Abstract:Here, we review the progresses of researches on the biological effects of the hypomagnetic field (HMF) and propose that a magnetic field with magnetic induction of "0 < |B| ≤ 5 μT" is defined as a hypomagnetic field (HMF)．Interplanetary space is a natural hypomagnetic field．The astronauts, enabled by space sciences thriving in the recent decades, are spending longer time in the hypomagnetic outer space, e.g．landing on the moon and heading to mars. The effects of HMF on many aspects of biological processes, especially the adverse impacts on the functions of the central nervous system, remind us that the astronauts would suffer from potential risks due to the HMF exposure．Unfolding the mechanism of the biological responses to the HMF is the fundament for developing the counteractions of the adverse space environmental factors, and has recently become a hot topic in the field of space life sciences. Refining the concept of HMF and standardizing the HMF simulation systems for biological experiments will benefit the comparability of the HMF effects as described, and improve our understanding of how HMF influences homeostasis, cell signaling pathways and cognitive behaviors, and to what extent HMF contribute to such disturbances.

Abstract:Nucleosome is the building unit of eukaryotic chromatin, the location of histone octamer on the DNA sequence is called nucleosome positioning. With the advent of high throughout technologies such as ChIP-chip and ChIP-seq. large-scale nucleosome positioning atlas of multiple model organisms have been measured, which attract many researchers to investigate nucleosome positioning and its functions on transcriptional regulation. In this paper, we first introduce the concept of nucleosome positioning and summarize the regular patterns of nucleosome positioning on genetic region, then review the major advances of functions of nucleosome positioning on transcriptional initiation, elongation, divergence of expression patterns and alternative splicing.

Abstract:The emergence of superbug, resistant to every widely used commercial antibiotics, has led to increasing environmental and health risks. Antimicrobial peptides (AMPs), which represent one of most promising substitutes for antibiotics, are earning interests on account of efficiency in fighting against pathogens and difference in action mechanism between AMPs and antibiotics from researchers all over the world. Indeed, early studies showed that AMPs were found extensively in nature, and had high antimicrobial activities and broad antimicrobial spectrum. Unfortunately, prior obstacles were urgently surmounted because of cytotoxicity, stability, and production cost of AMPs. Accordingly, to overcome these disadvantages, contemporary researchers are trying to apply rational methods and advanced technology to develop modified antimicrobial peptides. AMP mimetics, AMP congeners, hybrid AMPs, AMP conjugates, stabilized AMPs and immobilized AMPs have all emerged and have application potentials in husbandry, food and medicine. This review outlines recent advances of these modified antimicrobial peptides.

Abstract:Autophagy wildly exists in eucaryotic cells which is essential vital phenomena.Autophagy is an important mechanism that makes cells adapting the environment change, defensing invasion of pathogenic microorganism and maintaining homeostasis. The activity of autophagy fluctuates in many lung diseases, it closely related with the lung diseases' occurrences and developments. Autophagy has happened in pulmonary emphysema, chronic obstructive pulmonary disease, lung cancer, pulmonary tuberculosis and many other lung diseases, and plays an important role in these diseases. This review summarized it from the perspective of relationship of autophagy and lung diseases. It helps to understand the effect that autophagy produced in lung diseases and so as to further study the regulation of autophagy and to provide new ideas for the therapy of lung diseases.

Abstract:开花是高等植物发育过程中一个非常重要的转化过程，它能够保证植物的正常发育和后代的延续，并且有重要的农业价值和观赏价值[1]．开花时间的调控是一个非常复杂的过程，受到自身发育信号和外部环境因素的共同影响[2-3]．FLC是拟南芥开花调节过程中的中心抑制因子，其在拟南芥顶端分生组织和叶片维管束的伴胞细胞中均有表达，并且这两个部位的FLC对开花时间都有重要的调节作用[4]．目前已知的多数影响开花的通路都通过调节顶端FLC的表达来调控植物开花时间，关于伴胞细胞中的FLC如何被调控的研究还非常少[1, 3]．
在动植物中都存在一类具有JmjC结构域的蛋白质，是一类保守的组蛋白脱甲基化酶[5]．我们实验室最近的工作表明，JMJ18是一个受植物自身发育调节的H3K4脱甲基化酶，JMJ18主要在伴胞细胞中表达，通过特异调节伴胞细胞中的FLC调控植物开花时间[6]．
Yang等[6]实验证实在体外全长的JMJ18可以特异性地以H3K4m3的多肽为底物，脱掉其上一个甲基生成H3K4m2．在拟南芥中，JMJ18主要在伴胞细胞中表达，并且表达水平受到植物自身发育进程的调控[4]．JMJ18功能缺失突变体呈现弱的晚花表型，而JMJ18的超表达植株呈现明显的早花表型，说明JMJ18参与了拟南芥开花时间的调控[4].尽管多个具有JmjC结构域的组蛋白脱甲基化酶，如 JMJ14、ELF6/JMJ11、REF6/JMJ12等都参与了拟南芥开花时间的调节，但是机制都不太清楚[5, 7]，并且目前没有发现可以直接调控FLC的JmjC蛋白．Yang等的实验证实JMJ18可以结合到FLC的染色质上，通过降低FLC的染色质H3K4m3和H3K4m2修饰抑制FLC表达．FLC表达水平的降低导致FT表达的释放，促进FT在伴胞细胞中积累．积累的FT从伴胞细胞进入筛管组织，进而运输到顶端分生组织，与顶端分生组织特异性表达的bZIP转录因子FD直接相互作用，通过调节下游基因SOC1和AP1调控植物开花进程(图1)．
最近的研究发现，植物开花时间除了受到春化作用、自主途径、光周期途径、GA途径等调控以外，还可以通过自身年龄衡量因子miR156和其靶基因SQUAMOSA PROMOTER BINDING-LIKE (SPLs)调节开花进程[8]．Yang等实验证实：JMJ18主要在韧皮部的伴胞细胞表达．并且同miR156类似，在植物营养生长时期，JMJ18随着发育进程的深入表达水平逐渐升高．SUC2启动子驱动JMJ18在维管伴胞细胞中表达时也出现早花表型并且依赖于FT．这些研究结果表明，同miR156类似，JMJ18受植物自身发育调节，也可能作为自身年龄衡量因子调控植物开花时间，不同点是JMJ18是通过组蛋白修饰直接调节FLC表达调控开花时间的自身年龄衡量因子．即可能有两条感受自身年龄的途径：miR156-SPLs和JMJ18-FLC/MAFs途径，让人感兴趣的是两个因子都是表观遗传调控因子，而且在每个途径中均是前者负调控后者，而且后者均为一个转录因子基因家族，这两个途径最后都调控FT表达．这两个途径之间的关系也是一个有待于研究的科学问题，这可能会对于我们理解自身年龄衡量因子在植物开花进程中的作用有一定的启示．

Abstract:The heme oxygenase HugZ from Helicobacter pylori plays essential roles in the colonization of the bacteria in human hosts and is required for the utilization of heme as the sole iron source. Residue His245, which is highly conserved, coordinates the heme iron through its sidechain imidazole group. Surprisingly, this residue was not required for the enzymatic activities of HugZ. To investigate the roles played by His245 in heme binding and enzymatic mechanisms of HugZ, we have solved the crystal structure of HugZ mutant H245A at 2.55Å resolution and found that a nearby histidine residue, His249, coordinates the heme iron. This substitution is made possible by the fact that both residues 245 and 249 are located in a flexible loop region ranged from Gly239 to the C-terminus. Similar structural features have not been observed in other heme oxygenases so far. We have also performed spectroscopic studies on the heme-binding properties of HugZ and relevant mutants and our results suggest that the flexible C-terminal loop region of HugZ and the presence of multiple histidine residues in this region may play important roles in heme recruiting and in the catalytic mechanisms of HugZ.

Abstract:The c-Jun amino-terminal kinase (JNK) is an important player in inflammation, proliferation, and apoptosis. Here, by using a yeast two-hybrid technology, p65 subunit of NF-κB transcription factor was identified as a partner of JNK3. We show that JNK3 physically associated with p65 in vivo and in vitro. Overexpression of JNK3 inhibited NF-κB- dependent transcription induced by TNFα. It was demonstrated that JNK3 decreased NF-κB binding to its cognate DNA sequences and NF-κB target genes expression. Taken together, these data suggest that JNK3 may function in vivo as a modulator in suppressing the transcriptional activity of p65.

Abstract:Oxidored-nitro domain containing protein 1 (NOR1) is a candidate tumor suppressor gene that is down-regulated in nasopharyngeal carcinoma (NPC). In the present study, NOR1 stable transfected NPC 5-8F cells were established. As a result, the 5-8F cells expressing NOR1 showed dramatic morphological changes comparing with the control, such as less lamellipodia protrusions and membrane ruffles at the periphery of the cells. Ectopic expression of NOR1 in NPC 5-8F cells also inhibited microvillus formation on the surface of tumor cells due to filamentous actin rearrangement. Further more, realtime RT-PCR assay revealed that ectopic expression of NOR1 suppressed the expression level of FZD5 and FZD7, and then attenuated β-catenin nuclear translocation. This first report provides experimental proof to probe the function of NOR1 gene in the process of lamellipodia formation and the Wnt signaling in NPC cells.

Abstract:Protein Tau is a very unequal phosphoric microtubule associated protein, which affect the transport of substances in the axons of the neurons, whose phosphorylation is one of the key methods to regulate neuronal function. The hyperphosphorylation of protein Tau can damage the learning and memory of rats. The impairment of learning-memory induced by electroconvulsive shock in depressed rats is relevant to the function failure of glutamic acid signal system. The phosphorylation of protein Tau can be up-regulated by the individual stress level through the excitatory neurotransmission system. The mechanisms of 2, 6-diisopropylphenol effect on the central nerve system relate to inhibiting the release of glutamic acid and the activity of NMDAR. And the 2, 6-diisopropylphenol can protects against the impairment of learning-memory induced by electroconvulsive shock in depressed rats though inhibiting the excitotoxicty of glutamate. The rise of glutamic acid which induced by electroconvulsive shock in depressed rats can lead to the impairment of learning-memory through up-regulating the hyperphosphorylation of protein Tau? The 2, 6-diisopropylphenol can protect against this process? This study explore the reversion of the 2, 6-diisopropylphenol against the impairment of learning-memory and the hyperphosphorylation of protein Tau induced by electroconvulsive shock in depressed rats, in order to provide experimental evidence for neuropsychological mechanisms on improving learning and memory and the clinical intervention treatment. According to the design of factorial analysis, two intervention factors were set up: the electroconvulsive shock (two levels: no disposition; a course of electroconvulsive shock) and the 2, 6- diisopropylphenol (two levels: 5 ml Saline was injected peritoneally; 5 ml 2, 6-diisopropylphenol was injected peritoneally by dosage of 100 mg/kg). Thirty-two adult depression model rats whose olfactory bulbs were removed were randomly divided into four experimental groups (n=8, in each group): group Ⅰ(5 ml 2, 6-diisopropylphenol was injected peritoneally in the Sprague-Dawley rats by dosage of 100 mg/kg); group Ⅱ(5 ml 2, 6- diisopropylphenol was injected peritoneally in the Sprague-Dawley rats by dosage of 100 mg/kg and giving a course of electroconvulsive shock); group Ⅲ(5ml Saline was injected peritoneally in the Sprague-Dawley rats); group Ⅳ(5 ml saline was injected peritoneally in the Sprague-Dawley rats and giving a course of electroconvulsive shock). The Morris water maze test started within 1 day after the course of electroconvulsive shock finished in order to evaluate learning-memory. The hippocampus was removed from rats within 1 day after the Morris water maze test finished. The content of glutamate in the hippocampus of rats was detected by high performance liquid chromatography. The content of Protein Tau which includes Tau-5 (Total protein Tau), p-PHF1^Ser396/404, p-AT8^Ser199/202, p-12E8^Ser262, GSK-3β^1H8 and PP-2A in the hippocampus of rats was detected with Western blotting. The electroconvulsive shock and the 2, 6-diisopropylphenol can induce the impairment of learning-memory in depressed rats, extending the evasive latency time and shortening the space exploration time. And both influences present subtract effect. The electroconvulsive shock can significantly up-regulate the content of glutamate in the hippocampus of depressed rats which was reduced by 2, 6-diisopropylphenol. And both influences present subtract effect. The electroconvulsive shock and the 2, 6-diisopropylphenol does not affect the total protein Tau and protein PP-2A in the hippocampus of rats. The electroconvulsive shock can up-regulate the hyperphosphorylation of protein Tau and the expression of GSK-3β^1H8 in the hippocampus of depressed rats, which is reduced by 2, 6- diisopropylphenol. And both influences present subtract effect. Our results indicate that the electroconvulsive shock up-regulates the content of glutamate in the hippocampus of depressed rats, which up-regulates the hyperphosphorylation of protein Tau through up-regulating the expression of GSK-3β^1H8, and further induce the impairment of learning-memory in depressed rats. Wheareas, the 2, 6-diisopropylphenol protects against the impairment of learning-memory and reduce the hyperphosphorylation of protein Tau induced by electroconvulsive shock in depressed rats through reducing the expression of GSK-3β^1H8 and the content of glutamate in the hippocampus.

Abstract:Understanding the connection between sensory input and motor output is challenging. There is a need for good model systems to evaluate the molecular and neural mechanism of animal behavior. Here we show a new system for analyzing preference and plasticity of Drosophila egg-laying behavior. We found that selection of egg-laying site in flies is a good model to investigate the food preference in Drosophila. On sugar food with lower concentration, flies showed significant preference that was reduced upon the inhibition of olfactory pathway. Moreover, to examine the plasticity of egg-laying behavior, a new learning paradigm was devised. We associated light-dark cycle of egg-laying with different food conditions and found that flies could maintain egg-laying memory at least 3 days after training. This egg-laying system provides the basis for further study of molecular and neural mechanism underlying the relationship between environment and behavior.

Abstract:PROL4 (proline-rich protein 4) was screened out in lung cancer cells for its defective expression in our previous study. By transfection of PROL4 into lung adenocarcinoma cell line LTEP-a-2, a stable cell strain was acquired. It was shown that in PROL4 expressing cells, compared to the vector control cells, the serum dependence of cell growth was markedly enhanced, soft agar colony-forming ability was suppressed. The tumor growth was also significantly restrained by PROL4 in vivo experiments. Furthermore, PROL4 transfected cancer cell strains were found to display an elevated sensitivity to cisplatin treatment than mock-transfectant control cells, and the sensitivity up-regulation was closely related to the rate of cell apoptosis induced by PROL4 and cisplatin cooperately. These results suggest that PROL4 is potentially a new genetic engineering target to enhance the chemotherapeutic effects of cisplatin in lung cancer treatment.