The dsRNA isolated from Escherichia coli infected with the MS2 bacteriophage induces the production of interferons.

Viral infections pose a significant threat to public health, and the production of interferons represents one of the most critical antiviral innate immune responses of the host. Consequently, the screening and identification of compounds or reagents that induce interferon production are of paramount importance. This study commenced with the cultivation of host bacterium 15,597, followed by the infection of Escherichia coli with the MS2 bacteriophage. Utilizing the J2 capture technique, a class of dsRNA mixtures (MS2+15,597) was isolated from the E. coli infected with the MS2 bacteriophage. Subsequent investigations were conducted on the immunostimulatory activity of the MS2+15,597 mixture. The results indicated that the dsRNA mixtures (MS2+15,597) extracted from E. coli infected with the MS2 bacteriophage possess the capability to activate innate immunity, thereby inducing the production of interferon-ß. These dsRNA mixtures can activate the RIG-I and TLR3 pattern recognition receptors, stimulating the expression of interferon stimulatory factors 3/7, which in turn triggers the NF-κB signaling pathway, culminating in the cellular production of interferon-ß to achieve antiviral effects. This study offers novel insights and strategies for the development of broad-spectrum antiviral drugs, potentially providing new modalities for future antiviral therapies.

FAIRE-MS reveals mitotic retention of transcriptional regulators on a proteome-wide scale.

Mitosis entails global and dramatic alterations, such as higher-order chromatin organization disruption, concomitant with global transcription downregulation. Cells reliably re-establishing gene expression patterns upon mitotic exit and maintaining cellular identities remain poorly understood. Previous studies indicated that certain transcription factors (TFs) remain associated with individual loci during mitosis and serve as mitotic bookmarkers. However, it is unclear which regulatory factors remain bound to the compacted mitotic chromosomes. We developed formaldehyde-assisted isolation of regulatory elements-coupled mass spectrometry (FAIRE-MS) that combines FAIRE-based open chromatin-associated protein pull-down and mass spectrometry (MS) to quantify the open chromatin-associated proteome during the interphase and mitosis. We identified 189 interphase and mitosis maintained (IM) regulatory factors using FAIRE-MS and found intrinsically disordered proteins and regions (IDP(R)s) are highly enriched, which plays a crucial role in liquid-liquid phase separation (LLPS) and chromatin organization during the cell cycle. Notably, in these IDP(R)s, we identified mitotic bookmarkers, such as CEBPB, HMGB1, and TFAP2A, and several factors, including MAX, HMGB3, hnRNP A2/B1, FUS, hnRNP D, and TIAL1, which are at least partially bound to the mitotic chromosome. Furthermore, it will be essential to study whether these IDP(R)s through LLPS helps cells transit from mitosis to the G1 phase during the cell cycle.

Incidence of acute kidney injury after hematopoietic stem cell transplantation in children: a systematic review and meta-analysis.

While acute kidney injury (AKI) has been reported after hematopoietic stem cell transplantation (HCT) in children, the incidence of this condition in the pediatric population has not been fully addressed. To assess the incidence of pediatric AKI after HCT treatment,we conducted a systematic literature review. Databases PubMed, Embase, Cochrane Library, and WOS were searched as of June 2022 to identify studies on the incidence and the risk of death in AKI children undergoing HCT. Random effects and generic inverse variance methods were used, and effect estimates were subsequently derived from individual studies. Twelve cohort studies with 2 159 HCT cases were included in this analysis. The combined estimated incidence of AKI and severe AKI (stage AKI III) was 51% (95% confidence interval (CI) 39-64%) and 12% (95%CI 4-24%), respectively. The estimated incidence of AKI based on RIFLE (pRIFLE), AKIN, and KDIGO criteria was 61% (95%CI 40-82% score I 95.1%), 64% (95%CI 49-79% score I 90.4%), and 51% (95%CI 2-100% score 99.0%), respectively. However, we found no significant correlation between the years of publication of the included studies and the incidence of AKI.  Conclusions: AKI affects approximately half of the children after HCT. With the advancements in medical techniques, it is expected that AKI in this population will decrease gradually. What is Known: • Hematopoietic stem cell transplantation is recognized as a treatment for malignant and non-malignant diseases in children. • Hematopoietic stem cell transplantation causes acute kidney injury in children. What is New: • This metanalysis showed that the overall frequency of post-HCT AKI in children is 51%. • The frequency of severe AKI after HCT was found to be 12%.

The role of ZNF143 overexpression in rat liver cell proliferation.

BACKGROUND: Zinc finger protein 143(ZNF143), a member of the Krüppel C2H2-type zinc finger protein family, is strongly associated with cell cycle regulation and cancer development. A recent study suggested that ZNF143 plays as a transcriptional activator that promotes hepatocellular cancer (HCC) cell proliferation and cell cycle transition. However, the exact biological role of ZNF143 in liver regeneration and normal liver cell proliferation has not yet been investigated. METHODS: In our study, we constructed a stable rat liver cell line (BRL-3A) overexpressing ZNF143 and then integrated RNA-seq and Cleavage Under Targets and Tagmentation (CUT&Tag) data to identify the mechanism underlying differential gene expression. RESULTS: Our results show that ZNF143 expression is upregulated during the proliferation phase of liver regeneration after 2/3 partial hepatectomy (PH). The cell counting kit-8 (CCK-8) assay, EdU staining and RNA-seq data analyses revealed that ZNF143 overexpression (OE) significantly inhibited BRL-3A cell proliferation and cell cycle progression. We then performed CUT&Tag assays and found that approximately 10% of ZNF143-binding sites (BSs) were significantly changed genome-wide by ZNF143 OE. However, CCCTC-binding factor (CTCF) binding to chromatin was not affected. Interestingly, the integration analysis of RNA-seq and CUT&Tag data showed that some of genes affected by ZNF143 differential BSs are in the center of each gene regulation module. Gene ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses indicated that these genes are critical in the maintenance of cell identity. CONCLUSION: These results indicated that the expression level of ZNF143 in the liver is important for the maintenance of cell identity. ZNF143 plays different roles in HCC and normal liver cells and may be considered as a potential therapeutic target in liver disease.

ZNF143 is dynamically bound to a subset of its interphase sites during mitosis.

During mitosis, transcription is ceased, chromatin becomes condensed, many chromatin features are lost, and most transcription factors (TFs) are excluded from chromosomes. The mechanism on how daughter cells maintain cell identity after exiting mitosis remains unclear. A subset of multiple lineage-specific and general TFs remains bound to mitotic chromosomes during mitosis, thereby suggesting a potential mechanism termed mitotic bookmarking. Here, genome-wide binding analysis of TF ZNF143 in human A549 lung epithelial cells reveals that ZNF143 remains partially associated with its interphase-specific genomic regions during mitosis. Genome distribution analysis shows that 80% of these regions preferentially localize to promoters. In addition, ZNF143 in mitosis may could recruit other relative TFs when the cells re-enter into G1 phase and rapidly initiates gene transcription. These results suggest that the dynamic binding of ZNF143 during cell cycle has a potential mitotic bookmarking role in maintaining cell fate and identity.

Optimization and quality control of genome-wide Hi-C library preparation.

Highest-throughput chromosome conformation capture (Hi-C) is one of the key assays for genome- wide chromatin interaction studies. It is a time-consuming process that involves many steps and many different kinds of reagents, consumables, and equipments. At present, the reproducibility is unsatisfactory. By optimizing the key steps of the Hi-C experiment, such as crosslinking, pretreatment of digestion, inactivation of restriction enzyme, and in situ ligation etc., we established a robust Hi-C procedure and prepared two biological replicates of Hi-C libraries from the GM12878 cells. After preliminary quality control by Sanger sequencing, the two replicates were high-throughput sequenced. The bioinformatics analysis of the raw sequencing data revealed the mapping-ability and pair-mate rate of the raw data were around 90% and 72%, respectively. Additionally, after removal of self-circular ligations and dangling-end products, more than 96% of the valid pairs were reached. Genome-wide interactome profiling shows clear topological associated domains (TADs), which is consistent with previous reports. Further correlation analysis showed that the two biological replicates strongly correlate with each other in terms of both bin coverage and all bin pairs. All these results indicated that the optimized Hi-C procedure is robust and stable, which will be very helpful for the wide applications of the Hi-C assay.

Involvement of aberrant miR-139/Jun feedback loop in human gastric cancer.

Accumulating evidence indicates that some miRNAs could form feedback loops with their targets to fine-tune tissue homeostasis, while disruption of these loops constitutes an essential step towards human tumorigenesis. In this study, we report the identification of a novel negative feedback loop formed between miR-139 and its oncogenic target Jun. In this loop, miR-139 could inhibit Jun expression by targeting a conserved site on its 3'-UTR, whereas Jun could induce miR-139 expression in a dose dependent manner through a distant upstream regulatory element. Interestingly, aberration in this loop was found in human gastric cancer, where miR-139 was down-regulated and inversely correlated with Jun expression. Further functional analysis showed that restored expression of miR-139 in gastric cancer cells significantly induces apoptosis, and inhibits cell migration and proliferation as well as tumour growth through targeting Jun. Thus, our data strongly suggests a role of aberrant miR-139/Jun negative feedback loop in the development of human gastric cancer and miR-139 as a potential therapeutic target for gastric cancer. Given that miR-139 and Jun are deregulated in many cancers, our findings here might have broader implication in other types of human cancers.

GC3-biased gene domains in mammalian genomes.

MOTIVATION: Synonymous codon usage bias has been shown to be correlated with many genomic features among different organisms. However, the biological significance of codon bias with respect to gene function and genome organization remains unclear. RESULTS: Guanine and cytosine content at the third codon position (GC3) could be used as a good indicator of codon bias. Here, we used relative GC3 bias values to compare the strength of GC3 bias of genes in human and mouse. We reported, for the first time, that GC3-rich and GC3-poor gene products might have distinct sub-cellular spatial distributions. Moreover, we extended the view of genomic gene domains and identified conserved GC3 biased gene domains along chromosomes. Our results indicated that similar GC3 biased genes might be co-translated in specific spatial regions to share local translational machineries, and that GC3 could be involved in the organization of genome architecture. AVAILABILITY AND IMPLEMENTATION: Source code is available upon request from the authors. CONTACT: zhaozh@nic.bmi.ac.cn or zany1983@gmail.com SUPPLEMENTARY INFORMATION: Supplementary data are available at Bioinformatics online.

Construction of CTCF degradation cell line by CRISPR/Cas9 mediated genome editing.

The CCCTC-binding factor (CTCF) is the main insulator protein described in vertebrates. It plays fundamental roles during diverse cellular processes. CTCF gene knockout mice led to death during embryonic development. To further explore the functions of CTCF, we employed a CRISPR/Cas9-based genome engineering strategy to in-frame insert the mitosis-special degradation domain (MD) of cyclin B into the upstream open reading frame of CTCF gene. Fusion protein is designed to degrade during mitosis leaded by MD. As a control group, mutation of a single arginine (R42A) within the destruction box inactivates the MD leading to constitutive expression of MD*-CTCF. The homozygous clones were obtained via the screening by puromycin when coexpressed with puromycin resistence gene. The protein level of CTCF in MD-CTCF cell line was about 10% of wild-type cells throughout cell cycles by the analyses of Western blotting and immunofluorescence. There was no significant difference between MD*-CTCF cell line and wild type. Flow cytometry results showed prolonged G1 phase in MD-CTCF cell line. Taken together, we demonstrated the feasibility of efficiently inserting MD domain into genome with the CRISPR/Cas9 technology and reported the first CTCF-specific degradation human cell line.

A possible role of Drosophila CTCF in mitotic bookmarking and maintaining chromatin domains during the cell cycle.

BACKGROUND: The CCCTC-binding factor (CTCF) is a highly conserved insulator protein that plays various roles in many cellular processes. CTCF is one of the main architecture proteins in higher eukaryotes, and in combination with other architecture proteins and regulators, also shapes the three-dimensional organization of a genome. Experiments show CTCF partially remains associated with chromatin during mitosis. However, the role of CTCF in the maintenance and propagation of genome architectures throughout the cell cycle remains elusive. RESULTS: We performed a comprehensive bioinformatics analysis on public datasets of Drosophila CTCF (dCTCF). We characterized dCTCF-binding sites according to their occupancy status during the cell cycle, and identified three classes: interphase-mitosis-common (IM), interphase-only (IO) and mitosis-only (MO) sites. Integrated function analysis showed dCTCF-binding sites of different classes might be involved in different biological processes, and IM sites were more conserved and more intensely bound. dCTCF-binding sites of the same class preferentially localized closer to each other, and were highly enriched at chromatin syntenic and topologically associating domains boundaries. CONCLUSIONS: Our results revealed different functions of dCTCF during the cell cycle and suggested that dCTCF might contribute to the establishment of the three-dimensional architecture of the Drosophila genome by maintaining local chromatin compartments throughout the whole cell cycle.

Functional screening for miRNAs targeting Smad4 identified miR-199a as a negative regulator of TGF-ß signalling pathway.

The transforming growth factor-ß (TGF-ß) signalling pathway participates in various biological processes. Dysregulation of Smad4, a central cellular transducer of TGF-ß signalling, is implicated in a wide range of human diseases and developmental disorders. However, the mechanisms underlying Smad4 dysregulation are not fully understood. Using a functional screening approach based on luciferase reporter assays, we identified 39 microRNAs (miRNAs) as potential regulators of Smad4 from an expression library of 388 human miRNAs. The screening was supported by bioinformatic analysis, as 24 of 39 identified miRNAs were also predicted to target Smad4. MiR-199a, one of the identified miRNAs, was inversely correlated with Smad4 expression in various human cancer cell lines and gastric cancer tissues, and repressed Smad4 expression and blocked canonical TGF-ß transcriptional responses in cell lines. These effects were dependent on the presence of a conserved, but not perfect seed paired, miR-199a-binding site in the Smad4 3'-untranslated region (UTR). Overexpression of miR-199a significantly inhibited the ability of TGF-ß to induce gastric cancer cell growth arrest and apoptosis in vitro, and promoted anchorage-independent growth in soft agar, suggesting that miR-199a plays an oncogenic role in human gastric tumourigenesis. In conclusion, our functional screening uncovers multiple miRNAs that regulate the cellular responsiveness to TGF-ß signalling and reveals important roles of miR-199a in gastric cancer by directly targeting Smad4.

The microbiomic signature of hemorrhoids and comparison with associated microbiomes.

Hemorrhoids are a common ailment that can cause significant disruptions to one's daily life. While some researchers have speculated about a potential link between hemorrhoid development and gut microbes, there is currently insufficient evidence to support this claim. In this study, we collected samples from 60 hemorrhoid patients and analyzed the composition and characteristics of microbiomes in hemorrhoids. PCoA results revealed distinct differences between the microbiomes of hemorrhoids, skin-originated microbiomes, and gut microbes, highlighting the complex nature of hemorrhoidal microbiomes. The distribution characteristics of Staphylococcus suggest that the skin microbiome influences the microbiome of hemorrhoids. Additionally, we observed higher levels of Prevotella in two cases of thrombosed hemorrhoids compared to non-thrombosed hemorrhoids. This finding suggests that Prevotella may play a crucial role in the development of thrombosed hemorrhoids.

Microbiomic signatures of anal fistula and putative sources of microbes.

Anal fistula is a common perianal disease that typically develops from an abscess caused by in-flammation in the area. It has long been believed that intestinal microbes play a significant role in its development, considering its close relation to the intestinal environment. This work attempts to identify the microbiomic signatures of anal fistula, and putative sources of microbes by analyzing microbiomes of 7 anal fistula-associated sites in 12 patients. This study found that microbes in anal fistulas may originate from the skin surface in addition to the intestinal tract. This finding was further validated by NMDS analysis, which also indicated that the microbial communities in the inner and outer openings of the fistula were more similar to their surrounding environments. Using MaAslin2, the characteristics of the microbiome were examined, demonstrating a higher similarity between the abundant bacteria in the anal fistula samples and those found on the skin surface. Moreover, pin-to-pair analysis conducted on all subjects consistently showed a higher abundance of skin-sourced bacteria in anal fistulas. This study identifies the microbiomic signatures of anal fistula, and provides novel insights into the origin of microorganisms in anal fistulas.

Breaking the intrinsic activity barriers of bilayer metal oxides for catalytic CO2 reduction.

The photocatalytic CO2 reduction reaction is severely limited by sluggish charge kinetics. To address this issue, a strategy utilizing non-metal-doped layered double hydroxide (LDH) has been developed to control the electronic structure of spindle-shaped nanoflowers, resulting in efficient photocatalytic CO2 reduction. The results demonstrate that the designed catalyst yields 263.16 µmol g-1 h-1 for the photoreduction of CO2 to CO. Furthermore, the in situ Fourier transform infrared spectrum (FT-IR) analysis demonstrate that the specific S-ligand (S-bridge) facilitates CO2 activation, ensuring the continuous production of *COOH. The hydrothermal-assisted ionic liquid method proposed in this study offers guidance for modifying catalysts.

Learning curve for flexible bronchoscope-guided orotracheal intubation for anesthesiology residents: A cumulative sum analysis.

BACKGROUND: Endotracheal intubation with a flexible bronchoscope is a well-recognized airway management technique that anesthesiologists must master. Skill acquisition and knowledge must reach an appropriate level before trainees perform independent practice on patients. There are a paucity of evidence-based outcome measures of trainee competence in performing flexible bronchoscopy. The objectives of this study were to 1) construct a learning curve for flexible bronchoscope-guided orotracheal intubation for anesthesiology residents using the CUSUM method and 2) determine the number of procedures required to achieve proficiency. METHODS: This study included 12 first-year anesthesiology residents with no previous experience with flexible bronchoscopic intubation. Trainees attended theoretical and simulation training and performed flexible bronchoscope-guided orotracheal intubation in adult patients with normal airways under general anesthesia. Number of intubation attempts, intubation success rate, time to intubation, and incidence of dental and mucosal injuries were recorded. The cumulative sum (CUSUM) method was used to evaluate the learning curve of flexible bronchoscope-guided orotracheal intubation. RESULTS: Trainees performed flexible bronchoscope-guided orotracheal intubation on 364 patients. First-attempt intubation success occurred in 317 (87.1%) patients. Second-attempt intubation success occurred in 23 (6.3%) patients. Overall, the flexible bronchoscope-guided orotracheal intubation success rate was 93.4% (range, 85.3% to 100%). The mean number of orotracheal intubation procedures per trainee was 31 ± 5 (range, 23 to 40). All trainees crossed the lower decision boundary (H0) after 15.1 ± 5.6 procedures (range, 8 to 25 procedures). There was a significant decrease in median intubation time [39s (IQR: 30, 50) vs. 76s (IQR: 54, 119)] (P < 0.001) after crossing the lower decision boundary (H0) compared to before. There were no dental, mucosa, arytenoid or vocal cord trauma events associated with intubation. CONCLUSIONS: Learning curves constructed with CUSUM analysis showed that all trainees (anesthesiologist residents) included in this study achieved competence (intubation success rates ≥ 80%) in flexible bronchoscope-guided orotracheal intubation. Trainees needed to perform 15 (range, 8 to 25) procedures to achieve proficiency. There was wide variability between trainees. TRIAL REGISTRATION: Trial registration: Chinese Clinical Trial Register, ChiCTR 2000032166.

Research on the Mechanism and Control Technology of Coal Wall Sloughing in the Ultra-Large Mining Height Working Face.

One of the primary factors affecting safe and effective mining in fully mechanized mining faces with large mining heights is coal wall sloughing. This paper establishes the mechanical model of the coal wall and uses the deflection theory for the mechanics of materials to find the maximum point of the deflection of the coal wall, which is the most easily deformed and damaged during the mining process, based on the mining production conditions of the 12-2up108 working face in the Jinjitan Coal Mine. In order to simulate the characteristics of the coal wall in the large mining height working face at various mining heights, the FLAC-3D numerical method was used. The stability of the mining area was assessed in conjunction with the multi-factor fuzzy comprehensive evaluation mathematical model, and the corresponding control of the coal wall was suggested. The study demonstrates that: (1) The working surface at Jinjitan Coal Mine 112-2up108 is a typical drum-out sloughing. The coal wall is most likely to sustain damage at the point where it contacts the roof when the frictional resistance between the coal seam and the roof and floor is less than the uniform load, and at 0.578 times the mining height when the frictional resistance between the coal seam and the roof and floor is greater than the uniform load. (2) In the working face with a large mining height, mining height of the coal wall is one of the significant influencing factors. With increasing mining height, the coal wall's height also rises nonlinearly, as does the depth of the coal wall in the working face with the large mining height. The growth is linear. The coal wall's maximum deflection value point moves up and the slab's height significantly increases when the mining height exceeds 7.5 m. (3) The Jinjitan Coal Mine should be supported by a pressurized and enhanced composite support bracket with a support force greater than 0.245 MPa and a support plate of 3500 mm because it belongs to a Class I stable coal wall, according to a thorough evaluation of a multi-factor fuzzy mathematical model. The working face's mining pressure is continuously and dynamically monitored, and the stress is released in a timely manner to prevent the occurrence of dynamic disasters.

Deubiquitinating enzyme Josephin-2 stabilizes PHGDH to promote a cancer stem cell phenotype in hepatocellular carcinoma.

BACKGROUND: Deubiquitinating enzymes (DUBs) have been shown to be possible targets for hepatocellular carcinoma (HCC) treatment. OBJECTIVE: This study was designed to reveal the effect and underlying mechanism of Josephin-2, a relatively newly defined DUB, in HCC progression. METHODS: SNU-387 and PLC/PRF/5 cells were used for in vitro functional assays. The levels of Josephin-2 and phosphoglycerate dehydrogenase (PHGDH) were determined using RT-qPCR and western blotting. Cell proliferation, migration and invasion were assessed by CCK-8, colony formation and Transwell. Spheroid-forming assay was performed to assess the cancer stem cell (CSC)-phenotype of HCC cells. A xenograft mice model was applied to verify the effect of Josephin-2 on HCC cell growth in vivo. RESULTS: Herein, we showed that Josephin-2 expression was negatively correlated with HCC patient survival in data from the online database. Cell experiments indicated that knockdown of Josephin-2 attenuated HCC cell malignant biological behaviors. Besides, Josephin-2 silencing also decreased the spheroid-formation while inhibited the expression of CSC biomarkers (CD133, OCT4, SOX2 and EpCAM) in HCC cells. Mechanistically, Josephin-2 had a deubiquitinating activity towards the regulation of PHGDH protein, the rate-limiting enzyme in the first step of serine biosynthesis pathway. Depletion of Josephin-2 enhanced the ubiquitination degradation of PHGDH and ultimately inhibited the proliferation and CSC-phenotype of HCC in vitro and in vivo. CONCLUSION: Our work uncovered the regulatory effects of Josephin-2 on PHGDH protein stability and profiled its contribution in HCC malignant progression, which might provide a potential therapeutic target for HCC.

Role of PDLIM1 in hepatic stellate cell activation and liver fibrosis progression.

Liver fibrosis is caused by chronic hepatic injury and may lead to cirrhosis, and even hepatocellular carcinoma. When hepatic stellate cells (HSCs) are activated by liver injury, they transdifferentiate into myofibroblasts, which secrete extracellular matrix proteins that generate the fibrous scar. Therefore, it is extremely urgent to find safe and effective drugs for HSCs activation treatment to prevent liver against fibrosis. Here, we reported that PDZ and LIM domain protein 1 (PDLIM1), a highly conserved cytoskeleton organization regulator, was significantly up-regulated in fibrotic liver tissues and TGF-ß-treated HSC-T6 cells. Through transcriptome analysis, we found that knockdown of PDLIM1 resulted in a significant downregulation of genes related to inflammation and immune-related pathways in HSC-T6 cells. Moreover, PDLIM1 knockdown significantly inhibited the activation of HSC-T6 cells and the trans-differentiation of HSC-T6 cells into myofibroblasts. Mechanistically, PDLIM1 is involved in the regulation of TGF-ß-mediated signaling pathways in HSCs activation. Thus, targeting PDLIM1 may provide an alternative method to suppress HSCs activation during liver injury. CCCTC-binding factor (CTCF), a master regulator of genome architecture, is upregulated during HSCs activation. PDLIM1 knockdown also indirectly reduced CTCF protein expression, however, CTCF binding to chromatin was not significantly altered by CUT&Tag analysis. We speculate that CTCF may cooperate with PDLIM1 to activate HSCs in other ways. Our results suggest that PDLIM1 can accelerate the activation of HSCs and liver fibrosis progression and could be a potential biomarker for monitoring response to anti-fibrotic therapy.

Genome-wide identification of GTE family proteins in sugarcane (Saccharum spontaneum) reveals that SsGTEL3a confers drought tolerance.

The bromodomain is a highly conserved protein domain that specifically binds to acetylated lysine residues in histones, thereby activating transcription of target genes. Although some progress in Global Transcription Factor Group E (GTE) has been achieved in numerous animals and a few plant species, no systematic analysis of GTE gene families has been reported yet in sugarcane. In our study, 37 GTE and GTE-Like (GTEL) genes were characterized in the Saccharum spontaneum. All SsGTE/SsGTEL members were heterogeneously located on all chromosomes of the sugarcane genome and divided into five groups. Transcriptome data showed that SsGTEL3a was expressed at significantly higher levels under drought stress in drought-resistant varieties than in drought-sensitive varieties. Moreover, the overexpression of SsGTEL3a significantly improved the drought tolerance in Arabidopsis through improving the scavenging ability of reactive oxygen species. Additionally, an interaction between ScFAR1 and SsGTEL3a was identified, with ScFAR1 showing a positive response to drought stress in bacterium. In summary, this systematic analysis of GTE gene family in sugarcane and functional research of SsGTEL3a broadened deeper insight into their evolutionary dynamics and functional properties and provided new candidate genes for drought-resistant molecular breeding of sugarcane.

dbGSRV: A manually curated database of genetic susceptibility to respiratory virus.

Human genetics has been proposed to play an essential role in inter-individual differences in respiratory virus infection occurrence and outcomes. To systematically understand human genetic contributions to respiratory virus infection, we developed the database dbGSRV, a manually curated database that integrated the host genetic susceptibility and severity studies of respiratory viruses scattered over literatures in PubMed. At present, dbGSRV contains 1932 records of genetic association studies relating 1010 unique variants and seven respiratory viruses, manually curated from 168 published articles. Users can access the records by quick searching, batch searching, advanced searching and browsing. Reference information, infection status, population information, mutation information and disease relationship are provided for each record, as well as hyperlinks to public databases in convenient of users accessing more information. In addition, a visual overview of the topological network relationship between respiratory viruses and associated genes is provided. Therefore, dbGSRV offers a convenient resource for researchers to browse and retrieve genetic associations with respiratory viruses, which may inspire future studies and provide new insights in our understanding and treatment of respiratory virus infection. Database URL: http://www.ehbio.com/dbGSRV/front/.