蛹虫草组学研究进展

作为虫草属的模式种,蛹虫草是目前虫草类真菌中研究和应用最为广泛的物种之一。随着基因组序列的公布,蛹虫草组学水平的研究近年来取得了明显的进展。本文从基因组、线粒体基因组、甲基化组、转录组、蛋白质组、代谢网络等角度对蛹虫草组学水平的研究现状进行综述,期望对进一步推动蛹虫草的深入研究提供帮助。     

Expression Changes of NMDA and AMPA Receptor Subunits in the Hippocampus in rats with Diabetes Induced by Streptozotocin Coupled with Memory Impairment

Neurochemical Research - Cognitive impairment in diabetes (CID) is a severe chronic complication of diabetes mellitus (DM). It has been hypothesized that diabetes can lead to cognitive dysfunction...     

Expression of ssDNA in mammalian cells

Antisense therapy involves the use of antisense oligonucleotides for altering targeted gene function. However, the low efficiency of cell delivery of antisense oligonucleotides has limited the efficacy of antisense therapeutic approaches. RNA-based antisense or ribozyme oligonucleotides can be either synthesized endogenously (e.g., by a viral vector) or delivered exogenously. However, there is presently no vector delivery system available for DNA-based oligonucleotides. Recently, a novel ssDNA expression vector that can generate intracellularly any ssDNA molecule, such as antisense oligonucleotide or DNA enzyme, has been developed in our laboratory. Here we describe an improved expression vector based on the first-generation two-vector system. To test this new expression vector, we chose to express a single-stranded "10-23" DNA enzyme targeting c-raf mRNA in the human lung carcinoma A549 cell line. After introduction into cells by transient transfection, c-raf-cleaving DNA enzymes produced by this expression vector can significantly suppress the expression of c-raf mRNA. Furthermore, the expressed c-raf DNA enzymes induced cell apoptosis, as indicated by genomic DNA fragmentation assay. Our study further demonstrates the feasibility of using this novel ssDNA expression technology to produce intracellularly any sequence of interest, including antisense oligonucleotides and DNA enzyme molecules.     

Cloning and characterization of a new isoform of mouse interleukin-18

Interleukin-18 （IL-18） is a novel proinflammatory cytokine with potent interferon （IFN）-γ inducing activity that plays an important biological role in the enhancement of the activity of natural killer cells and cytotoxic T lymphocytes, In this study, we have identified a novel short form of IL- 18 in mouse, named IL-18s. IL-18s might be an alternative splicing variant of IL-18 and its cDNA contains a 57 bp in-frame deletion, Like IL-18, IL-18s is also widely expressed in mouse tissues, It was suggested that IL-18s might have a caspase- 1-dependent mechanism for maturation and secretion similar to that of IL- 18： when transfected in COS-7 cells, pro-IL-18s （22 kDa） could be detected, and the mature IL-18s （16 kDa） could also be detected when combined with caspase-1. We observed that recombinant mouse IL-18s did not show any IL-18-like function, and IL-18s could enhance the ability of IL-18 to increase IFN-γ production by approximately 40% in mouse splenocytes. This effect was observed primarily at relative low concentrations of IL-18, suggesting that IL- 18s might regulate the activity of IL- 18 in the physiological conditions,     

Complete Genome Sequence of Aeromonas hydrophila Phage CC2

Aeromonas hydrophila is one of the major pathogenic bacteria for fish and people. To develop an effective antimicrobial agent, we isolated a bacteriophage from sewage, named CC2, and sequenced its genome. Comparative genome analysis of phage CC2 with its relatives revealed that phage CC2 has higher sequence homology to A. salmonicida phage 65 than to A. hydrophila phage Aeh1. Here, we announce the complete genome sequence of CC2 and report major findings from the genomic analysis.     

The evolutionary convergence of mid-Mesozoic lacewings and Cenozoic butterflies

Mid-Mesozoic kalligrammatid lacewings (Neuroptera) entered the fossil record 165 million years ago (Ma) and disappeared 45 Ma later. Extant papilionoid butterflies (Lepidoptera) probably originated 80–70 Ma, long after kalligrammatids became extinct. Although poor preservation of kalligrammatid fossils previously prevented their detailed morphological and ecological characterization, we examine new, well-preserved, kalligrammatid fossils from Middle Jurassic and Early Cretaceous sites in northeastern China to unravel a surprising array of similar morphological and ecological features in these two, unrelated clades. We used polarized light and epifluorescence photography, SEM imaging, energy dispersive spectrometry and time-of-flight secondary ion mass spectrometry to examine kalligrammatid fossils and their environment. We mapped the evolution of specific traits onto a kalligrammatid phylogeny and discovered that these extinct lacewings convergently evolved wing eyespots that possibly contained melanin, and wing scales, elongate tubular proboscides, similar feeding styles, and seed–plant associations, similar to butterflies. Long-proboscid kalligrammatid lacewings lived in ecosystems with gymnosperm–insect relationships and likely accessed bennettitalean pollination drops and pollen. This system later was replaced by mid-Cretaceous angiosperms and their insect pollinators.     

Novel mutations in TARDBP (TDP-43) in patients with familial amyotrophic lateral sclerosis

The TAR DNA-binding protein 43 (TDP-43) has been identified as the major disease protein in amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration with ubiquitin inclusions (FTLD-U), defining a novel class of neurodegenerative conditions: the TDP-43 proteinopathies. The first pathogenic mutations in the gene encoding TDP-43 (TARDBP) were recently reported in familial and sporadic ALS patients, supporting a direct role for TDP-43 in neurodegeneration. In this study, we report the identification and functional analyses of two novel and one known mutation in TARDBP that we identified as a result of extensive mutation analyses in a cohort of 296 patients with variable neurodegenerative diseases associated with TDP-43 histopathology. Three different heterozygous missense mutations in exon 6 of TARDBP (p.M337V, p.N345K, and p.I383V) were identified in the analysis of 92 familial ALS patients (3.3%), while no mutations were detected in 24 patients with sporadic ALS or 180 patients with other TDP-43-positive neurodegenerative diseases. The presence of p.M337V, p.N345K, and p.I383V was excluded in 825 controls and 652 additional sporadic ALS patients. All three mutations affect highly conserved amino acid residues in the C-terminal part of TDP-43 known to be involved in protein-protein interactions. Biochemical analysis of TDP-43 in ALS patient cell lines revealed a substantial increase in caspase cleaved fragments, including the approximately 25 kDa fragment, compared to control cell lines. Our findings support TARDBP mutations as a cause of ALS. Based on the specific C-terminal location of the mutations and the accumulation of a smaller C-terminal fragment, we speculate that TARDBP mutations may cause a toxic gain of function through novel protein interactions or intracellular accumulation of TDP-43 fragments leading to apoptosis.