Identification of Cu-binding proteins in embryos of germinating rice in response to Cu toxicity

Seed germination, an early and important process for the growth and development of plants, is hypersensitive to environmental changes. Copper (Cu) is a necessary micronutrient for plants; however, an excessive dose of Cu had an extremely negative effect at the cellular level as a result of inevitable binding to proteins. In contrast, some structural motifs of proteins can bind free Cu ions and relieve Cu toxicity. This study aimed to understand the expression characteristics of Cu-binding proteins induced by excess Cu during rice seed germination. We investigated Cu-binding proteins in germinating rice embryos treated with 200 µM Cu using a Sephadex G-50 column or immobilized Cu affinity chromatography combined with two-dimensional gel electrophoresis. Proteomics analysis indicated that 12 protein spots exhibited a?>?2.0-fold increase in intensity in response to Cu toxicity as compared with controls. Among nine proteins in ten spots identified as Cu-binding proteins, three proteins (from four spots) were involved in antioxidative defense: copper, zinc superoxide dismutase, glutathione S-transferase and protein disulfide isomerase. These results show that reactive oxygen species may be involved in the expression regulation of Cu-binding proteins in germinating rice in response to Cu stress.     

不同经营模式对蒙古栎次生林叶功能性状和土壤理化性质的影响

植物功能性状是连接植物与环境的桥梁,能反映植物对外部环境的适应机制。以黑龙江省哈尔滨市丹青河实验林场3种经营模式下的蒙古栎天然次生林为研究对象,对其叶功能性状进行研究,探讨叶功能性状与土壤理化性质间的关系,对于理解植物对环境的适应机制及植物群落的构建具有重要意义。研究结果表明:(1)除土壤全钾、速效钾、有机碳含量外,不同经营模式下的土壤理化性质相差不大;(2)不同经营模式下的叶功能性状差异较大,目标树经营模式的单叶面积极显著大于综合抚育模式和无干扰模式(P0.01),目标树经营模式的叶氮、叶有机碳含量极显著小于综合抚育模式和无干扰模式(P0.01);单叶面积与叶氮含量、叶有机碳含量间均存在极显著负向相关关系(P0.01),叶氮含量与叶有机碳含量间存在极显著正向相关关系(P0.01);(3)土壤有机碳对单叶面积、叶氮含量、叶磷含量、叶有机碳含量均有显著影响。可见,不同经营模式下的蒙古栎天然次生林自我恢复能力较强,在采取不同程度的抚育后均未造成林地土壤养分的损失,土壤有机碳是影响不同经营模式下蒙古栎天然次生林叶功能性状变异的主要因素,蒙古栎天然次生林群落通过功能性状的耦合协调或组合来适应环境,植物功能性状对土壤理化性质的响应是一个长期的过程,仍需加强长期监测和更多研究。     

SIRT2 Plays Significant Roles in Lipopolysaccharides-Induced Neuroinflammation and Brain Injury in Mice

Several recent studies have suggested seemingly contrasting roles of SIRT2 in inflammation: Our previous cell culture study has indicated that SIRT2 siRNA-produced decrease in SIRT2 levels can lead to significant inhibition of lipopolysaccharides (LPS)-induced activation of BV2 microglia, suggesting that SIRT2 is required for LPS-induced microglial activation. In contrast, some studies have suggested that SIRT2 deficiency can lead to increased inflammation. In our current study, we used a mouse model of neuroinflammation to determine the roles of SIRT2 in LPS-induced inflammation. We found that administration of SIRT2 inhibitor AGK2 can significantly decrease LPS-induced increases in CD11b signals and the mRNA of TNF-α and IL-6. We further found that AGK2 can block LPS-induced nuclear translocation of NFκB. In addition, our study has shown that AGK2 can decrease not only LPS-induced increase in TUNEL signals—a marker of apoptosis-like damage, but also LPS-induced increases in the levels of active Caspase-3 and Bax. Collectively, our current in vivo study, together with our previous cell culture study, has suggested that SIRT2 is required for LPS-induced neuroinflammation and brain injury.

     

Unexpected complexity of multidrug resistance in the mcr-1-harbouring Escherichia coli

正Dear Editor,The discovery that the mobile colistin resistance gene(mcr-1)is encoded by plasmids and is prevalent in food animals and human beings worldwide(Hasman et al.,2015;Liu et al.,2015)has challenged greatly our traditional idea that polymyxin(consisting of two isoforms:polymyxin B and polymyxin E(colistin))acts as an ultimate line of refuge in the clinical treatment against the severe infections by the multidrug-resistant Gram-negative pathogens(Nation et al.,2015;Paterson and Harris,2015).To make matters     

Isolation and Characterization of a Novel Noncoding RNA from Nickel-Induced Lung Cancer

Noncoding RNAs have drawn significant attention in carcinogenesis. In this study, we identified a novel gene named nickel-related gene1 (NRG1) associated with nickel-induced cancer. By using rapid amplification of cDNA end PCR, we obtained the full length of the cDNA. The sequence was analyzed by using related bioinformatics software and comparative genomics methods. The results showed that NRG1 was located on chromosome 2q12, within intron2 of ADAMTS6, a disintegrin and metalloproteinase with thrombospondin motifs. And, NRG1 had a high level of homology (76?%) to rat LINE1 sequence RL1.3 (long interspersed middle repetitive DNA). What's more, there was no continuous open reading frame present in NRG1 sequence. Taken together, these data demonstrate that NRG1 is a novel noncoding RNA, and we predicted it may be a transposon-like gene. The identification of NRG1 emphasized the potential role of noncoding RNA in nickel carcinogenesis.     

Diversified variants of the mcr-1-carrying plasmid reservoir in the swine lung microbiota

正Dear Editor,Emergence of bacteria with multiple drug resistance is a major problem in global public health.Polymyxin comprising polymyxin E(colistin)and polymyxin B is generally recognized as the last-resort antibiotics with broad-spectrum     

Synthesis and acrosin inhibitory activity of methyl 5-substituted-1H-benzo[d]imidazol-2-yl carbamate derivatives

A series of novel methyl 5-substituted 1H-benzo[d]imidazol-2-ylcarbamates were designed, synthesized, and their acrosin inhibitory activities evaluated in vitro. The results of acrosin inhibitory activity showed that all title compounds were more potent than the control TLCK. Compound 4w displayed the most potent acrosin inhibitory activity among all the compounds, with an IC(50) of 6.3×10(-5)M. The studies provide a new structural class for the development of novel acrosin inhibitory agents.     

The negative c-Myc target onzin affects proliferation and apoptosis via its obligate interaction with phospholipid scramblase 1

Onzin, the product of a negatively c-Myc-regulated target gene, is highly expressed in myeloid cells. As a result of its interaction with and activation of Akt1 and Mdm2, onzin down-regulates p53. The apoptotic sensitivity of several cell lines is thus directly related to onzin levels. We have conducted a search for additional onzin-interacting proteins and identified phospholipid scramblase 1 (PLSCR1), an endofacial membrane protein, which is proposed to mediate the bidirectional movement of plasma membrane phospholipids during proliferation and apoptosis. PLSCR1 interacts with the same cysteine-rich domain of onzin as do Akt1 and Mdm2, whereas the onzin-interacting domain of PLSCR1 centers around, but does not require, a previously identified palmitoylation signal. Depletion of endogenous PLSCR1 in myeloid cells leads to a phenotype that mimics that of onzin overexpression, providing evidence that PLSCR1 is a physiologic regulator of onzin. In contrast, PLSCR1 overexpression in fibroblasts, which normally do not express onzin, affects neither growth nor apoptosis unless onzin is coexpressed, in which case PLSCR1 completely abrogates onzin's positive effects on proliferation and survival. These findings demonstrate a functional interdependence between onzin and PLSCR1. They further suggest a contiguous link between the earliest events mediated by c-Myc and the latest ones, which culminate at the cell surface and lead to phospholipid reshuffling and cell death.