澜沧江流域水生昆虫群落分类多样性和功能多样性海拔格局的空间尺度依赖性

群落分类多样性和功能多样性的海拔格局研究, 是了解生物多样性空间分布现状、揭示多样性维持和变化机制的重要途径。当前对水生昆虫分类多样性和功能多样性沿海拔梯度分布格局, 及其尺度依赖性依旧缺乏深入研究。本文基于2013-2018年在云南澜沧江流域500-3,900 m海拔梯度共149个溪流点位的水生昆虫群落调查数据, 利用线性或二次回归模型探索并比较了局部尺度(点位尺度)和不同区域尺度(100 m、150 m、200 m、250 m海拔段)的分类多样性指数(物种丰富度指数、Simpson多样性指数和物种均匀度指数)和功能多样性指数(树状图功能多样性指数(dbFD)、Rao二次熵指数(RaoQ)和功能均匀度指数(FEve))的海拔格局。结果表明, 在局部尺度, 物种丰富度指数和dbFD指数沿海拔梯度均无显著分布特征, Simpson多样性指数、RaoQ指数、物种均匀度指数和FEve指数沿海拔梯度呈现U型或者单调递减趋势。在区域尺度, 随着区域海拔带宽度的增加, 物种丰富度指数沿海拔呈不显著的单调递减格局, 但dbFD指数沿海拔分布由U型转变为单调递减趋势; Simpson多样性指数和RaoQ指数沿海拔梯度由显著U型趋势转变为无显著分布特征; 物种均匀度指数沿海拔梯度无显著分布特征, 但FEve指数呈显著增加的海拔格局。综上, 群落分类多样性指数和功能多样性指数沿海拔梯度分布存在局部和区域尺度的空间差异, 但区域尺度下二者海拔格局随海拔带宽度的增加存在一定程度的一致性。     

生态系统的多稳态与突变

许多生态系统可能在短时间内发生难以预料的状态突变, 其中一些生态系统突变的机理可以用多稳态理论进行解释。近年来生态系统的多稳态和突变现象及其机理吸引了研究者和管理者的广泛关注。本文重点对生态系统多稳态的理论基础、识别方法及稳态转换发生的早期预警信号进行综述, 并基于典型生态系统过程对现实世界中可能观测到的稳态转换进行实例分析, 最后对多稳态概念框架和理论应用中的潜在争议进行讨论, 以期为非线性生态系统动态的理论研究、管理实践和生物多样性保护等提供参考。     

Meeting report on the 2019 international symposium of molecular design breeding in animals (Yangling,China) with the consensus on genome-editing agricultural animals and their regulation

Transgenic Research -     

The phylogenetic range of bacterial and viral pathogens of vertebrates

Many major human pathogens are multihost pathogens, able to infect other vertebrate species. Describing the general patterns of host–pathogen associations across pathogen taxa is therefore important to understand risk factors for human disease emergence. However, there is a lack of comprehensive curated databases for this purpose, with most previous efforts focusing on viruses. Here, we report the largest manually compiled host–pathogen association database, covering 2,595 bacteria and viruses infecting 2,656 vertebrate hosts. We also build a tree for host species using nine mitochondrial genes, giving a quantitative measure of the phylogenetic similarity of hosts. We find that the majority of bacteria and viruses are specialists infecting only a single host species, with bacteria having a significantly higher proportion of specialists compared to viruses. Conversely, multihost viruses have a more restricted host range than multihost bacteria. We perform multiple analyses of factors associated with pathogen richness per host species and the pathogen traits associated with greater host range and zoonotic potential. We show that factors previously identified as important for zoonotic potential in viruses—such as phylogenetic range, research effort, and being vector‐borne—are also predictive in bacteria. We find that the fraction of pathogens shared between two hosts decreases with the phylogenetic distance between them. Our results suggest that host phylogenetic similarity is the primary factor for host‐switching in pathogens.     

Meiofauna promotes litter decomposition in stream ecosystems depending on leaf species

Litter decomposition, a fundamental process of nutrient cycling and energy flow in freshwater ecosystems, is driven by a diverse array of decomposers. As an important component of the heterotrophic food web, meiofauna can provide a trophic link between leaf‐associated microbes (i.e., bacteria and fungi)/plant detritus and macroinvertebrates, though their contribution to litter decomposition is not well understood. To investigate the role of different decomposer communities in litter decomposition, especially meiofauna, we compared the litter decomposition of three leaf species with different lignin to nitrogen ratios in litter bags with different mesh sizes (0.05, 0.25, and 2 mm) in a forested stream, in China for 78 days. The meiofauna significantly enhanced the decomposition of leaves of high‐and medium‐ quality, while decreasing (negative effect) or increasing (positive effect) the fungal biomass and diversity. Macrofauna and meiofauna together contributed to the decomposition of low‐quality leaf species. The presence of meiofauna and macrofauna triggered different aspects of the microbial community, with their effects on litter decomposition varying as a function of leaf quality. This study reveals that the meiofauna increased the trophic complexity and modulated their interactions with microbes, highlighting the important yet underestimated role of meiofauna in detritus‐based ecosystems.     

Brain tumors: Cancer stem-like cells interact with tumor microenvironment

Cancer stem-like cells (CSCs) with potential of self-renewal drive tumorigenesis. Brain tumor microenvironment (TME) has been identified as a critical regulator of malignancy progression. Many researchers are searching new ways to characterize tumors with the goal of predicting how they respond to treatment. Here, we describe the striking parallels between normal stem cells and CSCs. We review the microenvironmental aspects of brain tumors, in particular composition and vital roles of immune cells infiltrating glioma and medulloblastoma. By highlighting that CSCs cooperate with TME via various cellular communication approaches, we discuss the recent advances in therapeutic strategies targeting the components of TME. Identification of the complex and interconnected factors can facilitate the development of promising treatments for these deadly malignancies.     

6-gingerol protects nucleus pulposus-derived mesenchymal stem cells from oxidative injury by activating autophagy

BACKGROUNDTo date, there has been no effective treatment for intervertebral disc degeneration (IDD). Nucleus pulposus-derived mesenchymal stem cells (NPMSCs) showed encouraging results in IDD treatment, but the overexpression of reactive oxygen species (ROS) impaired the endogenous repair abilities of NPMSCs. 6-gingerol (6-GIN) is an antioxidant and anti-inflammatory reagent that might protect NPMSCs from injury.AIMTo investigate the effect of 6-GIN on NPMSCs under oxidative conditions and the potential mechanism.METHODSThe cholecystokinin-8 assay was used to evaluate the cytotoxicity of hydrogen peroxide and the protective effects of 6-GIN. ROS levels were measured by 2´7´-dichlorofluorescin diacetate analysis. Matrix metalloproteinase (MMP) was detected by the tetraethylbenzimidazolylcarbocyanine iodide assay. TUNEL assay and Annexin V/PI double-staining were used to determine the apoptosis rate. Additionally, autophagy-related proteins (Beclin-1, LC-3, and p62), apoptosis-associated proteins (Bcl-2, Bax, and caspase-3), and PI3K/Akt signaling pathway-related proteins (PI3K and Akt) were evaluated by Western blot analysis. Autophagosomes were detected by transmission electron microscopy in NPMSCs. LC-3 was also detected by immunofluorescence. The mRNA expression of collagen II and aggrecan was evaluated by real-time polymerase chain reaction (RT-PCR), and the changes in collagen II and MMP-13 expression were verified through an immunofluorescence assay.RESULTS6-GIN exhibited protective effects against hydrogen peroxide-induced injury in NPMSCs, decreased hydrogen peroxide-induced intracellular ROS levels, and inhibited cell apoptosis. 6-GIN could increase Bcl-2 expression and decrease Bax and caspase-3 expression. The MMP, Annexin V-FITC/PI flow cytometry and TUNEL assay results further confirmed that 6-GIN treatment significantly inhibited NPMSC apoptosis induced by hydrogen peroxide. 6-GIN treatment promoted extracellular matrix (ECM) expression by reducing the oxidative stress injury-induced increase in MMP-13 expression. 6-GIN activated autophagy by increasing the expression of autophagy-related markers (Beclin-1 and LC-3) and decreasing the expression of p62. Autophagosomes were visualized by transmission electron microscopy. Pretreatment with 3-MA and BAF further confirmed that 6-GIN-mediated stimulation of autophagy did not reduce autophagosome turnover but increased autophagic flux. The PI3K/Akt pathway was also found to be activated by 6-GIN. 6-GIN inhibited NPMSC apoptosis and ECM degeneration, in which autophagy and the PI3K/Akt pathway were involved.CONCLUSION6-GIN efficiently decreases ROS levels, attenuates hydrogen peroxide-induced NPMSCs apoptosis, and protects the ECM from degeneration. 6-GIN is a promising candidate for treating IDD.     

Examining differences in phylogenetic composition enhances understanding of the phylogenetic structure of the shrub community in the northeastern Qinghai‐Tibetan Plateau

Periodic climatic oscillations and species dispersal during the postglacial period are two important causes of plant assemblage and distribution on the Qinghai‐Tibet Plateau (QTP). To improve our understanding of the bio‐geological histories of shrub communities on the QTP, we tested two hypotheses. First, the intensity of climatic oscillations played a filtering role during community structuring. Second, species dispersal during the postglacial period contributed to the recovery of species and phylogenetic diversity and the emergence of phylogenetic overdispersion. To test these hypotheses, we investigated and compared the shrub communities in the alpine and desert habitats of the northeastern QTP. Notably, we observed higher levels of species and phylogenetic diversity in the alpine habitat than in the desert habitat, leading to phylogenetic overdispersion in the alpine shrub communities versus phylogenetic clustering in the desert shrub communities. This phylogenetic overdispersion increased with greater climate anomalies. These results suggest that (a) although climate anomalies strongly affect shrub communities, these phenomena do not act as a filter for shrub community structuring, and (b) species dispersal increases phylogenetic diversity and overdispersion in a community. Moreover, our investigation of the phylogenetic community composition revealed a larger number of plant clades in the alpine shrub communities than in the desert shrub communities, which provided insights into plant clade‐level differences in the phylogenetic structures of alpine and desert shrub communities in the northeastern QTP.     

Rapamycin inhibits AR signaling pathway in prostate cancer by interacting with the FK1 domain of FKBP51

Reactivation of the androgen receptor signaling pathway in the emasculated environment is the main reason for the occurrence of castration-resistant prostate cancer (CRPC). The immunophilin FKBP51, as a co-chaperone protein, together with Hsp90 help the correct folding of AR. Rapamycin is a known small-molecule inhibitor of FKBP51, but its effect on the FKBP51/AR signaling pathway is not clear. In this study, the interaction mechanism between FKBP51 and rapamycin was investigated using steady-state fluorescence quenching, X-ray crystallization, MTT assay, and qRT-PCR. Steady-state fluorescence quenching assay showed that rapamycin could interact with FKBP51. The crystal of the rapamycin-FKBP51 complex indicated that rapamycin occupies the hydrophobic binding pocket of FK1 domain which is vital for AR activity. The residues involving rapamycin binding are mainly hydrophobic and may overlap with the AR interaction site. Further assays showed that rapamycin could inhibit the androgen-dependent growth of human prostate cancer cells by down-regulating the expression levels of AR activated downstream genes. Taken together, our study demonstrates that rapamycin suppresses AR signaling pathway by interfering with the interaction between AR and FKBP51. The results of this study not only can provide useful information about the interaction mechanism between rapamycin and FKBP51, but also can provide new clues for the treatment of prostate cancer and castration-resistant prostate cancer.     

Dexamethasone does not ameliorate gliosis in a mouse model of neurodegenerative disease

Prolonged neuroinflammation is a driving force for neurodegenerative disease, and agents against inflammatory responses are regarded as potential treatment strategies. Here we aimed to evaluate the prevention effects on gliosis by dexamethasone (DEX), an anti-inflammation drug. We used DEX to treat the nicastrin conditional knockout (cKO) mouse, a neurodegenerative mouse model. DEX (10 mg/kg) was given to 2.5-month-old nicastrin cKO mice, which have not started to display neurodegeneration and gliosis, for 2 months. Immunohistochemistry (IHC) and Western blotting techniques were used to detect changes in neuroinflammatory responses. We found that activation of glial fibrillary acidic protein (GFAP) positive or ionized calcium binding adapter molecule1 (Iba1) positive cells was not inhibited in nicastrin cKO mice treated with DEX as compared to those treated with saline. These data suggest that DEX does not prevent or ameliorate gliosis in a neurodegenerative mouse model when given prior to neuronal or synaptic loss.