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• Despite a much higher proportion of intragenic heterochromatin-containing genes in crop genomes, the importance of intragenic heterochromatin in crop development remains unclear. Intragenic heterochromatin can be recognised by a protein complex, ASI1–AIPP1–EDM2 (AAE) complex, to regulate alternative polyadenylation. • Here, we investigated the impact of rice ASI1 on global poly(A) site usage through poly(A) sequencing and ASI1-dependent regulation on rice development. • We found that OsASI1 is essential for rice pollen development and flowering. OsASI1 dysfunction has an important impact on global poly(A) site usage, which is closely related to heterochromatin marks. Intriguingly, OsASI1 interacts with the intronic heterochromatin of OsXRNL, a nuclear XRN family exonuclease gene involved in the processing of an miRNA precursor, to promote the processing of full-length OsXRNL and regulate miRNA abundance. We found that OsASI1-mediated regulation of pollen development partially depends on OsXRNL. Finally, we characterised the rice AAE complex and its involvement in alternative polyadenylation and pollen development. • Our findings help to elucidate an epigenetic mechanism governing miRNA abundance and rice development, and provide a valuable resource for studying the epigenetic mechanisms of many important processes in crops.

A12-week experiment was conducted to evaluate the influences of thiamine ongrowth performance, and intestinal mitochondrial biogenesis and function of Megalobramaamblycephala fed a high-carbohydrate (HC) diet. Fish (24·73 (sem 0·45) g) were randomly assigned to one of four diets: two carbohydrate (CHO) levels (30 and 45 %) and two thiamine levels (0 and 1·5 mg/kg). HC diets significantly decreased DGC, GRMBW, FIMBW, intestinal activities of amylase, lipase, Na+, K+-ATPase, CK, complexes I, III and IV, intestinal ML, number of mitochondrial per field, ΔΨm, the P-AMPK: T-AMPK ratio, PGC-1β protein expression as well as the transcriptions of AMPKα1, AMPKα2, PGC-1β, mitochondrial transcription factor A, Opa-1, ND-1 and COX-1 and 2, while the opposite was true for ATP, AMP and reactive oxygen species, and the transcriptions of dynamin-related protein-1, fission-1 and mitochondrial fission factor. Dietarythiamine concentrations significantly increased DGC, GRMBW, intestinal activities of amylase, Na+, K+-ATPase, CK, complexes I and IV, intestinal ML, number of mitochondrial per field, ΔΨm, the P-AMPK:T-AMPK ratio, PGC-1β protein expression as well as the transcriptions of AMPKα1, AMPKα2, PGC-1β, Opa-1, ND-1, COX-1 and 2, SGLT-1 and GLUT-2. Furthermore, a significant interaction between dietary CHO and thiamine was observed in DGC, GRMBW, intestinal activities of amylase, CK, complexes I and IV, ΔΨm, the AMP:ATP ratio, the P-AMPK:T-AMPK ratio, PGC-1β protein expression as well as the transcriptions of AMPKα1, AMPKα2, PGC-1β, Opa-1, COX-1 and 2, SGLT-1 and GLUT-2. Overall, thiamine supplementation improved growth performance, and intestinal mitochondrial biogenesis and function of M. amblycephala fed HC diets.

Invertebrates rely heavily on immune-like molecules with highly diversified variability so as to counteract infections. However, the mechanisms and the relationship between this variability and functionalities are not well understood. Here, we showed that the C-terminal domain of hemocyanin (HMC) from shrimp contained an evolutionary conserved domain with highly variable genetic sequence, which is structurally homologous to immunoglobulin (Ig). This domain is responsible for recognizing and binding to bacteria or red blood cells, initiating agglutination and hemolysis. Furthermore, when HMC is separated into three fractions using anti-human IgM, IgG, or IgA, the subpopulation, which reacted with anti-human IgM (HMC-M), showed the most significant antimicrobial activity. The high potency of HMC-M is a consequence of glycosylation, as it contains high abundance of α-d-mannose relative to α-d-glucose and -acetyl-d-galactosamine. Thus, the removal of these glycans abolished the antimicrobial activity of HMC-M. Our results present a comprehensive investigation of the role of HMC in fighting against infections through genetic variability and epigenetic modification.

Background Posthemorrhagic hydrocephalus (PHH) is a frequent and significant complication that impacts the prognosis of patients suffering from intraventricular hemorrhage (IVH). However, the underlying mechanism is uncertain. Neuronal pyroptosis is characterized by neuronal lysis and destruction, along with the release of inflammatory factors. Autophagy is known to inhibit inflammation, and histone deacetylase-6 (HDAC6) is implicated in the regulation of both autophagy and the NLRP3 inflammasome. However, the role of these proteins in the regulation of neuronal pyroptosis in an IVH model has not been determined. Methods In this study, an IVH mouse (6–8 weeks) model was generated via the intracerebroventricular administration of autologous blood at a volume of 40 µL/animal. After the surgical operation, we monitored the mice at various time points, assessing ventricle size via MRI. Additionally, during both the acute (3 days) and chronic (28 days) phases post-surgery, we examined neuronal cell damage and ventricular cilia, as well as neurological function, using HE staining, Nissl staining, scanning electron microscopy, and behavioral experiments such as neurological function scoring and water maze tests. Finally, we detected activation of the pyroptosis and autophagy pathway through western blotting and immunofluorescence staining. Results Autophagy induction attenuated cerebral neuronal pyroptosis caused by acute-phase autologous blood injection. HDAC6 was implicated in regulating pyroptosis in the acute phase IVH through its influence on the transcription of nuclear factor kappa-B (NF-κB). Furthermore, HDAC6 regulates excessive autophagic activation in neurons in the chronic phase of IVH. Treatment with ricolinostat improved neurological deficits and ventricular damage during the acute phase of IVH. Moreover, it alleviated mood, memory, and learning deficits in the chronic phase of IVH while also improving PHH. Conclusions Enhanced autophagy attenuates activation of the NOD-like receptor protein 3 (NLRP3) inflammasome and inhibits neuronal pyroptosis in the acute phase of IVH. HDAC6 plays an important role in regulating the interaction between autophagy and pyroptosis. Ricolinostat treatment significantly attenuated the upregulation of inflammatory factors and neurological impairments induced by pyroptosis in the acute phase of IVH. In addition, ricolinostat effectively reduced excessive autophagy and apoptosis in neurons in the chronic phase and attenuated the formation of PHH.

Dimethylated histone H3 Lys9 (H3K9me2) is a conserved heterochromatic mark catalyzed by SUPPRESSOR OF VARIEGATION 3-9 HOMOLOG (SUVH) methyltransferases in plants. However, the mechanism underlying the locus specificity of SUVH enzymes has long been elusive. Here, we show that a conserved N-terminal motif is essential for SUVH6-mediated H3K9me2 deposition in planta. The SUVH6 N-terminal peptide can be recognized by the bromo-adjacent homology (BAH) domain of the RNA- and chromatin-binding protein ANTI-SILENCING 1 (ASI1), which has been shown to function in a complex to confer gene expression regulation. Structural data indicate that a classic aromatic cage of ASI1-BAH domain specifically recognizes an arginine residue of SUVH6 through extensive hydrogen bonding interactions. A classic aromatic cage of ASI1 specifically recognizes an arginine residue of SUVH6 through extensive cation-π interactions, playing a key role in recognition. The SUVH6-ASI1 module confers locus-specific H3K9me2 deposition at most SUVH6 target loci and gives rise to distinct regulation of gene expression depending on the target loci, either conferring transcriptional silencing or posttranscriptional processing of mRNA. More importantly, such mechanism is conserved in multiple plant species, indicating a coordinated evolutionary process between SUVH6 and ASI1. In summary, our findings uncover a conserved mechanism for the locus specificity of H3K9 methylation in planta. These findings provide mechanistic insights into the delicate regulation of H3K9 methylation homeostasis in plants.

The thermal scratch significantly influences the surface quality of the stainless steel in cold strip rolling. The thermal scratch has a close relation to the rolling parameters, the rolls surface and the emulsions used in rolling. In order to explain the thermal scratch on the strip surface, the cold roiling process of SUS430 stainless steel strip was investigated in the laboratory. The thermal scratch defect occurs frequently in the second rolling pass （maximum reduction in height is 32.3 ~）, especially on the lower surface of strips. When concentration and temperature of the emulsion are the same, the thermal scratch on the surface o{ the strip is aggravated with increasing the roll surface roughness. With the same roll surface roughness and emulsion concentration, the thermal scratch is obviously more severe at an emulsion temperature of 63 ℃ than 55 ℃. With the same roll surface roughness and emulsion tempera- ture, the thermal scratch is distinctly weaker at the emulsion concentration of 6 % than that of 3 %.

Post-transcriptional regulatory mechanisms play important roles in the regulation of LC-PUFA biosynthesis. Our previous study revealed that miR-33 could increase the expression of fatty acyl desaturases (fads2) in the rabbitfish Siganus canaliculatus, but the specific mechanism is unknown. Here, we confirmed that miR-33 could target the 3′UTR of insulin-induced gene 1 (insig1), resulting in downregulation of its protein level in the rabbitfish hepatocyte line (SCHL). In vitro overexpression of miR-33 inhibited the mRNA level of insig1 and increased the mRNA levels of Δ6Δ5 fads2 and elovl5, as well as srebp1. In SCHL cells, proteolytic activation of sterol-regulatory-element-binding protein-1 (Srebp1) was blocked by Insig1, with overexpression of insig1 decreasing mature Srebp1 level, while inhibition of insig1 led to the opposite effect. Srebp1 could enhance the promoter activity of Δ6Δ5 fads2 and elovl5, whose expression levels decreased with knockdown of srebp1 in SCHL. Overexpression of miR-33 also resulted in a higher conversion of 18:3n-3 to 18:4n-3 and 20:5n-3 to 22:5n-3, linked to desaturation and elongation via Δ6Δ5 Fads2 and Elovl5, respectively. The results suggested that the mechanism by which miR-33 regulates LC-PUFA biosynthesis in rabbitfish is through enhancing the expression of srebp1 by targeting insig1. The findings here provide more insight to the mechanism of miRNAs involvement in the regulation of LC-PUFA biosynthesis in teleosts.

Aim： To discover novel hepatitis C virus （HCV） inhibitors and elucidate the mechanism of action of the active compounds. Methods： HCV subgenomic replicon-based luciferase reporter cell line was used to screen 1200 synthetic compounds with novel structures. HuhT.5.1 cell line stably transfected with HCV NS3/4A protease reporter was established to investigate the anti-HCV mechanism of the active compounds. The active compounds were further examined in an in vitro HCV infection assay to confirm their anti-HCV activity. Results： After two-round screening in the anti-HCV replicon assay, some 2,4-diaminoquinazoline derivatives and carboxamide analogues were found to possess anti-HCV replicon activities （the IC50 values were less than 5 μmol/L）. Among them, two representative compounds HZ-1157 and LZ-110618-6 inhibited HCV NS3/4A protease with IC50 values of 1.0 and 0.68 μmol/L, respectively. Furthermore, HZ-1157 and LZ-110618-6 inhibited HCV infection in vitro with IC50values of 0.82 and 0.11 μmol/L, respectively. Conclusion： Some 2,4-diaminoquinazoline derivatives and carboxamide analogues have been identified as novel anti-HCV compounds.

Dear Editor, MicroRNAs （miRNAs） are small non-coding RNAs of -22 nucleotides （nt） in length that bind to the 3＇UTRs of their target mRNAs, leading to translational inhibition or mRNA degradation （Bartel, 2009）. miRNAs regulate the expression of hundreds of genes involved in various biological processes, such as apoptosis, migration, metastasis, and autophagy （Flynt and Lai, 2008; Frankel and Lund, 2012; Ventura and Jacks, 2009）. Previous studies have indicated that miRNAs may act as oncogenes or antioncogenes in tumorigenesis of various cancers （Hammond, 2015）.

Background： Major side branch （SB） occlusion is one of the most serious complications during percutaneous coronary intervention （PCI） for bifurcation lesions. We aimed to characterize the incidence and predictors of major SB occlusion during coronary bifurcation intervention. Methods： We selected consecutive patients undergoing PCI （using one stent or provisional two stent strategy） for bifurcation lesions with major SB. All clinical characteristics, coronary angiography findings, PCI procedural factors and quantitative coronary angiographic analysis data were collected. Multivariate logistic regression analysis was performed to identify independent predictors of SB occlusion. SB occlusion after main vessel （MV） stenting was defined as no blood flow or any thrombolysis in myocardial infarction （TIMI） flow grade decrease in SB after MV stenting. Results： Among all 652 bifurcation lesions, 32 （4.91%） SBs occluded. No blood flow occurred in 18 lesions and TIMI flow grade decreasing occurred in 14 lesions. In multivariate analysis, diameter ratio between MV/SB （odds ratio [OR]： 7.71,95% confidence interval [C/]： 1.53-38.85, P = 0.01）, bifurcation angle （OR： 1.03, 95% CI： 1.02-1.05, P 〈 0.01）, diameter stenosis of SB before MV stenting （OR： 1.05, 95% CI： 1.03-1.07, P〈 0.01）, TIMI flow grade of SB before MV stenting （OR： 3.59, 95% CI： 1.48-8.72, P〈 0.01） and left ventricular eject fraction （LVEF） （OR： 1.06, 95% Cl： 1.02-1.11, P 〈 0.01） were independent predictors of SB occlusion. Conclusions： Among clinical and angiographic findings, diameter ratio between MV/SB, bifurcation angle, diameter stenosis of SB before MV stenting, TIMI flow grade of SB before MV stenting and LVEF were predictive of major SB occlusion after MV stenting.