Antiviral phagocytosis is regulated by a novel Rab-dependent complex in shrimp penaeus japonicus

Rab GTPases are involved in phagosome formation and maturation. However, the role of Rab GTPases in phagocytosis against virus infection remains unknown. In this study, it was found that a Rab gene ( PjRab) from marine shrimp was upregulated in virus-resistant shrimp, suggesting that Rab GTPase was involved in the innate response to virus. The RNAi and mRNA assays revealed that the PjRab protein could regulate shrimp hemocytic phagocytosis through a protein complex consisting of the PjRab, beta-actin, tropomyosin, and envelope protein VP466 of shrimp white spot syndrome virus (WSSV). It was further demonstrated that the PjRab gene silencing by RNAi caused the increase in the number of WSSV copies, indicating that the PjRab might be an intracellular virus recognition protein employed by a host to increase the phagocytic activity. Therefore, our study presents a novel Rab-dependent signaling complex, in which the Rab GTPase might detect virus infection as an intracellular virus recognition protein and trigger downstream phagocytic defense against virus in crustacean for the first time. This discovery would improve our understanding of the still poorly understood molecular events involved in innate immune response against virus infection of invertebrates.     

Generation of an external guide sequence library for a reverse genetic screen in Caenorhabditis elegans

Background  

A method for inhibiting the expression of particular genes using external guide sequences (EGSs) has been developed in bacteria, mammalian cells and maize cells.     

Localization of CD26/DPPIV in nucleus and its nuclear translocation enhanced by anti-CD26 monoclonal antibody with anti-tumor effect

Background  

CD26 is a type II, cell surface glycoprotein known as dipeptidyl peptidase (DPP) IV. Previous studies have revealed CD26 expression in T cell leukemia/lymphoma and malignant mesothelioma, and an inhibitory effect of anti-CD26 monoclonal antibody (mAb) against the growth of CD26+ cancer cells in vitro and in vivo. The function of CD26 in tumor development is unknown and the machinery with which the CD26 mAb induces its anti-tumor effect remains uncharacterized.     

湿地植物根系泌氧及其在自然基质中的扩散效应研究进展

湿地植物根系径向泌氧(ROL)是构造根际氧化-还原异质微生态系统的核心要素,其扩散层为好氧、厌氧微生物提供了良好生境并促进其代谢活动,使湿地植物根际成为有机物降解、物质循环及生命活动最为强烈的场所,已有成果证明湿地植物根系ROL的强弱与污染物的去除效果密切相关。因此,开展湿地植物根系ROL及其在自然基质中的扩散效应研究,对于了解湿地植物根系ROL机理及其根际氧环境特征,进而发挥湿地植物的污染去除功能具有十分重要的意义。基于此,首先归纳了湿地植物根系ROL特征及其受影响机制的研究现状,而后从种属差异、时空分布及对微生物的影响等方面对根系ROL在自然基质中的扩散效应国内外研究成果进行了总结,最终根据研究现状与不足对今后的研究方向进行了简要展望。创新之处在于:1)提出影响根系氧供给及氧输送释放通道的环境、生物等因素,阐述了其对根系ROL的影响机制;2)着重阐述了目前研究较少提及的根系ROL扩散效应测定方法。     

挺水植物与浮叶植物光合荧光特性的差异

为探讨自然生境中不同生活型水生植物光合生理特征的差异,选取4种挺水植物菖蒲(Acorus calamus L.)、再力花(Thalia dealbata Fraser)、梭鱼草(Pontederia cordata L.)、茭草(Zizania latifolia(Griseb.)Stapf),以及4种浮叶植物黄睡莲(Nymphaea mexicana Zucc.)、莼菜(Brasenia schreberi J.F.Gmel.)、金银莲花(Nymphoides indica(L.)O.Kuntze)、菱(Trapa bispinosa Roxb.)为研究对象,比较其叶绿素荧光参数、色素组成和比叶重的差异。研究发现,高光强下挺水植物电子传递速率(ETR)、非光化学淬灭(NPQ)等光合荧光参数、以及低光强下ETR拟合曲线的初始斜率(α)均值显著大于浮叶植物。不同挺水植物间光系统Ⅱ(PSⅡ)最大光化学效率(F_v/F_m)、ETR、NPQ、最大潜在电子传递速率(Ps)、最大电子传递速率(ETR_m)及饱和光强(E_m)变化幅度较大;不同浮叶植物间上述参数变化幅度较小。挺水植物叶绿素(Chls)、类胡萝卜素(Cars)含量均值也高于浮叶植物。但由于比叶重(SLW)的影响,不同水生植物间单位叶面积和单位叶鲜重色素含量的变化规律略有不同。挺水植物中再力花、梭鱼草光合能力较强,其光合荧光参数和色素比例均符合典型阳生型特征;菖蒲、茭草光合能力略弱,部分指标符合阴生型特征。4种浮叶植物各指标均符合阳生型特征。实验推测,挺水植物和浮叶植物由于叶片所处环境不同,其光合适应机制存在明显分化。挺水植物叶片所处环境异质性较大,因而不同物种之间光合参数适应范围也大;浮叶植物叶片所处环境相对均一,因而光合参数差异也小。浮叶植物也不依赖NPQ进行高光保护。在湿地植被恢复工具种筛选过程中应综合考虑环境异质性和不同物种光适应能力的差异。     

哈维氏弧菌胞外蛋白酶基因的表型克隆与序列分析

哈维氏弧菌是引起大黄鱼疾病的主要致病菌之一,胞外蛋白酶是哈维氏弧菌GYC1108-1的主要致病因子。利用表型克隆技术,用Sau3AⅠ将提取的哈维氏弧菌基因组DNA酶切成短片段,纯化回收1-5 kb的片段与BamH I酶切的pUC118在T4连接酶的作用下进行连接,并转化感受态细胞TG1,在含0.5%脱脂奶和100μg/mL氨苄青霉素的LB平板上筛选胞外蛋白酶阳性株,命名为YZ。测定阳性株YZ的胞外蛋白酶活性,并对阳性株的重组质粒的插入片段进行序列测定,分析开放阅读框,确定胞外蛋白酶基因编码区。发现蛋白酶基因的ORF编码531个氨基酸,在起始密码子ATG上游存在一个核糖体结合位点(SD),其上游的启动区与大肠杆菌的σ70启动区和枯草芽孢杆菌的启动区高度同源。在终止子(TAG)下游,存在两个反向重复序列,为推导的2个转录终止子。哈维氏弧菌胞外蛋白酶基因的克隆与诠释为哈维氏弧菌致病机理和疫苗的开发奠定了基础。     

变溶菌素(Mutanolysin)研究历史和发展前景

变溶菌素(Ｍｕｔａｎｏｌｙｓｉｎ)是由球孢链霉菌(Ｓｔｒｅｐｔｏｍｙｃｅｓｇｌｏｂｉｓｐｏｒｕｓ)的培养液制备的由多种不同溶菌酶组成的粗酶液。这种溶菌酶群在防治龋齿、从细菌细胞壁制取免疫活性物质等方面及一些科研领域有着良好的应用前景,其研究越来越受到广泛?..     

光照和生长阶段对菖蒲根系泌氧的影响

以自然湖泊沉积物为研究基质,利用微型电机控制溶氧微电极实现纵向精确微位移,在照光与遮光条件下,对典型湿地植物菖蒲幼苗、成株根系根基部起总根长1/4处(根1/4)、根系中部(根1/2)、从根基部起总根长3/4处(根3/4)及根尖(根1)处根系微界面径向溶氧浓度变化进行原位精确测定。结果表明:无论有无光照,菖蒲幼苗、成株根系不同部位均存在从根表面至沉积物氧饱和度由高到低的氧扩散层,其厚度0.18—0.68 mm;根1/2、3/4、1处氧扩散能力菖蒲成株较幼苗显著增强(P<0.01),根1/4处二者则无显著差异(P>0.05);光照对菖蒲幼苗、成株根系不同部位氧扩散能力的影响存在差异,光照对菖蒲幼苗根1/2及菖蒲成株根1/2、根3/4处影响显著(照光组显著高于遮光组,P<0.01),而对菖蒲幼苗根1/4、根3/4、根1及菖蒲成株根1/4、根1处无显著影响(P>0.05);从根系泌氧空间差异上看,照光条件下菖蒲幼苗、成株分别表现为根1/2>根3/4≈根1≈根1/4(P<0.01,P>0.05)和根1/2>根3/4>根1>根1/4(P<0.01),遮光条件下菖蒲幼苗、成株分别表现为根1/2≈根3/4≈根1≈根1/4(P>0.05)和根1/2>根3/4≈根1>根1/4(P<0.01,P>0.05)。     

p38α‐MAPK‐deficient myeloid cells ameliorate symptoms and pathology of APP‐transgenic Alzheimer's disease mice

Alzheimer''s disease (AD), the most common cause of dementia in the elderly, is pathologically characterized by extracellular deposition of amyloid‐β peptides (Aβ) and microglia‐dominated inflammatory activation in the brain. p38α‐MAPK is activated in both neurons and microglia. How p38α‐MAPK in microglia contributes to AD pathogenesis remains unclear. In this study, we conditionally knocked out p38α‐MAPK in all myeloid cells or specifically in microglia of APP‐transgenic mice, and examined animals for AD‐associated pathologies (i.e., cognitive deficits, Aβ pathology, and neuroinflammation) and individual microglia for their inflammatory activation and Aβ internalization at different disease stages (e.g., at 4 and 9 months of age). Our experiments showed that p38α‐MAPK‐deficient myeloid cells were more effective than p38α‐MAPK‐deficient microglia in reducing cerebral Aβ and neuronal impairment in APP‐transgenic mice. Deficiency of p38α‐MAPK in myeloid cells inhibited inflammatory activation of individual microglia at 4 months but enhanced it at 9 months. Inflammatory activation promoted microglial internalization of Aβ. Interestingly, p38α‐MAPK‐deficient myeloid cells reduced IL‐17a‐expressing CD4‐positive lymphocytes in 9 but not 4‐month‐old APP‐transgenic mice. By cross‐breeding APP‐transgenic mice with Il‐17a‐knockout mice, we observed that IL‐17a deficiency potentially activated microglia and reduced Aβ deposition in the brain as shown in 9‐month‐old myeloid p38α‐MAPK‐deficient AD mice. Thus, p38α‐MAPK deficiency in all myeloid cells, but not only in microglia, prevents AD progression. IL‐17a‐expressing lymphocytes may partially mediate the pathogenic role of p38α‐MAPK in peripheral myeloid cells. Our study supports p38α‐MAPK as a therapeutic target for AD patients.