In sight the behavior of natural Bletilla striata polysaccharide hydrocolloids by molecular dynamics method.

Plant polysaccharides, distinguished by diverse glycosidic bonds and various cyclic sugar units, constitute a subclass of primary metabolites ubiquitously found in nature. Contrary to common understanding, plant polysaccharides typically form hydrocolloids upon dissolution in water, even though both excessively high and low temperatures impede this process. Bletilla striata polysaccharides (BSP), chosen for this kinetic study due to their regular repeating units, help elucidate the relationship between polysaccharide gelation and temperature. It is suggested that elevated temperatures enhance the mobility of BSP molecular chains, resulting in a notable acceleration of hydrogen bond breakage between BSP and water molecules and consequently, compromising the conformational stability of BSPs to some extent. This study unveils the unique relationship between polysaccharide dissolution processes and temperature from a kinetics perspective. Consequently, the conclusion provides a dynamical basis for comprehending the extraction and preparation of natural plant polysaccharide hydrocolloids, pharmaceuticals and related fields.

Radiation-targeted immunotherapy: A new perspective in cancer radiotherapy.

In contemporary oncology, radiation therapy and immunotherapy stand as critical treatments, each with distinct mechanisms and outcomes. Radiation therapy, a key player in cancer management, targets cancer cells by damaging their DNA with ionizing radiation. Its effectiveness is heightened when used alongside other treatments like surgery and chemotherapy. Employing varied radiation types like X-rays, gamma rays, and proton beams, this approach aims to minimize damage to healthy tissue. However, it is not without risks, including potential damage to surrounding normal cells and side effects ranging from skin inflammation to serious long-term complications. Conversely, immunotherapy marks a revolutionary step in cancer treatment, leveraging the body's immune system to target and destroy cancer cells. It manipulates the immune system's specificity and memory, offering a versatile approach either alone or in combination with other treatments. Immunotherapy is known for its targeted action, long-lasting responses, and fewer side effects compared to traditional therapies. The interaction between radiation therapy and immunotherapy is intricate, with potential for both synergistic and antagonistic effects. Their combined use can be more effective than either treatment alone, but careful consideration of timing and sequence is essential. This review explores the impact of various radiation therapy regimens on immunotherapy, focusing on changes in the immune microenvironment, immune protein expression, and epigenetic factors, emphasizing the need for personalized treatment strategies and ongoing research to enhance the efficacy of these combined therapies in cancer care.

P53-response circRNA_0006420 aggravates lung cancer radiotherapy resistance by promoting formation of HUR/PTBP1 complex.

BACKGROUND: p53 wild-type lung cancer cells can develop radiation resistance. Circular RNA (circRNA) consists of a family of transcripts with exclusive structures. circRNA is critical in tumorigenesis and is a potential biomarker or therapeutic target. It is uncertain how circRNA expression and functions are regulated post-radiation in p53 wild-type cancer cells. METHODS: A549 or H1299 cells were divided into p53-wt and p53-KO groups by CRISPR/Cas9; both groups were subjected to 4 Gy ionizing radiation (IR: p53-wt-IR and p53-KO-IR). RNA-seq, CCK8, cell cycle, and other functional and mechanism experiments were performed in vivo. p53 gene knockout mice were generated to test the cell results in vitro. RESULTS: circRNAs were found in differential groups. circRNA_0006420 (IRSense) was upregulated in p53-wt cells but had the same expression level as p53-KO cells after radiation, indicating that p53 silencing prevents its upregulation after IR. In the presence of p53, upregulated IRSense post-radiation induces G2/M arrest by regulating DNA damage repair (DDR) pathway-related proteins. Meanwhile, upregulated IRSense post-radiation aggravates the radiation-induced epithelial-mesenchymal transition (EMT). Interestingly, in the presence of p53, it promotes IRSense/HUR/PTBP1 complex formation resulting in the promotion of the radiation-induced EMT. Moreover, c-Jun regulates the upregulation of p53 transcription after radiation treatment. For these lung cancer cells with p53, upregulated IRSense aggravates lung cancer cell proliferation and increases radiation resistance by interacting with HUR (ElAV-like protein 1) and PTBP1 (polypyrimidine tract-binding protein 1) in the nucleus. CONCLUSIONS: Lung cancer cells retaining p53 may upregulate circRNA_0006420 (IRSense) expression post radiation to form an IRSense/HUR/PTBP1 complex leading to radiotherapy resistance. This study furthers our understanding of the roles of circRNA in regulating the effect of radiotherapy and provides novel therapeutic avenues for effective clinical lung cancer therapies.

Nanoparticles-induced potential toxicity on human health: Applications, toxicity mechanisms, and evaluation models.

Nanoparticles (NPs) have become one of the most popular objects of scientific study during the past decades. However, despite wealth of study reports, still there is a gap, particularly in health toxicology studies, underlying mechanisms, and related evaluation models to deeply understanding the NPs risk effects. In this review, we first present a comprehensive landscape of the applications of NPs on health, especially addressing the role of NPs in medical diagnosis, therapy. Then, the toxicity of NPs on health systems is introduced. We describe in detail the effects of NPs on various systems, including respiratory, nervous, endocrine, immune, and reproductive systems, and the carcinogenicity of NPs. Furthermore, we unravels the underlying mechanisms of NPs including ROS accumulation, mitochondrial damage, inflammatory reaction, apoptosis, DNA damage, cell cycle, and epigenetic regulation. In addition, the classical study models such as cell lines and mice and the emerging models such as 3D organoids used for evaluating the toxicity or scientific study are both introduced. Overall, this review presents a critical summary and evaluation of the state of understanding of NPs, giving readers more better understanding of the NPs toxicology to remedy key gaps in knowledge and techniques.

TXNL4B regulates radioresistance by controlling the PRP3-mediated alternative splicing of FANCI.

Ionizing radiation (IR) has been extensively used for cancer therapy, but the radioresistance hinders and undermines the radiotherapy efficacy in clinics greatly. Here, we reported that the spliceosomal protein thioredoxin-like 4B (TXNL4B) is highly expressed in lung tissues from lung cancer patients with radiotherapy. Lung cancer cells with TXNL4B knockdown illustrate increased sensitivity to IR. Mechanistically, TXNL4B interacts with RNA processing factor 3 (PRP3) and co-localizes in the nucleus post-IR. Nuclear localization of PRP3 promotes the alternative splicing of the Fanconi anemia group I protein (FANCI) transcript variants, FANCI-12 and FANCI-13. PRP3 regulates alternative splicing of FANCI toward the two variants, FANCI-12 and FANCI-13. Radioresistance was greatly enhanced through the combination of PRP31 and PRP8, the critical components of core spliceosome promoted by PRP3. Notably, the inhibition of PRP3 to suppress the production of FANCI-12 would deprive PRP31 and PRP8 of such interaction. As a result, cell cycle G2/M arrest was induced, DNA damage repair was delayed, and radiosensitivity was improved. Collectively, our study highlights potential novel underlying mechanisms of the involvement of TXNL4B and alternative splicing in radioresistance. The results would benefit potential cancer radiotherapy.

Lactobacillus rhamnosus GG ameliorates radiation-induced lung fibrosis via lncRNASNHG17/PTBP1/NICD axis modulation.

Radiation-induced pulmonary fibrosis (RIPF) is a major side effect experienced for patients with thoracic cancers after radiotherapy. RIPF is poor prognosis and limited therapeutic options available in clinic. Lactobacillus rhamnosus GG (LGG) is advantaged and widely used for health promotion. However. Whether LGG is applicable for prevention of RIPF and relative underlying mechanism is poorly understood. Here, we reported a unique comprehensive analysis of the impact of LGG and its' derived lncRNA SNHG17 on radiation-induced epithelial-mesenchymal transition (EMT) in vitro and RIPF in vivo. As revealed by high-throughput sequencing, SNHG17 expression was decreased by LGG treatment in A549 cells post radiation and markedly attenuated the radiation-induced EMT progression (p < 0.01). SNHG17 overexpression correlated with poor overall survival in patients with lung cancer. Mechanistically, SNHG17 can stabilize PTBP1 expression through binding to its 3'UTR, whereas the activated PTBP1 can bind with the NICD part of Notch1 to upregulate Notch1 expression and aggravated EMT and lung fibrosis post radiation. However, SNHG17 knockdown inhibited PTBP1 and Notch1 expression and produced the opposite results. Notably, A549 cells treated with LGG also promoted cell apoptosis and increased cell G2/M arrest post radiation. Mice of RIPF treated with LGG decreased SNHG17 expression and attenuated lung fibrosis. Altogether, these data reveal that modulation of radiation-induced EMT and lung fibrosis by treatment with LGG associates with a decrease in SNHG17 expression and the inhibition of SNHG17/PTBP1/Nothch1 axis. Collectively, our results indicate that LGG exerts protective effects in RIPF and SNHG17 holds a potential marker of RIPF recovery in patients with thoracic cancers.

Potential role of gut microbiota-LCA-INSR axis in high fat-diet-induced non-alcoholic fatty liver dysfunction: From perspective of radiation variation.

Non-alcoholic fatty liver disease (NAFLD) is a progressive disease of the liver covering a range of conditions from hepatic steatosis to liver fibrosis. NAFLD could be induced by High-fat-diet(HFD). Ionizing radiation is widely used in medical diagnosis and therapy as well as is a common risk factor in occupational environment. Whether the exposure of various dose of radiation has effects on HFD-induced NAFLD remains unclear. Here, we reported that radiation exposure promoted HFD-induced NAFLD in a dose-response manner. Furthermore, the gut microbiota composition had significant difference among mice with or without radiation treatment. Specifically, the Bacteroidetes/Firmicutes ratio, the abundance of A. muciniphila, Butyricococcus, and Clostridiaceae decreased significantly in the mice with co-exposure of high dose of radiation and HFD treatment. A fecal transplantation trial (FMT) further verified the role of gut microbiota in the regulation of the liver response to co-exposure of high dose of radiation and HFD treatment. Notably, the gut microbiome analysis showed plasma lithocholic acid (LCA) level increased in the mice with co-exposure of high dose of radiation and HFD treatment. Following antibiotic and probiotic treatments there was a significantly decreased LCA bile acid concentration and subsequent promotion of INSR/PI3K/Akt insulin signaling in the liver tissues. Our results demonstrate that the co-exposure of radiation and HFD aggravates the HFD-induced NAFLD through gut microbiota-LCA-INSR axis. Probiotics supplementation is a potential way to protect against co-exposure of radiation and HFD-induced liver damage. Meanwhile, our study provide a new insight that population with potential HFD-induced damage should pay more attention on preventing from liver damage while exposing radiation.

Low-dose radiation exaggerates HFD-induced metabolic dysfunction by gut microbiota through PA-PYCR1 axis.

Co-exposure of High-fat-diet (HFD) behavior and environmental low-dose radiation (LDR) is common among majority occupational workers, but the synergism of this co-exposure in metabolic health is poorly understood. This study aimed to investigate the impact of gut microbiota and its metabolites on the regulation of HFD accompanied by LDR-associated with metabolic dysfunction and insulin resistance. Here, we reported that Parasutterella was markedly elevated in the gut microbiota of mice in co-exposure of HFD and LDR, accompanied by increased pyrrolidinecarboxylic acid (PA) level in both intestine and plasma. Transplantation of fecal microbiota from mice with co-exposure HFD and LDR with metabolic dysfunction resulted in increased disruption of metabolic dysfunction, insulin resistance and increased PYCR1 (Pyrroline-5-carboxylate reductase 1) expression. Mechanistically, intestinal barrier was damaged more serious in mice with co-exposure of HFD and LDR, leading high PA level in plasma, activating PYCR1 expression to inhibit insulin Akt/mTOR (AKT kinase-transforming protein/Serine threonine-protein kinase) signaling pathway to aggravate HFD-induced metabolic impairments. This study suggests a new avenue for interventions against western diet companied with low dose radiation exposure-driven metabolic impairments.

Amomum tsao-ko essential oil, a novel anti-COVID-19 Omicron spike protein natural products: A computational study.

Since the outbreak of COVID-19, this virus has been constantly mutating. The latest mutant Omicron has been identified as VOC by WHO. The main reason for its concern is the mutation of 46 amino acids in spike protein, which has brought the global epidemic prevention into another difficulty. Herbal aromatic plant Amomum tsao-ko was excavated from formula 1 and 2 for the treatment of COVID-19 in China, and its active components were extracted and identified. Molecular dynamics simulation and Fpocket were applied to find the key sites on RBDOmicron, and molecular docking was also used to reveal the interaction between A. tsao-ko essential oil (AEO) and RBDOmicron. The AEO components were analyzed and identified by GC/Q-TOF MS. There were 20 kinds of AEO with a relative area percentage of more than 1%, and they were related to the three active centres of RBDOmicron. In this study, virtual screening was used to mine the essential oil components of medicinal plants, and it was found that the components could interact with the spike protein RBD in aerosol to block the interaction of RBD and hACE2, thus cutting off the transmission route and protecting the host. This study has certain guiding significance in the modernization of Traditional Chinese medicine and the prevention of COVID-19.

Selective Aerobic Oxidation of Csp3-H Bonds Catalyzed by Yeast-Derived Nitrogen, Phosphorus, and Oxygen Codoped Carbon Materials.

Nitrogen, phosphorus, and oxygen codoped carbon catalysts were successfully synthesized using dried yeast powder as a pyrolysis precursor. The yeast-derived heteroatom-doped carbon (yeast@C) catalysts exhibited outstanding performance in the oxidation of Csp3-H bonds to ketones and esters, giving excellent product yields (of up to 98% yield) without organic solvents at low O2 pressure (0.1 MPa). The catalytic oxidation protocol exhibited a broad range of substrates (38 examples) with good functional group tolerance, excellent regioselectivity, and synthetic utility. The yeast-derived heteroatom-doped carbon catalysts showed good reusability and stability after recycling six times without any significant loss of activity. Experimental results and DFT calculations proved the important role of N-oxide (N+-O-) on the surface of yeast@C and a reasonable carbon radical mechanism.

Helicobacter pylori and Alzheimer's Disease-Related Metabolic Dysfunction: Activation of TLR4/Myd88 Inflammation Pathway from p53 Perspective and a Case Study of Low-Dose Radiation Intervention.

Gut dysbiosis is observed in Alzheimer's disease (AD) and is frequently associated with AD-induced metabolic dysfunction. However, the extent and specific underlying molecular mechanisms triggered by alterations of gut microbiota composition and function mediating AD-induced metabolic dysfunction in AD remain incompletely uncovered. Here, we indicate that Helicobacter pylori (H. pylori) is abundant in AD patients with relative metabolic dysfunction. Fecal microbiota transplantation from the AD patients promoted metabolic dysfunction in mice and increased gut permeability. H. pylori increased gut permeability through activation of the TLR4/Myd88 inflammation pathway in a p53-dependent manner, leading to metabolic dysfunction. Moreover, p53 deficiency reduced bile acid concentration, leading to an increased abundance of H. pylori colonization. Overall, these data identify H. pylori as a key promoter of AD-induced metabolic dysfunction.

Potential liver damage due to co-exposure to As, Cd, and Pb in mining areas: Association analysis and research trends from a Chinese perspective.

There is global concern regarding the public health hazards of environmental exposure to multiple toxic heavy metals. The effects of toxic heavy metals on liver function have been suggested in previous reports, but the association between exposure to multiple toxic heavy metals and liver function has not been elucidated. The aim of this study was to investigate the effects of exposure to multiple toxic heavy metals, arsenic(As), lead(Pb), and cadmium(Cd), on liver function through population-based and animal studies. A total of 3590 participants were enrolled from the mining areas in Western Hunan Province. The concentrations of As, Pb, and Cd in the urine and plasma samples were determined using quadrupole inductively coupled plasma mass spectrometry (ICP-MS). Bayesian kernel machine regression (BKMR) was employed for the joint association assay. An animal study was conducted to further verify the cumulative effects of metals on liver damage-related parameters such as alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) levels. Research trends regarding toxic metals were also explored to obtain in-depth understanding of the current knowledge in this field. Typically, for single-exposure analysis, in most mines, Pb exhibited a significantly negative association with ALT levels, whereas for cumulative effects analysis, when As, Pb, and Cd concentrations were at the 50thpercentile, a significantly negative effect on liver ALT levels was observed. Furthermore, animal studies have shown that co-exposure to As, Pb, and Cd could aggravate liver dysfunction in mice compared to that in the single-metal treated group (p < 0.05). From 1990 to 2019, 1965 projects relating to As, Pb, and Cd research have been initiated, and the total RMB(RenMingBi) funded was approximately 800 million in China, as opposed to 2500 projects in the US with an approximate amount of US$ 1 billion, which is substantially greater than that of China. Finally, from a global viewpoint, scientists should continue to substantially contribute to the field of heavy metal contamination through more extensive academic investigation, global cooperation, and the development of novel control methods. Overall, this study identified that elevated combined concentrations of As, Pb, and Cd were significantly negatively associated with liver function.

Transcriptomic and metabolomic profiling reveal the p53-dependent benzeneacetic acid attenuation of silica-induced epithelial-mesenchymal transition in human bronchial epithelial cells.

BACKGROUND: Silica exposure underlies the development of silicosis, one of the most serious occupational hazards worldwide. We aimed to explore the interaction of the silica-induced epithelial-mesenchymal transition (EMT)-related transcripts with the cellular metabolism regulated by p53. METHODS: We knocked out p53 using CRISPR/Cas9 in the human bronchial epithelial (HBE) cell line. The transcriptomic and metabolomic analyses and integrative omics were conducted using microarrays, GC-MS, and MetaboAnalyst, respectively. RESULTS: Fifty-two mRNAs showed significantly altered expression in the HBE p53-KO cells post-silica exposure. A total of 42 metabolites were putatively involved in p53-dependent silica-mediated HBE cell dysfunction. Through integrated data analysis, we obtained five significant p53-dependent metabolic pathways including phenylalanine, glyoxylate, dicarboxylate, and linoleic acid metabolism, and the citrate cycle. Through metabolite screening, we further identified that benzeneacetic acid, a key regulation metabolite in the phenylalanine metabolic pathway, attenuated the silica-induced EMT in HBE cells in a p53-dependent manner. Interestingly, despite the extensive p53-related published literature, the clinical translation of these studies remains unsubstantial. CONCLUSIONS: Our study offers new insights into the molecular mechanisms by which epithelial cells respond to silica exposure and provide fresh perspective and direction for future clinical biomarker research and potential clinically sustainable and translatable role of p53.

GTPase Activity of MxB Contributes to Its Nuclear Location, Interaction with Nucleoporins and Anti-HIV-1 Activity.

The human myxovirus resistance 2 (Mx2/MxB) protein, a member of interferon (IFN)-inducible dynamin-like large GTPases, restricts a number of virus infections. Inhibition of these viruses occurs at poorly-defined steps after viral entry and has a common requirement for MxB oligomerization. However, the GTPase activity is essential for the anti-viral effects of MxB against herpesviruses and HBV but not HIV-1. To understand the role of MxB GTPase activity, including GTP binding and GTP hydrolysis, in restriction of HIV-1 infection, we genetically separated these two functions and evaluated their contributions to restriction. We found that both the GTP binding and hydrolysis function of MxB involved in the restriction of HIV-1 replication. The GTPase activity of MxB contributed to its nuclear location, interaction with nucleoporins (NUPs) and HIV-1 capsids. Furthermore, MxB disrupted the association between NUPs and HIV-1 cores dependently upon its GTPase activity. The function of GTPase activity was therefore multi-faceted, led to fundamentally distinct mechanisms employed by wild-type MxB and GTPase activity defective MxB mutations to restrict HIV-1 replication.

A gut dysbiotic microbiota-based hypothesis of human-to-human transmission of non-communicable diseases.

Non-communicable diseases (NCDs) have replaced communicable diseases as the leading cause of premature death worldwide over the past century. Increasing numbers of studies have reported a link between NCDs and dysbiotic gut microbiota. Some gut microbiota, such as Helicobacter pylori, have been implicated in person-to-person transmission. Based on these reports, we develop a hypothesis regarding dysbiotic microbiota-associated NCDs, and explore how the presence of communicable NCDs could be confirmedexperimentally. We have also reviewed reports on environmental factors, including a high-fat diet, alcohol, smoking, exercise, radiation and air pollution, which have been associated with dysbiotic microbiota, and determined whether any of these parameters were also associated with NCDs. This review discusses the potential mechanism by which dysbiotic microbiota induced by environmental factors are directly or indirectly involved in person-to-person transmission. The hypothetical interplay between the environment, gut microbiota and host can be tested through high-throughput sequencing, animal models, and cell studies, although each of these modalities presents specific challenges. Confirmation of a causative association of dysbiotic microbiota with NCDs would represent a paradigm shift in efforts to prevent and control these diseases, and should stimulate additional studies on the associations among environmental factors, gut microbiota, and NCDs.

MxB impedes the NUP358-mediated HIV-1 pre-integration complex nuclear import and viral replication cooperatively with CPSF6.

BACKGROUND: The human myxovirus resistance 2 (Mx2/MxB) protein was originally found to regulate cytoplasmic-nuclear transport but was recently reported to restrict HIV-1 replication by binding to HIV-1 capsid (CA), preventing uncoating, the nuclear import of pre-integration complex (PIC) and viral DNA integration. This work explores the mechanisms of MxB-mediated HIV-1 inhibition. RESULTS: We demonstrated that MxB represses NUP358-mediated PIC nuclear import and HIV-1 replication. Moreover, MxB's effects on PIC nuclear import and HIV-1 replication depend critically on cofactor cleavage and polyadenylation specificity factor subunit 6 (CPSF6). MxB binds nucleoporin NUP358, blocks NUP358-CA interaction, thereby impeding the nuclear import of HIV-1 PIC with CPSF6 binding to PIC. More intriguingly, CPSF6's role in nuclear import depends on MxB, being a facilitator of HIV-1 nuclear import on its own, but becoming an inhibitor when MxB is present. CONCLUSIONS: Our work establishes that MxB impedes the NUP358-mediated HIV-1 nuclear import and viral replication cooperatively with CPSF6.

Correction to: Description of Wenzhouxiangella salilacus sp. nov., a moderate halophilic bacterium isolated from a salt lake in Xinjiang Province, China.

In the original publication of the article, the deposit accession numbers of strain 15181T in the acknowledgment section were incorrectly provided as "KCTC 62172T and MCCC 1K03442T".

Elevated expression of miR-146a correlates with high levels of immune cell exhaustion markers and suppresses cellular immune function in chronic HIV-1-infected patients.

Functional exhaustion of immune cells is a defining characteristic of HIV-1 chronic infections, exhibiting dysregulation of cellular immune responses and expression of co-inhibitory receptors. Although the molecular mechanisms controlling immune-cell exhaustion retains largely unknown, immune checkpoint blockade strategy has shown inspiring potential to reinvigorate T cell functions in chronic infections. In this study, we investigated peripheral blood mononuclear cells (PBMCs) exhaustion markers from 109 chronic HIV-1-infected patients and found they correlated positively with microRNA-146a, which was inversely correlated with CD4+ T cell count. Intriguingly, ex vivo neutralization of miR-146a in PBMCs from chronic HIV-1 infection exhibited an elevated antiviral cytokines production as well as the expression of GZMB and perforin, while simultaneously, decreased the inhibitory receptors expression such as PD-1, CTLA-4, TIM-3 and LAG-3. These results highlight the importance of miR-146a to HIV-1 induced immune cell exhaustion, and uncover a novel layer of HIV/AIDS pathogenesis and provide potential targets for improved immune intervention.

Alkalilacustris brevis gen. nov., sp. nov., isolated from a soda lake.

A Gram-stain-negative, aerobic, non-pigmented and short-rod-shaped bacterium, designated 34079T, was isolated from a water sample of a soda lake in Jilin, a province of China. Strain 34079T grew at 10-50 °C (optimum, 35 °C), pH 7-10 (optimum, pH 8.0-8.5). NaCl was required for growth at the concentration range 1-10.0 % (w/v), with an optimum at 2.5-4 % (w/v). Chemotaxonomic analysis indicated that the sole respiratory quinone was Q-10. The predominant cellular fatty acids (>5 %) were summed feature 8 (C18 : 1 ω7c/C18 : 1 ω6c) and C16 : 0. The major polar lipids consisted of diphosphatidylglycerol, phosphatidylglycerol, phosphatidylcholine, three unidentified amino lipids, one unidentified amino phosphoglycolipid, one phosphoglycolipid, one unidentified glycolipid, three unidentified phospholipids and two unidentified lipids. The DNA G+C content was 65.6 mol%. Phylogenetic analysis based on 16S rRNA gene sequences revealed that strain 34079T formed a distinct lineage in the clade of the family 'Rhodobacteraceae' with the highest sequence similarity of 96.1 % to Pararhodobacter aggregans, followed by Rhodobaca bogoriensis DSM 18756T (95.7 %) and Roseibaca ekhonensis DSM 11469T (94.7 %). The distinct biochemical, chemotaxonomic and phylogenetic differences from the previously described taxa supported that strain 34079T represents a novel species of a new genus, for which the name Alkalilacustris brevis gen. nov., sp. nov. is proposed. The type strain is 34079T (=KCTC 62428T=MCCC 1K03493T).

Pseudomonas mangrovi sp. nov., isolated from mangrove soil.

A Gram-stain-negative, aerobic, non-motile, short-rod-shaped bacterium, designated as strain TC11T, was isolated from rhizosphere soil of mangrove forest (Kandeliaobovata) in Fugong village, Zhangzhou, Fujian, China. Strain TC11T grew at 15-45 °C (optimum, 35 °C), 0-8 % (w/v) NaCl (optimum, 1 %, w/v) and pH 5.5-9.5 (optimum, pH 7.5). Phylogenetic analyses revealed that strain TC11T belonged to a clade of the genus Pseudomonas and showed the highest sequence similarity of 98.4 % to Pseudomonas fluvialis ASS-1T, followed by Pseudomonas oleovorans subsp.oleovorans DSM 1045T (97.9 %), Pseudomonas indoloxydans JCM 14246T (97.7 %), Pseudomonas guguanensis JCM 18416T(97.6 %) and Pseudomonas alcaliphila JCM 10630T (97.5 %) on the basis of their 16S rRNA gene sequences. The DNA G+C content was 64.3 mol%. In silico DNA-DNA hybridization and average nucleotide identity values between strain TC11T and the reference strains were 19-22 % and 72-78 %, respectively. Studies based on the three housekeeping genes, rpoB, gyrB and rpoD, further confirmed that strain TC11T is a novel member of the genus Pseudomonas. The major fatty acids of strain TC11Twere C16 : 0, summed feature 8 (C18 : 1ω6c/C18 : 1ω7c) and summed feature 3 (C16 : 1ω7c/C16 : 1ω6c). The sole isoprenoid quinone was Q-9. The major polar lipids were phosphatidylethanolamine, phosphatidylglycerol and diphosphatidylglycerol. Based on the phenotypic, chemotaxonomic and phylogenetic properties, strain TC11T represents a novel species of the genus Pseudomonas, for which the name Pseudomonasmangrovi sp. nov., is proposed. The type strain is TC11T (=KCTC 62159=MCCC 1K03499).