms remain largely unclear. Here, we demonstrate that TIP60 acetylates Bub1 at K424 and K431 on kinetochores in early mitosis. This acetylation increases the kinase activity of Bub1 to phosphorylate centromeric histone H2A at T120 (H2ApT120), which recruits Aurora B and Shugoshin 1 (Sgo1) to regulate centromere integrity, protect centromeric cohesion, and ensure the subsequent faithful chromosome segregation. Expression of the non-acetylated Bub1 mutant reduces its kinase activity, decreases the level of H2ApT120, and disrupts the recruitment of centromere proteins and chromosome congression, leading to genomic instability of daughter cells. When cells exit mitosis, HDAC1-regulated deacetylation of Bub1 decreases H2ApT120 levels and thereby promotes the departure of centromeric CPC and Sgo1, ensuring timely centromeres disassembly. Collectively, our results reveal a molecular mechanism by which the acetylation and deacetylation cycle of Bub1 modulates the phosphorylation of H2A at T120 for recruitment of Aurora B and Sgo1 to the centromeres, ensuring faithful chromosome segregation during mitosis. [ABSTRACT FROM AUTHOR]

A reed (Arundo donax) was acetylated to prevent serious cheilitis (reed allergy) in woodwind musicians in contact with the vibrating plate made of the reed. The reed was acetylated almost completely at 120 °C for 8 to 24 h. The maximum weight% gain (WPG) of the reed was lower than that of wood, reflecting a lower number of active reaction sites. The WPG of the inner part of the reed was slightly higher than that of the outer part, probably because the reactivity of the parenchyma cells is higher than that of the bundle sheaths. The acetylated reeds were tested by eleven skilled musicians suffering from the reed allergy. Eight musicians reported no allergic reactions. Three musicians reacted with the acetylated reed, but the reactions were much weaker than those induced by the unmodified reed. Thus, acetylation has been proven effective in preventing reed allergy. The patch test was not sufficient to detect allergies because although some musicians tested negative in the patch test, their mouths reacted seriously. [ABSTRACT FROM AUTHOR]

Post-translational modifications (PTMs), as epigenetic modifications, are significant in the interaction between virus and its host. However, it is unclear whether rotavirus (RV) causes changes in both the host cell epigenetic protein modification and the regulatory mechanism of viral replication. Here, we analyzed the proteome of Caco-2 cells to determine if acetylation modification occurred within the cells after RV infection. We found that glyceraldehyde-3-phosphate dehydrogenase (GAPDH), a protein involved in glycolysis, was deacetylated at lysine 219 via histone deacetylase 9 (HDAC9) in 50 h after the RV infection. Remarkably, the deacetylation of GAPDH promoted RV replication. Finally, we found that glycolysis was alterable in Caco-2 cells by RV or the deacetylation of GAPDH lysine 219, using the Seahorse XF Glycolysis Stress Test. In conclusion, our results demonstrate for the first time that RV infection promoted deacetylation of GAPDH at lysine 219 in order to increase its own viral replication in Caco-2 cells. [ABSTRACT FROM AUTHOR]

Paper-based separator for lithium-ion battery application has attracted great attention due to its good electrolyte affinity and thermal stability. To avoid the short circuit by the micron-sized pores of paper and improve the electrochemical properties of paper-based separator, cellulose fibers were acetylated followed by wet papermaking and metal-organic framework coating. Due to the strong intermolecular interaction between acetylated cellulose fibers and N,N-dimethylformamide, the resulting separator exhibited compact microstructure. The zeolitic imidazolate framework-8 coating endowed the separator with enhanced electrolyte affinity (electrolyte contact angle of 0°), ionic conductivity (1.26 mS·cm−1), interfacial compatibility (284 Ω), lithium ion transfer number (0.61) and electrochemical stability window (4.96 V). The assembled LiFePO4/Li battery displayed an initial discharge capacity of 146.10 mAh·g−1 at 0.5 C with capacity retention of 99.71% after 100 cycles and good rate performance. Our proposed strategy would provide a novel perspective for the design of high-performance paper-based separators for battery applications. [ABSTRACT FROM AUTHOR]

RNA base editing relies on the introduction of adenosine-to-inosine changes into target RNAs in a highly programmable manner in order to repair disease-causing mutations. Here, we propose that RNA base editing could be broadly applied to perturb protein function by removal of regulatory phosphorylation and acetylation sites. We demonstrate the feasibility on more than 70 sites in various signaling proteins and identify key determinants for high editing efficiency and potent down-stream effects. For the JAK/STAT pathway, we demonstrate both, negative and positive regulation. To achieve high editing efficiency over a broad codon scope, we applied an improved version of the SNAP-ADAR tool. The transient nature of RNA base editing enables the comparably fast (hours to days), dose-dependent (thus partial) and reversible manipulation of regulatory sites, which is a key advantage over DNA (base) editing approaches. In summary, PTM interference might become a valuable field of application of RNA base editing. RNA base editing enables a precise, reversible and doseable change of genetic information. Here, authors propose base editing as a method to control post-translational modifications via removal of regulatory phosphorylation and acetylation sites, applying the approach to modulation of the JAK/STAT pathway via editing of wildtype alleles. [ABSTRACT FROM AUTHOR]

Viral myocarditis (VMC) is the major reason for sudden cardiac death among both children and young adults. Of these, coxsackievirus B3 (CVB3) is the most common causative agent of myocarditis. Recently, the role of signaling pathways in the pathogenesis of VMC has been evaluated in several studies, which has provided a new perspective on identifying potential therapeutic targets for this hitherto incurable disease. In the present study, in vivo and in vitro experiments showed that CVB3 infection leads to increased Bim expression and triggers apoptosis. In addition, by knocking down Bim using RNAi, we further confirmed the biological function of Bim in apoptosis induced by CVB3 infection. We additionally found that Bim and forkhead box O1 class (FOXO1) inhibition significantly increased the viability of CVB3-infected cells while blocking viral replication and viral release. Moreover, CVB3-induced Bim expression was directly dependent on FOXO1 acetylation, which is catalyzed by the co-regulation of CBP and SirTs. Furthermore, the acetylation of FOXO1 was an important step in Bim activation and apoptosis induced by CVB3 infection. The findings of this study suggest that CVB3 infection induces apoptosis through the FOXO1 acetylation-Bim pathway, thus providing new insights for developing potential therapeutic targets for enteroviral myocarditis. [ABSTRACT FROM AUTHOR]

Sorption of water has a profound effect on the material properties of wood. The uptake of water vapour in wood and other materials releases more heat than the condensation of vapour to liquid water. This excess energy provides insights to the interactions and energy state of the absorbed water molecules. Modification of wood by acetylation is a common way of altering the wood-water interactions; however, very few data exist on how this and other types of modification affect the energy state of absorbed water in wood. This study is the first to use sorption calorimetry on modified wood to explore the effect of acetylation on wood-water interactions. Acetylation decreased the strength of the interactions between wood and water as seen from a decrease in differential enthalpy of mixing, both overall and in the dry state. It appears that acetylation removes or hinders the most-energetic interactions or bonding configurations of water in wood, perhaps because acetylation reduces the number of water-accessible hydroxyls more than it reduces the amount of absorbed water molecules. [ABSTRACT FROM AUTHOR]

We herein described a biogenic route for the in situ supporting silver nanoparticles on hydroxymethylated lignin (HL) coated Fe3O4 (iron oxide) magnetic nanoparticles using the Cydonia oblonga flower extract (Fe3O4@HL/Ag NPs) and its catalytic activity in the acetylation of alcohols and subsequent its biological activity are investigated. The successful fabrication of Fe3O4@HL/Ag NPs was established by using advanced analytical techniques such as Fourier Transformed Infra-Red spectroscopy, Transmission Electron Microscopy, Field Emission Scanning Electron Microscopy, Energy Dispersive X-ray spectroscopy, elemental mapping and Vibrating Sample Magnetization. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay was used to measure anti-thyroid cancer (on WRO, FTC133, BCPAP, TPC1, K1, and 8505C cells) properties of Fe3O4@HL/Ag NPs nanocomposite. The findings indicate that in 3 days, the cancer cell survival percentage in various dilations reduced as much as the Fe3O4@HL/Ag NPs nanocomposite concentration increased. The best anticancer effect was reported at 1000 μg/ml dilation. MTT findings reveal that IC50 = 146, 181, 250, 141, 170, and 125 µg/ml is a Fe3O4@HL/Ag NPs nanocomposite concentration in which 50% of the WRO, FTC133, BCPAP, TPC1, K1, and 8505C thyroid carcinoma cells. The results indicated that these Fe3O4@HL/Ag NPs nanocomposite could inhibit thyroid cancer cells more strongly than normal cells. Fe3O4@HL/Ag NPs nanocomposite shows high antioxidant effects against DPPH. [ABSTRACT FROM AUTHOR]

The AMP-forming acetyl-CoA synthetase is regulated by lysine acetylation both in bacteria and eukaryotes. However, the underlying mechanism is poorly understood. The Bacillus subtilis acetyltransferase AcuA and the AMP-forming acetyl-CoA synthetase AcsA form an AcuA•AcsA complex, dissociating upon lysine acetylation of AcsA by AcuA. Crystal structures of AcsA from Chloroflexota bacterium in the apo form and in complex with acetyl-adenosine-5′-monophosphate (acetyl-AMP) support the flexible C-terminal domain adopting different conformations. AlphaFold2 predictions suggest binding of AcuA stabilizes AcsA in an undescribed conformation. We show the AcuA•AcsA complex dissociates upon acetyl-coenzyme A (acetyl-CoA) dependent acetylation of AcsA by AcuA. We discover an intrinsic phosphotransacetylase activity enabling AcuA•AcsA generating acetyl-CoA from acetyl-phosphate (AcP) and coenzyme A (CoA) used by AcuA to acetylate and inactivate AcsA. Here, we provide mechanistic insights into the regulation of AMP-forming acetyl-CoA synthetases by lysine acetylation and discover an intrinsic phosphotransacetylase allowing modulation of its activity based on AcP and CoA levels. AMP-forming acetyl-CoA synthetase (AcsA) is an essential enzyme in all domains of life. Here, the authors provide mechanistic insights into regulation of AcsA by lysine acetylation, uncovering a regulatory phosphotransacetylase activity. [ABSTRACT FROM AUTHOR]

In spite of its essential role in culture media, the precise influence of lactate on early mouse embryonic development remains elusive. Previous studies have implicated lactate accumulation in medium affecting histone acetylation. Recent research has underscored lactate-derived histone lactylation as a novel epigenetic modification in diverse cellular processes and diseases. Our investigation demonstrated that the absence of sodium lactate in the medium resulted in a pronounced 2-cell arrest at the late G2 phase in embryos. RNA-seq analysis revealed that the absence of sodium lactate significantly impaired the maternal-to-zygotic transition (MZT), particularly in zygotic gene activation (ZGA). Investigations were conducted employing Cut&Tag assays targeting the well-studied histone acetylation and lactylation sites, H3K18la and H3K27ac, respectively. The findings revealed a noticeable reduction in H3K18la modification under lactate deficiency, and this alteration showed a significant correlation with changes in gene expression. In contrast, H3K27ac exhibited minimal correlation. These results suggest that lactate may preferentially influence early embryonic development through H3K18la rather than H3K27ac modifications. [ABSTRACT FROM AUTHOR]

Since Robert Feulgen first stained DNA in the cell, visualizing genome chromatin has been a central issue in cell biology to uncover how chromatin is organized and behaves in the cell. To approach this issue, we have developed single-molecule imaging of nucleosomes, a basic unit of chromatin, to unveil local nucleosome behavior in living cells. In this study, we investigated behaviors of nucleosomes with various histone H4 mutants in living HeLa cells to address the role of H4 tail acetylation, including H4K16Ac and others, which are generally associated with more transcriptionally active chromatin regions. We ectopically expressed wild-type (wt) or mutated H4s (H4K16 point; H4K5,8,12,16 quadruple; and H4 tail deletion) fused with HaloTag in HeLa cells. Cells that expressed wtH4-Halo, H4K16-Halo mutants, and multiple H4-Halo mutants had euchromatin-concentrated distribution. Consistently, the genomic regions of the wtH4-Halo nucleosomes corresponded to Hi-C contact domains (or topologically associating domains, TADs) with active chromatin marks (A-compartment). Utilizing single-nucleosome imaging, we found that none of the H4 deacetylation or acetylation mimicked H4 mutants altered the overall local nucleosome motion. This finding suggests that H4 mutant nucleosomes embedded in the condensed euchromatic domains with excess endogenous H4 nucleosomes cannot cause an observable change in the local motion. Interestingly, H4 with four lysine-to-arginine mutations displayed a substantial freely diffusing fraction in the nucleoplasm, whereas H4 with a truncated N-terminal tail was incorporated in heterochromatic regions as well as euchromatin. Our study indicates the power of single-nucleosome imaging to understand individual histone/nucleosome behavior reflecting chromatin environments in living cells. [ABSTRACT FROM AUTHOR]

Paper sludge consists mainly of wet short cellulose fibers that are lost during papermaking and of residual chemicals used in the manufacturing process that remain dissolved in the water. Each ton of paper generates about 40–50 kg of dry sludge, of which 70% is primary sludge. Paper production, which exceeded 400 million tons globally in 2020, generates vast volumes of solid waste. Primary sludge is usually fiber-rich and hence suitable to be recycled back into the papermaking process. However, if the sludge is to be disposed of in landfills, sustainable practices must be developed in order to recover the fibers as they are valuable source for manufacturing high value-added products. This study investigates the valorization of paper sludge discarded by a filter paper manufacturer, with the purpose of producing cellulose acetate films for food packaging. The process involves recovering cellulose fibers from the sludge, purifying them and through acetylation reaction produce cellulose acetate films. FTIR spectra confirmed successful acetylation of fibers and also that acetyl groups reduced the hydrophilicity of cellulose—the contact angle was increased to over 80° from 50° in native cellulose. The films exhibited very good water barrier properties at both 50% and 90% relative humidity (RH). [ABSTRACT FROM AUTHOR]

This work aims to synthesize, characterize and determine the catalytic performance of MgO-KOH based catalysts using the glycerol acetylation reaction as a test. Acetylation of glycerol yields acetin compounds, which are considered high-value products with applications ranging from solvents in medicine to additives in gasoline. The catalysts were prepared by the co-precipitation method from the magnesium nitrate mixture as MgO precursor using KOH solutions at three different concentrations (1, 2, and 3 molar). Once obtained, the catalysts were characterized by Infrared and Raman spectroscopies, X-ray diffraction, scanning electronic microscopy, and nitrogen adsorption–desorption. The basic properties were determined using the thermal programmed CO2 desorption technique (TPD-CO2). The catalytic activity was evaluated in a glycerol/acetic acid esterification reaction carried out in a batch reactor at 70 °C, using a glycerol to acetic acid ratio of 1:3, 2 g of catalyst and for 110 min as the reaction conditions. The results show that catalysts have a high basicity with moderate strength and that they were highly active and stable. The catalyst with the highest amount of KOH was the most active, giving 95% glycerol conversion and 60% selectivity to higher acetin such as triacetate (TAGLY). The selectivity towards triacetin formation increased with increasing reaction time. In contrast, DAGLY formation decreased continuously as a function of time and glycerol monoacetate (MAGLY) formation remained almost constant throughout the reaction time. [ABSTRACT FROM AUTHOR]

The long noncoding DANCR functions as a tumor oncogene in many cancers, including colorectal cancer (CRC). However, the molecular mechanism of DANCR in CRC has not been explored. This study probed the function and potential mechanism by which DANCR contributes to the progression of CRC. The obtained data indicated that DANCR is overexpressed in CRC tissues and cell lines. Knockdown of DANCR hindered CRC cell proliferation, which was mediated by cyclin D1 and CDK4. Bioinformatic analysis, luciferase reporter assays and subcellular fractionation verified that DANCR directly binds to miR-508-5p. Moreover, DANCR acts as a miR-508-5p ceRNA to regulate expression of ATF1. In addition, upregulation of DANCR is attributed to H3K27 acetylation at the promoter region. In conclusion, our study confirmed that activation of lncRNA DANCR by H3K27 acetylation has an oncogenic role in CRC progression and provides a potential therapeutic target for CRC. [ABSTRACT FROM AUTHOR]

In all eukaryotes, acetylation of histone lysine residues correlates with transcription activation. Whether histone acetylation is a cause or consequence of transcription is debated. One model suggests that transcription promotes the recruitment and/or activation of acetyltransferases, and histone acetylation occurs as a consequence of ongoing transcription. However, the extent to which transcription shapes the global protein acetylation landscapes is not known. Here, we show that global protein acetylation remains virtually unaltered after acute transcription inhibition. Transcription inhibition ablates the co-transcriptionally occurring ubiquitylation of H2BK120 but does not reduce histone acetylation. The combined inhibition of transcription and CBP/p300 further demonstrates that acetyltransferases remain active and continue to acetylate histones independently of transcription. Together, these results show that histone acetylation is not a mere consequence of transcription; acetyltransferase recruitment and activation are uncoupled from the act of transcription, and histone and non-histone protein acetylation are sustained in the absence of ongoing transcription. Acetylation of histone lysine residues correlates with transcription activation, but it is currently debated whether histone acetylation is a cause or a consequence of transcription. Here, the authors show how global protein acetylation remains unaltered after acute inhibition of transcription, indicating that histone acetylation is not merely a consequence of transcription. [ABSTRACT FROM AUTHOR]

Facing increasing social, environmental, and economic pressure to substitute non-renewable fossil resources with renewable ones, hemicellulose has received attention as a substrate for the production of high-value products such as packaging materials because of its non-toxicity, abundance, and biodegradability. Hemicelluloses in the cell wall are naturally substituted with acetyl groups, and the degree and pattern of acetylation vary among plant species, tissue and cell types, and plant maturity. Hemicellulose acetylation influences features such as the flexural properties of wood, polysaccharide interactions, plant growth, and stress resistance. However, hemicellulose is deacetylated during its separation from other biomass polymers, mainly via alkaline solubilization. Therefore, when industrial applications require a certain degree of acetylation, chemical acetylation is necessary, which occurs through an esterification reaction that links acetyl groups to hemicellulose, catalyzed or not. Acetylation may enhance some features of hemicellulose-based packaging materials, such as mechanical strength, processability, thermal stability, hydrophobicity, and oxygen and water vapor permeability. This review provides an update on the latest advances in plant polysaccharide acetylation, including the acetylation mechanism in the plant cell wall as well as the influence of such esterification on plant properties and wood industrial application. Recent developments and progress in hemicellulose chemical acetylation strategies have been summarized, disclosing the advantages and disadvantages of different solvents and catalysts applied and acetylation evaluation methods. [ABSTRACT FROM AUTHOR]

Plastic film is widely produced and applied in many daily applications. Although it provides many benefits to human activity, the disposal of commercial plastics has always been a serious problem as it will contribute to landfilling issues and environmental pollution. Bioplastic film was invented to resolve part of this issue, as most of the plastic film produced from natural sources is biodegradable. However, the biodegradability and characteristics of the film are highly dependent on the type of raw material, production procedure, and chemical composition. In this study, extracted kapok cellulose was acetylated into cellulose acetate (CA) with various levels of acetic acid (17.5, 20, and 22.5 mL), acetic anhydride (5, 7.5, and 10 mL) and acetylation time (30, 45 and 60 min). The Box–Behnken design was applied to evaluate the quality of the produced film. The design showed that the level of acetic acid has a strong impact on CA's yield, acetic anhydride has a greater influence on tensile strength, and CA's solubility has a stronger connection with the acetylation time. All modeling equations developed were validated with the coefficient of determination, R2 more than 0.6. The optimized factor levels for the ductile-like film on acetic acid, acetic anhydride, and acetylation time are 20.530 mL, 9.546 mL, and 55.45 min, respectively. Whereas for brittle-like film, the optimized factor level is 22.399 mL, 10 mL, and 60 min, respectively. The ductility and brittleness of a plastic film can be modified by adjusting these level factors. [ABSTRACT FROM AUTHOR]

Sirtuin1 (SIRT1) activity decreases the tuberous sclerosis complex 2 (TSC2) lysine acetylation status, inhibiting the mechanistic target of rapamycin complex 1 (mTORC1) signalling and concomitantly, activating autophagy. This study analyzes the role of TSC2 acetylation levels in its translocation to the lysosome and the mitochondrial turnover in both mouse embryonic fibroblast (MEF) and in mouse insulinoma cells (MIN6) as a model of pancreatic β cells. Resveratrol (RESV), an activator of SIRT1 activity, promotes TSC2 deacetylation and its translocation to the lysosome, inhibiting mTORC1 activity. An improvement in mitochondrial turnover was also observed in cells treated with RESV, associated with an increase in the fissioned mitochondria, positive autophagic and mitophagic fluxes and an enhancement of mitochondrial biogenesis. This study proves that TSC2 in its deacetylated form is essential for regulating mTORC1 signalling and the maintenance of the mitochondrial quality control, which is involved in the homeostasis of pancreatic beta cells and prevents from several metabolic disorders such as Type 2 Diabetes Mellitus. [ABSTRACT FROM AUTHOR]

It is well known that preslaughter (antemortem) stress such as rough handling, transportation, a negative environment, physical discomfort, lack of consistent routine, and bad feed quality has a big impact on meat quality. The antemortem-induced poor meat quality is characterized by low pH, a pale and exudative appearance, and a soft texture. Previous studies indicate that antemortem stress plays a key role in regulating protein acetylation and glycolysis in postmortem (PM) muscle. However, the underlying molecular and biochemical mechanism is not clearly understood yet. In this study, we investigated the relationship between antemortem and protein acetylation and glycolysis using murine longissimus dorsi muscle isolated from ICR mice and murine muscle cell line C2C12 treated with epinephrine hydrochloride. Because adrenaline secretion increases in stressed animals, epinephrine hydrochloride was intraperitoneally injected epinephrine into mice to simulate pre-slaughter stress in this study to facilitate experimental operations and save experimental costs. Our findings demonstrated that protein acetylation in pyruvate kinase M1 (PKM1) form is significantly reduced by antemortem, and the reduced acetylation subsequently leads to an increase in PKM1 enzymatic activity which causes increased glycolysis in PM muscle. By using molecular approaches, we identified lysine 141 in PKM1 as a critical residue for acetylation. Our results in this study provide useful insight for controlling or improving meat quality in the future. [ABSTRACT FROM AUTHOR]

Hepatocellular carcinoma (HCC) is one of the malignancies with the worst prognosis worldwide, in the occurrence and development of which glycolysis plays a central role. This study uncovered a mechanism by which ZNF692 regulates ALDOA-dependent glycolysis in HCC cells. RT-qPCR and western blotting were used to detect the expression of ZNF692, KAT5, and ALDOA in HCC cell lines and a normal liver cell line. The influences of transfection-induced alterations in the expression of ZNF692, KAT5, and ALDOA on the functions of HepG2 cells were detected by performing MTT, flow cytometry, Transwell, cell scratch, and colony formation assays, and the levels of glucose and lactate were determined using assay kits. ChIP and luciferase reporter assays were conducted to validate the binding of ZNF692 to the KAT5 promoter, and co-IP assays to detect the interaction between KAT5 and ALDOA and the acetylation of ALDOA. ZNF692, KAT5, and ALDOA were highly expressed in human HCC samples and cell lines, and their expression levels were positively correlated in HCC. ZNF692, ALDOA, or KAT5 knockdown inhibited glycolysis, proliferation, invasion, and migration and promoted apoptosis in HepG2 cells. ZNF692 bound to the KAT5 promoter and promoted its activity. ALDOA acetylation levels were elevated in HCC cell lines. KAT5 bound to ALDOA and catalyzed ALDOA acetylation. ALDOA or KAT5 overexpression in the same time of ZNF692 knockdown, compared to ZNF692 knockdown only, stimulated glycolysis, proliferation, invasion, and migration and reduced apoptosis in HepG2 cells. ZNF692 promotes the acetylation modification and protein expression of ALDOA by catalyzing KAT5 transcription, thereby accelerating glycolysis to drive HCC cell development. [ABSTRACT FROM AUTHOR]

Gestational hypoxia inhibits mitochondrial function in the fetal heart and placenta contributing to fetal growth restriction and organ dysfunction. NAD + deficiency may contribute to a metabolic deficit by inhibiting oxidative phosphorylation and ATP synthesis. We tested the effects of nicotinamide riboside (NR), an NAD + precursor, as a treatment for reversing known mitochondrial dysfunction in hypoxic fetal hearts. Pregnant guinea pigs were housed in room air (normoxia) or placed in a hypoxic chamber (10.5%O2) for the last 14 days of gestation (term = 65 days) and administered either water or NR (1.6 mg/ml) in the drinking bottle. Fetuses were excised at term, and NAD + levels of maternal liver, placenta, and fetal heart ventricles were measured. Indices of mitochondrial function (complex IV activity, sirtuin 3 activity, protein acetylation) and ATP synthesis were measured in fetal heart ventricles of NR-treated/untreated normoxic and hypoxic animals. Hypoxia reduced fetal body weight in both sexes (p = 0.01), which was prevented by NR. Hypoxia had no effect on maternal liver NAD + levels but decreased (p = 0.04) placenta NAD + levels, the latter normalized with NR treatment. Hypoxia had no effect on fetal heart NAD + but decreased (p < 0.05) mitochondrial complex IV and sirtuin 3 activities, ATP content, and increased mitochondrial acetylation, which were all normalized with maternal NR. Hypoxia increased (p < 0.05) mitochondrial acetylation in female fetal hearts but had no effect on other mitochondrial indices. We conclude that maternal NR is an effective treatment for normalizing mitochondrial dysfunction and ATP synthesis in the hypoxic fetal heart. [ABSTRACT FROM AUTHOR]

Quick drying after water or sweat absorption is an important function of underwear. In this study, the hydroxy groups of cotton knitted fabrics (CFs) were partially acetylated, maintaining the original fabric structure. The following three heterogeneous acetylation processes were used: Ac-I (Ac2O/H2SO4/toluene), Ac-II (Ac2O/H2SO4/AcOH/water), and Ac-III (Ac2O/AcONa) systems (Ac2O, acetic anhydride; AcOH, acetic acid; AcONa, sodium acetate). Acetylated cotton knitted fabrics (AcCFs) with degree of substitution (DS) ≤ 0.5 and yields of > 80% were prepared. AcCFs prepared with the Ac-III system gave high degree of polymerization (DP) values of > 1500, whereas those prepared with the Ac-II system exhibited low DP values of ≤ 400. The moisture contents of AcCFs at 20 °C and 65% relative humidity decreased from 7.1 to 4.7% with increasing DS value up to 0.46; introducing hydrophobic acetyl groups into the CFs decreased their hydrophilic nature. Quick drying similar to that of a polyester fabric was achieved for some of the AcCFs with DS values of < 0.2. When the acetyl groups in the AcCFs were homogeneously distributed across each fiber width (achieved for AcCFs prepared with the Ac-II system), quick drying was evident in the AcCFs. The crystallinities and crystal widths of cellulose I for the AcCFs with DS values of ≤ 0.28 were almost unchanged compared with those of the original CFs. However, neither the crystallinities nor crystal widths of cellulose I were directly related to quick drying after water absorption. Thermal degradation of the AcCFs varied between the acetylation systems, and depended on the DP values and/or the presence of sulfate ester groups in the AcCFs. [ABSTRACT FROM AUTHOR]

Oil spills are significant environmental events that can harm marine life and human health globally. Booms, skimmers, dispersants and burning have drawbacks such as instability in strong currents and high costs, and can themselves cause environmental damage. Bioremediation using oil-degrading bacteria has been widely used but faces the risk of the bacteria being washed away under strong winds and currents, thus lowering their effectiveness. To enhance oil degradation effectiveness, immobilisation is commonly used to attach bacteria onto carriers which thereby act as a shield for the bacteria under harsh conditions. In this study, kapok fibre was used as an oil sorbent and carrier for bacterial immobilisation of Acinetobacter venetianus RAG-1. Kapok fibres were chosen due to their hollow lumen and waxy layer, which can be altered through acetylation to increase their hydrophobicity for potentially improved oil absorption and bacterial immobilisation. The highest degree of substitution achieved was 2.06 ± 0.05 using acetic anhydride with 0.2% sulphuric acid at 90 °C for an hour. The results showed that acetylated kapok fibres had a lower oil absorption capacity but higher reabsorption ratio than raw kapok fibres, which leads to better reusability. Scanning electron microscopy and viable cell counts showed that the bacteria were successfully immobilised onto kapok fibres. The number of bacteria immobilised showed no significant difference between acetylated and raw kapok fibres despite acetylated fibres having a rougher surface. Bacteria-immobilised acetylated fibres are effective as a reusable oil sorbent for their greater reabsorption ratio and likely to degrade oil simultaneously. [ABSTRACT FROM AUTHOR]

The main aim of this work was to study the role of the acetylation process of wheat straw pulp on its ability to rheologically modify two of the most important non-polar engineering fluid: bitumen and oil. Pulp was produced by a pilot-scale kraft pulping process from local wheat straw. Pulp was functionalized with acetic anhydride and sulfuric acid as a catalyst by modifying (temperature, pulp/acetic anhydride mass ratio, and reaction time. Further, chemical, morphological and thermal changes induced by the acetylation process were properly assessed. Acetylated wheat straw pulp dispersions in oil showed gel-like behaviour, with a mechanical spectrum characterized by higher values of the storage modulus (G′) and a minimum in the loss modulus (G″) at intermediate frequencies. The complex modulus (G*) for bitumen dispersions formulated with acetylated samples was up to 4 times higher than neat bitumen, and the phase angle (δ) indicated an enhancement in the elastic behavior parameters. The rheological response of these systems was associated with the microstructural network formed by pulp fibers and the balance between the physical and chemical changes of wheat straw fibers. According to the experimental results obtained, it can be concluded that acetylation is a relevant chemical treatment to modulate the rheological properties of wheat straw pulp dispersions in non-polar fluids, improving the compatibility between pulp fibers and these engineering fluids. Accordingly, this study provides valuable insights into the development of sustainable multiphasic materials (bitumen binders and semi-solid lubricants) for industrial applications. [ABSTRACT FROM AUTHOR]

Primary familial brain calcification (PFBC) is characterized by calcium deposition in the brain, causing progressive movement disorders, psychiatric symptoms, and cognitive decline. PFBC is a heterogeneous disorder currently linked to variants in six different genes, but most patients remain genetically undiagnosed. Here, we identify biallelic NAA60 variants in ten individuals from seven families with autosomal recessive PFBC. The NAA60 variants lead to loss-of-function with lack of protein N-terminal (Nt)-acetylation activity. We show that the phosphate importer SLC20A2 is a substrate of NAA60 in vitro. In cells, loss of NAA60 caused reduced surface levels of SLC20A2 and a reduction in extracellular phosphate uptake. This study establishes NAA60 as a causal gene for PFBC, provides a possible biochemical explanation of its disease-causing mechanisms and underscores NAA60-mediated Nt-acetylation of transmembrane proteins as a fundamental process for healthy neurobiological functioning. Most individuals with primary familial brain calcification (PFBC) remain genetically unsolved. Here the authors show that NAA60 biallelic variants cause PFBC, likely via reduced N-terminal acetylation and SLC20A2 levels with impaired phosphate uptake. [ABSTRACT FROM AUTHOR]

This study focuses on understanding the role of c-Myc, a cancer-associated transcription factor, in the penumbra following ischemic stroke. While its involvement in cell death and survival is recognized, its post-translational modifications, particularly acetylation, remain understudied in ischemia models. Investigating these modifications could have significant clinical implications for controlling c-Myc activity in the central nervous system. Although previous studies on c-Myc acetylation have been limited to non-neuronal cells, our research examines its expression in perifocal cells during stroke recovery to explore regulatory mechanisms via acetylation. We found that in peri-infarct neurons, c-Myc is upregulated with acetylation at K148 but not K323 during the acute phase of stroke, with SIRT2 deacetylase primarily affecting K148 acetylation. Molecular dynamics simulations suggest that lysine 148 plays a crucial role in stabilizing c-Myc spatial structure. Increased acetylation at K148 reduces c-Myc compaction, potentially limiting its nuclear penetration, promoting calpain-mediated cleavage, and decreasing nuclear localization. Additionally, cytoplasmic acetylation at K148 may alter c-Myc's interaction with unidentified proteins, potentially influencing its pro-apoptotic effects and promoting cytoplasmic accumulation. Targeting SIRT2 with selective inhibitors could be a promising avenue for future stroke therapy strategies. [ABSTRACT FROM AUTHOR]

The Escherichia coli TetR-related transcriptional regulator RutR is involved in the coordination of pyrimidine and purine metabolism. Here we report that lysine acetylation modulates RutR function. Applying the genetic code expansion concept, we produced site-specifically lysine-acetylated RutR proteins. The crystal structure of lysine-acetylated RutR reveals how acetylation switches off RutR-DNA-binding. We apply the genetic code expansion concept in E. coli in vivo revealing the consequences of RutR acetylation on the transcriptional level. We propose a model in which RutR acetylation follows different kinetic profiles either reacting non-enzymatically with acetyl-phosphate or enzymatically catalysed by the lysine acetyltransferases PatZ/YfiQ and YiaC. The NAD+-dependent sirtuin deacetylase CobB reverses enzymatic and non-enzymatic acetylation of RutR playing a dual regulatory and detoxifying role. By detecting cellular acetyl-CoA, NAD+ and acetyl-phosphate, bacteria apply lysine acetylation of transcriptional regulators to sense the cellular metabolic state directly adjusting gene expression to changing environmental conditions. The mechanisms underlying adaptation of bacteria to changing environmental conditions remain poorly understood. Here, the authors show bacteria using lysine acetylation of transcriptional regulators to adjust gene expression to changing conditions. [ABSTRACT FROM AUTHOR]

Aluminum is a known neurotoxin and a major environmental contributor to neurodegenerative diseases such as Alzheimer's disease (AD). We uesd a subchronic aluminum chloride exposure model in offspring rats by continuously treating them with AlCl3 solution from the date of birth until day 90 in this research. Then evaluated the neurobehavioral changes in rats, observed the ultrastructural changes of hippocampal synapses and neurons, and examined the level of hippocampal acetylated histone H3 (H3ac), the activity and protein expression of hippocampal HAT1 and G9a, and the protein expression level of H3K9 dimethylation (H3K9me2). The findings demonstrated that aluminum-treated offspring rats had impaired learning and memory abilities as well as ultrastructural alterations in hippocampal synapses and neurons. The level of histone H3ac was decreased along with decreased protein expression and activity of HAT1, while level of H3K9me2 was increased along with increased protein expression and activity of G9a. [ABSTRACT FROM AUTHOR]

Acetylation is a commercialised chemical wood modification technology that increases the durability of wood against microbial attack. However, the details of how acetylation protects the wood structure from fungal degradation are still unclear. In this study, we tested the hypothesis that the resistance against microbial attack depends on the localisation of acetylation within the cell wall. The methodology involved two types of acetylation (uniform and lumen interface modification), which were analysed by lab-scale degradation with Rhodonia placenta, chitin quantification, infrared spectroscopy, and Raman microspectroscopy. The location of the acetylation did not affect overall mass loss during degradation experiments. Instead, the mass loss was related to the intensity of the treatment. However, chemical imaging of the interface acetylated specimens showed that degradation primarily took place in cell wall regions that were less acetylated. It was also observed that the fungus required more fungal biomass (i.e., fungal mycelia) to degrade acetylated wood than untreated wood. Based on dimensions and comparison to a reference spectrum, several cross-sections of hyphae located within lumina were discovered in the Raman images. These hyphae showed presence of chitin, water and chelated metals within their walls, and could be separated into an inner and an outer part based on their chemistry as seen in the spectra. The outer part was distinguished by a relatively higher amount of water and less chelated iron than the inner part. [ABSTRACT FROM AUTHOR]

Composite films of cellulose nanofibers (CNFs) and poly(methyl methacrylate) (PMMA) are fabricated typically by solution-casting using an organic solvent (e.g., chloroform) that can dissolve PMMA. However, the preparation of the casting dope using the previously reported method requires multistep procedures for the solvent exchange of the CNF suspension from water to the organic solvent. Here we developed a facile method utilizing the cosolvency of PMMA in aqueous ethanol (EtOH aq.) to fabricate an optically transparent CNF-reinforced PMMA film. In this study, an acetylated-CNF (Ac-CNF) was used as a hydrophobic filler for compatibility with a hydrophobic PMMA matrix. First, an appropriate amount of EtOH was added dropwise to Ac-CNF aq. suspension to adjust the EtOH concentration to 80 vol%. PMMA was then added to the solution and dissolved under heating above the upper critical solution temperature to yield a clear casting dope. The dope is cast at 65 °C and then dried at 45 °C for 24 h in a closed oven to obtain an Ac-CNF/PMMA composite film. The composite film with 1% Ac-CNFs exhibited high total-light transmittance (93%) and low haze (4.4%), while 1.3-times higher tensile strength and Young's modulus than the neat PMMA film, indicating the effective reinforcement of PMMA by the well-dispersed Ac-CNFs. Thus, this method enables the facile preparation of an Ac-CNF/PMMA composite film with excellent transparency and enhanced mechanical performance. [ABSTRACT FROM AUTHOR]

Due to its role in apoptosis, differentiation, cell cycle arrest, and DNA damage repair in stress responses (oxidative stress, hypoxia, chemotherapeutic drugs, and UV irradiation or radiotherapy), FOXO3a is considered a key tumor suppressor that determines radiotherapeutic and chemotherapeutic responses in cancer cells. Mutations in the FOXO3a gene are rare, even in cancer cells. Post-translational regulations are the main mechanisms for inactivating FOXO3a. The subcellular localization, stability, transcriptional activity, and DNA binding affinity for FOXO3a can be modulated via various post-translational modifications, including phosphorylation, acetylation, and interactions with other transcriptional factors or regulators. This review summarizes how proteins that interact with FOXO3a engage in cancer progression. [ABSTRACT FROM AUTHOR]

Acetylation is a wood modification used to increase the durability. Although it is known that the wood moisture content is lowered, the exact mechanisms behind the increased durability are not known. However, since fungi need water in different locations for different purposes the location and state of water is most probably of importance in addition to the total moisture content. In a previous study, we used targeted acetylation to alter the wood–water interactions in different parts of the wood structure in water saturated and hygroscopic moisture states. The main range for fungal degradation is, however, between these moisture ranges. This study investigated the effect of targeted acetylation on location, state and amount of water at non-saturated, high moisture states using the pressure plate technique. Specimens were modified using acetic anhydride by two approaches: (1) uniform modification (2) interface modification acting on the cell wall-lumen interface. They were then conditioned to eight moisture states between 99.64 and 99.98% relative humidity in both absorption and desorption and the location and state of water was studied using Low Field Nuclear Magnetic Resonance, X-ray computed tomography and Differential Scanning Calorimetry. Capillary water was present at all the included moisture states for all specimen types, but the amounts of capillary water in absorption were small. Increasing degree of interface modification increased the amount of capillary water compared to untreated wood. In addition, the uniformly modified wood often had higher amounts of capillary water than the untreated wood. The amount of cell wall water was decreased by uniform modification, but slightly or not reduced by the interface modification. The combination of targeted modification and conditioning to high well-defined moisture states thus gave very different amounts of capillary water and cell wall water depending on the conditioning history (absorption or desorption) and choice of modification. This opens new possibilities for designing materials and moisture states for fungal degradation experiments of wood. [ABSTRACT FROM AUTHOR]

High rates of cardiac fatty acid oxidation during reperfusion of ischemic hearts contribute to contractile dysfunction. This study aimed to investigate whether lysine acetylation affects fatty acid oxidation rates and recovery in post-ischemic hearts. Isolated working hearts from Sprague Dawley rats were perfused with 1.2 mM palmitate and 5 mM glucose and subjected to 30 min of ischemia and 40 min of reperfusion. Cardiac function, fatty acid oxidation, glucose oxidation, and glycolysis rates were compared between pre- and post-ischemic hearts. The acetylation status of enzymes involved in cardiac energy metabolism was assessed in both groups. Reperfusion after ischemia resulted in only a 41% recovery of cardiac work. Fatty acid oxidation and glycolysis rates increased while glucose oxidation rates decreased. The contribution of fatty acid oxidation to ATP production and TCA cycle activity increased from 90 to 93% and from 94.9 to 98.3%, respectively, in post-ischemic hearts. However, the overall acetylation status and acetylation levels of metabolic enzymes did not change in response to ischemia and reperfusion. These findings suggest that acetylation may not contribute to the high rates of fatty acid oxidation and reduced glucose oxidation observed in post-ischemic hearts perfused with high levels of palmitate substrate. [ABSTRACT FROM AUTHOR]

The kinetics of the reaction of glycerol with acetic acid in the presence of natural aluminosilicates treated with nitric acid has been investigated. The influence of a molar ratio of the reagents, the reaction temperature and the catalyst mass fraction on glycerol conversion, as well as a rate of the accumulation of the products and their selectivities has been studied. It is established that in presence of clinoptilolite and trepel, monoacetin is the main product. In the case of bentonite, with the increase in the molar fraction of acetic acid and the catalyst mass fraction, the selectivity of monoacetin decreases due to a diacetin accumulation. [ABSTRACT FROM AUTHOR]

Immiscible and incompatibility between the hydrophilic fiber phase and hydrophobic matrix phase results in a poor stress transfer between the two phases and deterioration in mechanical, physical, and barrier properties. Thus, this study aims to enhance the compatibility between hydrophobic polybutylene adipate-co-terephthalate (PBAT) and hydrophilic nature corn starch (CS) by substituting native corn starch with acetylated corn starch (ACS). The acetylation treatment was used to improve the hydrophobicity of corn starch. The native corn starch was used as a reference to study the effect of acetylation. Challenges in incorporating fillers into hydrophobic PBAT were overcome by adding plasticizer; sorbitol (S) and compatibilizers; maleic anhydride (MAH) and dicumyl peroxide (DCP). The composite films were characterized by fourier transform infrared (FTIR), tensile properties, differential scanning calorimetry (DSC), water contact angle (WCA) measurement, and thermogravimetric analysis (TGA). The morphology of the composites was examined by scanning electron microscopy (SEM). The tensile properties of PBAT/ACS were improved by adding compatibilizers. Meanwhile, adding plasticizer improved the tensile properties of PBAT/CS. PBAT/ACS/MAH composite possessed a tensile strength of 15.47 MPa, modulus of 95.30 MPa, and strain at break of 170.81%, while PBAT/CS/30S composite possessed tensile strength of 8.59 MPa, modulus of 104.60 MPa and strain at break of 1037.91% which have potential use in packaging applications. [ABSTRACT FROM AUTHOR]

The regulation of cellular metabolism is a topic of interest for both fundamental and applied science, as the findings can be used in various biotechnological industries. One of the universal regulatory mechanisms that affects most cellular processes is the acetylation of lysine residues in central metabolic enzymes, such as glyceraldehyde-3-phosphate dehydrogenase. In this work, we investigated the effect of acetylation and deacetylation on the activity of both wild type and mutant E. coli glyceraldehyde-3-phosphate dehydrogenase. We found that in vitro acetylation of wild-type GAPDH by PatZ acetyltransferase increased its enzymatic activity by two-fold, while subsequent deacetylation restored the activity to initial level. For mutant forms of glyceraldehyde-3-phosphate dehydrogenase, we demonstrated that the introduction of additional acetylation sites due to mutations altered the impact of acetylation/deacetylation processes on glyceraldehyde-3-phosphate dehydrogenase activity. Our data suggest a re-evaluation of the role of acetylation in regulating glyceraldehyde-3-phosphate dehydrogenase activity and its involvement in E. coli metabolism. [ABSTRACT FROM AUTHOR]

Purpose: Anorexia nervosa (AN) is a neuropsychological public health concern with a socially disabling routine and affects a person’s healthy relationship with food. The role of the NNAT (Neuronatin) gene in AN is well established. The impact of mutation at the protein’s post-translational modification (PTM) site has been exclusively associated with the worsening of the protein’s biochemical dynamics. Methods: To understand the relationship between genotype and phenotype, it is essential to investigate the appropriate molecular stability of protein required for proper biological functioning. In this regard, we investigated the PTM-acetylation site of the NNAT gene in terms of 19 other specific amino acid probabilities in place of wild type (WT) through various in silico algorithms. Based on the highest pathogenic impact computed through the consensus classifier tool, we generated 3 residue-specific (K59D, P, W) structurally modified 3D models of NNAT. These models were further tested through the AutoDock Vina tool to compute the molecular drug binding affinities and inhibition constant (Ki) of structural variants and WT 3D models. Results: With trained in silico machine learning algorithms and consensus classifier; the three structural modifications (K59D, P, W), which were also the most deleterious substitution at the acetylation site of the NNAT gene, showed the highest structural destabilization and decreased molecular flexibility. The validation and quality assessment of the 3D model of these structural modifications and WT were performed. They were further docked with drugs used to manage AN, it was found that the ΔGbind (kcal/mol) values and the inhibition constants (Ki) were relatively lower in structurally modified models as compared to WT. Conclusion: We concluded that any future structural variation(s) at the PTM-acetylation site of the NNAT gene due to possible mutational consequences, will serve as a basis to explore its relationship with the propensity of developing AN. Level of evidence: No level of evidence—open access bioinformatics research. [ABSTRACT FROM AUTHOR]

Neurotrauma is among the main causes of human disability and mortality. However, the mechanisms that mediate the survival and death of cells in the peripheral nervous system are still not fully understood. The transcription factors p53 and E2F1 are the master regulators of basic cellular functions, including DNA repair, cell cycle, metabolism, and apoptosis. Overexpression of p53 and E2F1, shown in a number of experimental models of peripheral nerve injury, suggests an important role of these proteins in the pathogenesis of neurotrauma. This review discusses the epigenetic mechanisms of p53 and E2F1 activation and regulation, which may contribute to the survival or death of neurons and glial cells after traumatic injury. Prospects for further studies of the mechanisms of regulation of the p53 and E2F1 proteins, including those involving histone deacetylases, for the development of neuroprotectors are considered. [ABSTRACT FROM AUTHOR]

The recalcitrance of plant cell wall lignocellulosic biomass to deconstruction is a major hurdle to sustainable biofuel/bioproduct economy. A multitude of interactions stabilize lignocellulosic biomass structure. Among these, tight packing of hemicellulose-cellulose is partly responsible for biomass recalcitrance. Here, unrestrained molecular dynamics simulations are employed to understand the influence of the nature and pattern of naturally-occuring acetyl decorations of the xylan backbone on interactions with the (100) hydrophobic cellulose surface. Periodically O2-acetylated xylan (2AcX) assume twofold helical screw conformations that are stabilized by a combination of multiple hydrophobic contacts and hydrogen bonds with the hydrophobic cellulose surface. In contrast, acetylation at the O3 position in xylan obstructs interactions, thereby adopting threefold helical screw conformations that potentially preferably interact with lignin rather than cellulose. Fully acetylated xylan desorbs from the surface implying a minimum number of unsubstituted residues on the xylan backbone is required for interaction with the surface. The substituted residues must form ~ 20% fewer contacts than the unsubstituted residues to sustain stable twofold helical screw xylan conformations on the cellulose surface. Thus, specific roles of macromolecular conformations of cellulose and hemicellulose in influencing the supramolecular interactions and function of plant cell walls have been determined. [ABSTRACT FROM AUTHOR]