A new species of the genus Psilota Meigen, 1822 (Diptera: Syrphidae) from China.

The genus Psilota Meigen, 1822 is recorded for the first time from China, and the species Psilota bashanensis Huo and Zhao sp. nov. is described and illustrated based on the adult male. The complete cytochrome c oxidase subunit I (COI) gene of this new species has been successfully obtained and compared to that of other congeneric species. An updated key to adult males of the genus Psilota from the Palaearctic Region is also provided.

The complete mitochondrial genome of Eristalinus viridis (Coquillett, 1898) (Diptera: Syrphidae) and its phylogenetic implications.

The complete mitochondrial genome of Eristalinus viridis (Coquillett, 1898) was obtained for the first time using Next Generation Sequencing (NGS). The mitogenome assembly of E. viridis is 15,640 bp in length and its annotation confirms the presence of 13 protein-coding genes (PCGs), 22 transfer RNA genes (tRNAs), two ribosomal RNA genes (rRNAs), and one putative control region. The results of the phylogenetic analyses using Maximum Likelihood and Bayesian inference recover a highly supported sister relationship between E. viridis and Mallota bellus.

The complete mitochondrial genome of Melanostoma mellinum (Linnaeus, 1758) (Diptera: Syrphidae) and phylogenetic analysis.

In this study, the complete mitochondrial genome (mitogenome) of Melanostoma mellinum (Linnaeus, 1758) was sequenced using the-next generation sequencing technology. The assembled mitogenome of M. mellinum has a total length of 16,055bp and contains 13 protein-coding genes (PCGs), 22 transfer RNA genes (tRNAs), and 2 ribosomal RNA genes (rRNAs). The results of phylogenetic reconstruction based on the combined mitochondrial gene dataset indicated that M. mellinum belongs to Melanostoma genus with a close relationship to Melanostoma orientale, but the monophyly of the tribe Bacchini is not well supported.

Characterization and phylogenetic analysis of the complete mitochondrial genome of Lathyrophthalmus quinquestriatus (Fabricius, 1794)(Diptera, Syrphidae).

In this study, we present the complete mitogenome of Lathyrophthalmu quinquestriatus (Fabricius, 1794), which has a total length of 16,198 base pairs and includes 13 protein-coding genes, 22 transfer RNA genes, 2 ribosomal RNA genes and one putative control region. Most PCGs started with ATN codons except COX1 (CAA), and ended with TAA, TAG (ND3) or single T(ND5). The results of phylogenetic tree reconstruction show that the monophyly of subfamily Eristalinae is not supported, and the closer relationship between genus Lathyrophthalmus and Eristalinus.

A new species of the flower fly genus Criorhina Meigen (Diptera: Syrphidae) from mainland China.

The genus Criorhina consists of honey-bee and bumblebee mimic flower flies with a strongly produced face. It is widespread in the Holarctic and Oriental Regions. Criorhina adults are usually found flying near white spring flowers in woodlands and shrubs. The Chinese Criorhina fauna is poorly known and includes seven species. In our flower fly collection of Henan Province, northern China, an eighth new species was discovered: Criorhina rostrata Li, Huo Li sp. nov. This new species is here described and illustrated. The new species possess a very long proboscis, unique amongst the Criorhina species from mainland China. In addition, during the course of this study, Criorhina brevipila Loew, 1871 was also found to be present in mainland China, based on a specimen from our collection. A key to the species of Criorhina from mainland China is given.

Phytochemicals Content, Antioxidant and Antibacterial Activities of Sophora viciifolia.

The objective of this study is to compare the efficacy of ethanol extracts from different parts of Sophora viciifolia. The content of polyphenols, flavonoids, alkaloids, and antioxidant capacity, antimicrobial activity were investigated, and individual polyphenols and alkaloids were analyzed and quantified by ultra-high performance liquid chromatography (UPLC). The microdilution method was used to determine the antimicrobial activity of extracts from S. viciifolia on six strains. The results for extracts from the different parts (flowers, leaves, and fruit) were compared in varying concentrations to determine whether one extract source is superior to another. Testing verified that extracts from the different parts of S. viciifolia did vary, as expected. For example, extract from the leaves had the best antimicrobial activity against pathogenic Candida albicans, but all extracts had good antimicrobial activity against the six tested strains. These results reveal that the active substances in S. viciifolia are abundant and have good antioxidant and antimicrobial activities, which can provide theoretical support for the subsequent development and utilization of S. viciifolia extracts.

Microdon dentigiganteum sp. nov. and other Microdontinae species (Diptera: Syrphidae) from Northeast China.

Hoverflies (Diptera: Syrphidae) of the subfamily Microdontinae were surveyed in Northeast China. A total of six species were identified, including one new to science, Microdon dentigiganteum sp. nov. from Liaoning. This new species has a pair of very large-size posterior calcars on the scutellum and very wide flat tarsi. New records of Metadon spuribifasciatus (Huo, Ren et Zheng, 2007), Microdon analis (Macquart, 1842) and Microdon auricomus Coquillett, 1898 from Jilin province, and Microdon ignotus Violovitsh, 1976 and Microdon oitanus Shiraki, 1930 from Liaoning province are provided. A key to the six studied species and diagnostic figures are presented.

Aspergillus fumigatus phospholipase D may enhance reactive oxygen species production by accumulation of histone deacetylase 6.

Aspergillus fumigatus, an airborne pathogen, causes many diseases, including aspergilloma, invasive aspergillosis, and allergic bronchopulmonary aspergillosis. Phospholipase D (PLD) is an important virulence factor for A. fumigatus infection, but the manner by which PLD contributes to the virulence of this pathogen is not clear. Our results show that expression of A. fumigatus PLD in human cells was able to increase the production of reactive oxygen species (ROS), which play an important role in several signaling pathways as well as in lung infection. Meanwhile, A. fumigatus PLD was found to interact with human endogenous histone deacetylase 6 (HDAC6), a known regulator of ROS production and inflammatory responses; PLD significantly increased the expression level of HDAC6 protein without altering its mRNA level. These results suggest that A. fumigatus PLD may enhance the production of ROS via the accumulation of HDAC6, which may be involved in host immunomodulation during A. fumigatus infection.

New method for quantification of gasotransmitter hydrogen sulfide in biological matrices by LC-MS/MS.

Hydrogen sulfide exists widely in mammalian tissues and plays a vital role in physiological and pathophysiological processes. However, striking differences with orders of magnitude were observed for the detected hydrogen sulfide concentrations in biological matrices among different measurements in literature, which lead to the uncertainty for examination the biological relevance of hydrogen sulfide. Here, we developed and validated a liquid chromatography- mass spectrometry (LC-MS/MS) method for the determination of hydrogen sulfide in various biological matrices by determination of a derivative of hydrogen sulfide and monobromobimane named sulfide dibimane (SDB). 36S-labeled SDB was synthesized and validated for using as an internal standard. This method has been successfully used to measure hydrogen sulfide levels in a broad range of biological matrices, such as blood, plasma, tissues, cells, and enzymes, across different species. Moreover, a novel mode that hydrogen sulfide could loosely and non-covalently bind to human serum protein (HSA) and hemoglobin (HB) was revealed by using the developed method.

p75 neurotrophin receptor and its novel interaction partner, NIX, are involved in neuronal apoptosis after intracerebral hemorrhage.

Recently, NIX, a pro-apoptotic BH3-only protein, was found to be a novel p75 neurotrophin receptor (p75NTR) binding protein by screening a human fetal brain two-hybrid library in our laboratory. We further study the interaction of these two proteins and the possible roles of p75NTR and NIX in intracerebral hemorrhage (ICH)-induced neuronal death. Using the split-ubiquitin yeast two-hybrid system, we found that the "Copper" domain in p75NTR and the TM region in NIX were sufficient for the interaction of these two proteins. Co-immunoprecipitation and in vitro binding assays demonstrated the direct interaction between p75NTR and NIX. NIX protein was stabilized by p75NTR at post-translational levels. Moreover, p75NTR was able to work together with NIX to promote apoptosis and affected the NIX-induced JNK-p53-Bax pathway in neuronal PC12 cells. Previous work has indicated that p75NTR and NIX are induced in neurons in human ICH and the rat ICH model, respectively. We confirm that both p75NTR and NIX levels were up-regulated in glutamate-treated primary cortical neurons (a cellular in vitro model for ICH) and in the rat ICH model. Glutamate exposure increased the association between p75NTR and NIX and elevated the activation of the JNK-p53-Bax pathway and neuronal apoptosis; all of these observations were similar in the rat ICH model. Importantly, p75NTR and NIX appeared to be involved in cortical neuronal apoptosis, because knockdown of p75NTR or NIX not only inhibited the JNK pathway but also impaired neuronal apoptosis. Thus, p75NTR and NIX may play critical roles in ICH-induced neuronal apoptosis in vitro and in vivo.

The Natural Product Resveratrol Inhibits Yeast Cell Separation by Extensively Modulating the Transcriptional Landscape and Reprogramming the Intracellular Metabolome.

An increasing number of studies have shown that the promising compound resveratrol treats multiple diseases, such as cancer and aging; however, the resveratrol mode-of-action (MoA) remains largely unknown. Here, by virtue of multiple omics approaches, we adopted fission yeast as a model system with the goal of dissecting the common MoA of the anti-proliferative activity of resveratrol. We found that the anti-proliferative activity of resveratrol is mainly due to its unique role of inhibiting the separation of sister cells, similar phenotype with the C2H2 zinc finger transcription factor Ace2 knock-out strain. Microarray analysis shown that resveratrol has extensive impact on the fission yeast transcription levels. Among the changed gene's list, 40% of up-regulated genes are Core Environmental Stress Responses genes, and 57% of the down-regulated genes are periodically expressed. Moreover, resveratrol leverages the metabolome, which unbalances the intracellular pool sizes of several classes of amino acids, nucleosides, sugars and lipids, thus reflecting the remodulated metabolic networks. The complexity of the resveratrol MoA displayed in previous reports and our work demonstrates that multiple omics approaches must be applied together to obtain a complete picture of resveratrol's anti-proliferative function.

SCYL1-BP1 affects cell cycle arrest in human hepatocellular carcinoma cells via Cyclin F and RRM2.

The cell cycle is regulated via important biological mechanisms. Controlled expression of cell cycle regulatory proteins is crucial to maintain cell cycle progression. However, unbalanced protein expression leads to many diseases, such as cancer. Previous research suggests that SCYL1-BP1 function might be related to cell cycle progression and SCYL1-BP1 dysfunction to diseases through undefined mechanisms. In this research, an unbiased yeast two-hybrid screen was used to find protein(s) with potential biological relevance to SCYL1-BP1 function, and a novel interaction was recognized between SCYL1-BP1 and Cyclin F. This interaction was chosen as a paradigm to study SCYL1-BP1 function in cell cycle progression and its possible role in tumorigenesis. We found that SCYL1-BP1 binds to Cyclin F both in vivo and in vitro. SCYL1-BP1 overexpression promoted expression of the CCNF gene and simultaneously delayed Cyclin F protein degradation. SCYL1-BP1 knockdown reduced the expression of endogenous Cyclin F. It was also demonstrated in functional assays that SCYL1-BP1 overexpression induces G2/M arrest in cultured liver cells. Furthermore, SCYL1-BP1 sustained RRM2 protein expression by reducing its ubiquitination. Thus, we propose that SCYL1- BP1 affects the cell cycle through increasing steady state levels of Cyclin F and RRM2 proteins, thus constituting a dual regulatory circuit. This study provides a possible mechanism for SCYL1-BP1-mediated cell cycle regulation and related diseases.

Up-regulation of c-Fos associated with neuronal apoptosis following intracerebral hemorrhage.

The proto-oncogene c-Fos is an important member of the activating protein 1 (AP-1) transcription complex involved in major cellular functions such as transformation, proliferation, differentiation, and apoptosis. The expression of c-Fos is very tightly regulated and responses rapidly and transiently to a plethora of apoptotic stimuli. However, it is still unclear how c-Fos functions on neuronal activities following intracerebral hemorrhage (ICH). In the present studies, we uncovered that the up-regulation of c-Fos is related to neuronal apoptosis following ICH probably via FasL/Fas apoptotic pathway. From the results of Western blot and immunohistochemistry, we obtained that c-Fos is significantly up-regulated surrounding the hematoma following ICH and co-locates with active caspase-3 in the neurons. Besides, electrophoretic mobility shift assay exhibits high AP-1 DNA-binding activities in ICH groups due to the increase of c-Fos expression. In addition, there are concomitant up-regulation of Fas ligand (FasL), which is the target protein of AP-1, Fas, active caspase-8, and active caspase-3 in vivo and in vitro studies. What is more, our in vitro study showed that using c-Fos-specific RNA interference in primary cortical neurons, the expression of FasL and active caspase-3 are suppressed. Thus, our results indicated that c-Fos might exert its pro-apoptotic function on neuronal apoptosis following ICH.

Transcriptional profiling and dynamical regulation analysis identify potential kernel target genes of SCYL1-BP1 in HEK293T cells.

SCYL1-BP1 is thought to function in the p53 pathway through Mdm2 and hPirh2, and mutations in SCYL1-BP1 are associated with premature aging syndromes such as Geroderma Osteodysplasticum; however, these mechanisms are unclear. Here, we report significant alterations in miRNA expression levels when SCYL1-BP1 expression was inhibited by RNA interference in HEK293T cells. We functionally characterized the effects of potential kernel miRNA-target genes by miRNA-target network and protein-protein interaction network analysis. Importantly, we showed the diminished SCYL1-BP1 dramatically reduced the expression levels of EEA1, BMPR2 and BRCA2 in HEK293T cells. Thus, we infer that SCYL1-BP1 plays a critical function in HEK293T cell development and directly regulates miRNA-target genes, including, but not limited to, EEA1, BMPR2, and BRCA2, suggesting a new strategy for investigating the molecular mechanism of SCYL1-BP1.

Spazigasteroides a new genus from China with a black face and scutellum in the Syrphini (Diptera: Syrphidae).

In the present paper, the genus Spazigasteroides gen. nov. (Diptera, Syrphidae), with Spazigasteroides caeruleus sp. nov. as type species, is described from China. The new genus bears the following characters: Head strongly concave posteriorly and closely appressed to thorax so that the bare postpronota are entirely hidden. Face black in ground colour. Antennae short, with basoflagellomeres slightly longer than wide. Scutellum black. Postmetacoxal bridge

XPC promotes MDM2-mediated degradation of the p53 tumor suppressor.

Although ubiquitin receptor Rad23 has been implicated in bringing ubiquitylated p53 to the proteasome, how Rad23 recognizes p53 remains unclear. We demonstrate that XPC, a Rad23-binding protein, regulates p53 turnover. p53 protein in XPC-deficient cells remains ubiquitylated, but its association with the proteasome is drastically reduced, indicating that XPC regulates a postubiquitylation event. Furthermore, we found that XPC participates in the MDM2-mediated p53 degradation pathway via direct interaction with MDM2. XPC W690S pathogenic mutant is specifically defective for MDM2 binding and p53 degradation. p53 is known to become stabilized following UV irradiation but can be rendered unstable by XPC overexpression, underscoring a critical role of XPC in p53 regulation. Elucidation of the proteolytic role of XPC in cancer cells will help to unravel the detailed mechanisms underlying the coordination of DNA repair and proteolysis.

hABCF3, a TPD52L2 interacting partner, enhances the proliferation of human liver cancer cell lines in vitro.

In the present study, we characterized an evolutionarily conserved non-transmembrane ATP-binding cassette protein: hABCF3. Subcellular immunofluorescence staining demonstrated that hABCF3 localizes preferentially in cytoplasm, unlike its paralog protein hABCF1, which localizes in both cytoplasm and nucleus. Quantitative realtime PCR analysis revealed that hABCF3 is expressed in all tissues examined, with high expression level in heart, liver, and pancreas. Interestingly, ectopic hABCF3 promoted proliferation of human liver cancer cell lines. Moreover, knock down of hABCF3 protein expression by siRNA inhibited cell proliferation. In addition, we identified TPD52L2 (Tumor Protein D52-like 2) as a hABCF3 interacting protein via yeast two-hybrid. This interaction was further confirmed by in vivo co-immunoprecipitation and co-localization assays. Furthermore, we identified the interactional region of hABCF3 to be the first 200 amino acids uncharacterized region. Notably, the truncated version of hABCF3, which lacks the TPD52L2 binding region, remarkably impaired hABCF3-mediated cell proliferation. Taken together, these findings suggest that hABCF3 positively regulates cell proliferation, at least partially through the interaction with a tumor protein D52 protein family member: TPD52L2.

PPP3CC feedback regulates IP3-Ca2+ pathway through preventing ITPKC degradation.

ITPKC, a susceptibility gene of Kawasaki disease, encodes a kinase that negatively regulates intracellular Ca2+ level and inhibits calcineurin-dependent activation of NFAT by phosphorylating IP3. In this study, we identified a novel ITPKC-interacting protein, namely PPP3CC, using yeast two-hybrid. This interaction was further confirmed by GST pull-down and co-immunoprecipitation assays, and fluorescent microscopy showed co-localization of both proteins in the cell cytoplasm. Our functional studies demonstrated that PPP3CC positively influences the protein level of ITPKC, likely by inhibiting phosphorylation of ITPKC and consequently preventing ITPKC from ubiquitin-mediated protein degradation which requires phosphorylation. Importantly, the protein level of PPP3CC negatively correlates with the cellular level of IP3, suggesting a regulatory role of PPP3CC in the IP3-Ca2+ signaling pathway.

PTPN4 negatively regulates CrkI in human cell lines.

PTPN4 is a widely expressed non-receptor protein tyrosine phosphatase. Although its overexpression inhibits cell growth, the proteins with which it interacts to regulate cell growth are unknown. In this study, we identified CrkI as a PTPN4-interacting protein using a yeast two-hybrid, and confirmed this interaction using in vitro GST pull-down and co-immunoprecipitation and co-localization assays. We further determined the interactional regions as the SH3 domain of CrkI and the proline-rich region between amino acids 462 and 468 of PTPN4. Notably, overexpression of PTPN4 inhibits CrkI-mediated proliferation and wound healing of HEK293T cells, while knockdown of PTPN4 by siRNA in Hep3B cells enhances CrkI-mediated cell growth and motility. Moreover, our data show that ectopic expression of PTPN4 reduces the phosphorylation level of CrkI in HEK293T cells. These findings suggest that PTPN4 negatively regulates cell proliferation and motility through dephosphorylation of CrkI.