昆虫内共生菌研究概况

内共生菌与昆虫形成互惠共生关系,在宿主昆虫的生长、生殖、传播植物病害以及探讨生命起源与进化等等方面都有很重要的意义。从昆虫内共生菌的特点、内共生菌在昆虫体内的分布、对昆虫的影响、获得少或缺内共生菌的方法及其研究内共生菌的潜在意义等方面进行了综述。     

鳞翅目昆虫内共生菌研究进展

内共生菌(endosymbionts)与其昆虫宿主的共生关系是普遍存在的,它们彼此相互依赖、相互影响、协同进化.近年来,关于昆虫内共生菌的研究多以半翅目(Hemiptera)和双翅目(Diptera)昆虫为主,但数量不断增加的研究表明鳞翅目(Lepidoptera)昆虫与其体内共生菌的互作模式和机制也正在受到越来越多的...     

昆虫内共生菌及其功能研究进展

昆虫内共生菌与宿主之间的互作关系已逐渐成为昆虫学的研究热点之一。昆虫内共生菌具有协助宿主营养代谢、 逃避天敌攻击和增强抗药性等功能： 通过协助宿主营养代谢, 提供食物中缺乏的营养物质来弥补食物中营养物质的不足; 分泌抗菌肽、 毒素等物质以增强对外源寄生物等的防御能力, 抑制对宿主的不利影响; 同时, 也可以增强宿主抗逆性, 调控植物生理反应, 抑制植物对宿主的不利影响; 利用对抗逆性基因精确的表达调控来增强宿主抗药性等。因此, 内共生菌介导的宿主生物学性状的改变, 扩大了宿主昆虫的生态位, 成为昆虫生长发育过程中的重要调控因子。目前, 昆虫内共生菌的功能往往是通过研究宿主感染共生菌前后性状的变化而证实。近几年, 转录组学、 蛋白质组学、 基因组学等技术的进步, 促进了内共生菌与宿主昆虫共生机制研究的发展。通过研究内共生菌及其功能基因在昆虫种群动态中的作用, 特别是内共生菌感染对宿主生殖、 存活、 适应环境能力的影响, 将有利于揭示内共生菌与宿主的共生机制, 并最终为开发新的防控技术提供理论依据。本文针对昆虫内共生菌的功能进行了综述, 并对日后的研究方向进行了展望, 提供了研究昆虫内共生菌与宿主互作关系的方法及建议。     

昆虫内共生菌及其传病毒相关GroEL蛋白

昆虫传播的植物病毒种类多、危害大,其传病毒的能力与昆虫体内共生菌产生的GroEL蛋白关系密切,该蛋白是分子伴侣hsp60家族的成员,对病毒进入昆虫血体腔免遭破坏起着保护作用,也与昆虫传病毒的专一性有关。本对昆虫内共生菌及其产生的GroEL进行了综述,并分析了研究内共生菌及其产生的蛋白质的科学意义与发展趋势,为植物病毒病的防治研究提供了新的思路。     

昆虫内共生菌研究概况*

内共生菌与昆虫形成互惠共生关系,在宿主昆虫的生长、生殖、传播植物病害以及探讨生命起源与进化等等方面都有很重要的意义。从昆虫内共生菌的特点、内共生菌在昆虫体内的分布、对昆虫的影响、获得少或缺内共生菌的方法及其研究内共生菌的潜在意义等方面进行了综述。     

昆虫体外共生菌研究进展

昆虫体外共生菌是指能在体外与宿主发生互利共生关系的微生物。体外共生菌虽然不如肠道微生物那样普遍存在于昆虫中,但也在宿主生长发育过程中扮演着重要的角色。昆虫体外共生菌一般寄生于昆虫体表或体内特异器官(如储菌器),在特定时期转移到植物组织中。体外共生菌产生的挥发物能作为宿主定位寄主植物的信号物质,能为宿主提供生长发育所需的营养物质,还参与了宿主体外免疫。对昆虫体外共生菌的研究,不仅能进一步揭示昆虫与微生物之间的互作关系,丰富昆虫共生菌的研究,还能从共生菌的角度探索害虫引诱剂和昆虫免疫豁免机制。本文对昆虫体外共生菌寄生方式、传播途径、对宿主的影响等研究成果进行了综述,旨在为害虫综合防控提供新思路。     

防御素在免疫中的作用

哺乳动物的防御素是在体内形成的一种小分子杭菌性阳离子肽,是天然免疫中的一种类似抗生素的效应物质。防御素利用树突细胞和T细胞上的趋化因子受体,在微生物侵入后的获得性免疫调节上超重要作用。它也有一定的免疫佐剂活性。本文叙述了各种具有抗菌活性的防御素或抗菌肽的各项免疫活性。     

破译白蚁肠道内共生菌基因组

日本理化研究所的科学家日前完全破译了白蚁肠道内一种共生细菌的基因组,这将有助于研究白蚁高效分解木材的机制,为生物燃料的开发提供新线索。     

昆虫免疫防御系统的限制因素

本文主要针对昆虫对寄生物的免疫防御并从进化生态学的角度采阐述昆虫防御系统所存在的一些限制因素,如识别抗原失败、免疫特异性、防御代价、自体免疫、性别、资源利用率和寄生物的干扰等,而这些局限使得昆虫的免疫防御受到不同（自发或诱导的、广泛或具体的）免疫反应的影响。从而限制其持续的免疫防御。     

Host factors against plant viruses

Plant virus genome replication and movement is dependent on host resources and factors. However, plants respond to virus infection through several mechanisms, such as autophagy, ubiquitination, mRNA decay and gene silencing, that target viral components. Viral factors work in synchrony with pro-viral host factors during the infection cycle and are targeted by antiviral responses. Accordingly, establishment of virus infection is genetically determined by the availability of the pro-viral factors necessary for genome replication and movement, and by the balance between plant defence and viral suppression of defence responses. Sequential requirement of pro-viral factors and the antagonistic activity of antiviral factors suggest a two-step model to explain plant–virus interactions. At each step of the infection process, host factors with antiviral activity have been identified. Here we review our current understanding of host factors with antiviral activity against plant viruses.     

Parasite spread in experimental metapopulations: resistance,tolerance and host competence

Host competence, defined as the likelihood that a host will transmit infection, may be affected by an individual's resistance to infection and its ability to withstand damage caused by infection (tolerance). Host competence may therefore be one of the most important factors to impact host–parasite dynamics, yet the relationships among resistance, tolerance and competence are poorly understood. The objective of the present study was to determine whether individual host resistance (ability to resist or minimize infection) and/or tolerance (ability to withstand or minimize reduction in fitness due to infection) contributed to the competence (ability to spread infection) of hosts using guppies infected with the ectoparasite, Gyrodactylus turnbulli. This individual-fish level analysis used data collected from a previous metapopulation experiment that had tracked host–parasite dynamics at the metapopulation scale using individually marked guppies that were moved among experimental tanks within replicate metapopulations. Fish tolerance was measured as the residual from a fish's expected survival post-infection for a given parasite burden. Fish resistance was measured as the peak parasite load (– log-transformed). Host competence was measured as the incidence (number of new infections over two days after the arrival of a fish to a tank) weighted by the density of available uninfected fish in the tank. In contrast to the assumption of a trade-off between resistance and tolerance, individual fish tolerance and resistance were both negatively associated with competence. Connectivity (the number of fish with which an individual came into contact) was not associated with competence. Our results indicate that resistance and tolerance are both important to disease spread. These findings highlight the importance of understanding how individual defence against parasites may contribute to its competence as a host, and therefore impact metapopulation-level dynamics.     

A critical role for CARD9 in pneumocystis pneumonia host defence

Caspase recruitment domains‐containing protein 9 (CARD9) is an adaptor molecule critical for key signalling pathways initiated through C‐type lectin receptors (CLRs). Previous studies demonstrated that Pneumocystis organisms are recognised through a variety of CLRs. However, the role of the downstream CARD9 adaptor signalling protein in host defence against Pneumocystis infection remains to be elucidated. Herein, we analysed the role of CARD9 in host defence against Pneumocystis both in CD4‐depleted CARD9^?/? and immunocompetent hosts. Card9 gene‐disrupted (CARD9^?/?) mice were more susceptible to Pneumocystis, as evidenced by reduced fungal clearance in infected lungs compared to wild‐type (WT) infected mice. Our data suggests that this defect was due to impaired proinflammatory responses. Furthermore, CARD9^?/? macrophages were severely compromised in their ability to differentiate and express M1 and M2 macrophage polarisation markers, to enhanced mRNA expression for Dectin‐1 and Mincle, and most importantly, to kill Pneumocystis in vitro. Remarkably, compared to WT mice, and despite markedly increased organism burdens, CARD9^?/? animals did not exhibit worsened survival during pneumocystis pneumonia (PCP), perhaps related to decreased lung injury due to altered influx of inflammatory cells and decreased levels of proinflammatory cytokines in response to the organism. Finally, although innate phase cytokines were impaired in the CARD9^?/? animals during PCP, T‐helper cell cytokines were normal in immunocompetent CARD9^?/? animals infected with Pneumocystis. Taken together, our data demonstrate that CARD9 has a critical function in innate immune responses against Pneumocystis.     

Selective elimination of aphid endosymbionts: effects of antibiotic dose and host genotype, and fitness consequences

Multiple endosymbionts commonly coexist in the same host insects. In order to gain an understanding of the biological roles of the individual symbionts in such complex systems, experimental techniques for enabling the selective removal of a specific symbiont from the host are of great importance. By using the pea aphid-Buchnera-Serratia endosymbiotic system as a model, the efficacy, generality, and fitness consequences of selective elimination techniques at various antibiotic doses and under a variety of host genotypes were investigated. In all the disymbiotic aphid strains examined, the facultative symbiont Serratia was selectively eliminated by ampicillin treatment in a dose-dependent manner, suggesting a generality of the elimination technique irrespective of host genotype. However, fitness consequences of the Serratia elimination differed between the aphid strains, indicating substantial effects of host genotype. In all the disymbiotic aphid strains, the obligate symbiont Buchnera was selectively eliminated by rifampicin treatment irrespective of the antibiotic dose. However, the survival and reproduction of the Buchnera-free aphids varied in a dose-dependent manner, and the dose dependence was strikingly different between the aphid genotypes. These results provide a basis for the development of new protocols for manipulating insect endosymbiotic microbiota.     

The increasing role of phosphatidylethanolamine as a lipid receptor in the action of host defence peptides

Host defence peptides (HDPs) are antimicrobial agents produced by organisms across the prokaryotic and eukaryotic kingdoms. Many prokaryotes produce HDPs, which utilise lipid and protein receptors in the membranes of bacterial competitors to facilitate their antibacterial action and thereby survive in their niche environment. As a major example, it is well established that cinnamycin and duramycins from Streptomyces have a high affinity for phosphatidylethanolamine (PE) and exhibit activity against other Gram-positive organisms, such as Bacillus. In contrast, although eukaryotic HDPs utilise membrane interactive mechanisms to facilitate their antimicrobial activity, the prevailing view has long been that these mechanisms do not involve membrane receptors. However, this view has been recently challenged by reports that a number of eukaryotic HDPs such as plant cyclotides also use PE as a receptor to promote their antimicrobial activities. Here, we review current understanding of the mechanisms that underpin the use of PE as a receptor in the antimicrobial and other biological actions of HDPs and describe medical and biotechnical uses of these peptides, which range from tumour imaging and detection to inclusion in topical microbicidal gels to prevent the sexual transmission of HIV.     

不同寄主植物的烟粉虱(Bemisia tabaci)内共生菌传毒相关GroEL蛋白的一致性

通过对7种寄主植物上B型烟粉虱北京种群的内共生菌传毒相关groEL基因进行PCR扩增和测序,结合已有的相关序列,构建了groEL基因及其编码的GroEL蛋白的分子系统树。结果表明：烟粉虱内共生菌产生的groEL基因是一个非常保守的基因,北京不同寄主植物的烟粉虱内共生菌与IsraelB型烟粉虱内共生菌的groEL基因亲源关系非常近,位于同一进化分支,其编码的GroEL蛋白的分子系统树也基本上是一致的。不同物种的groEL基因及其编码的GroEL蛋白分别位于不同的分支,说明groEL基因及其编码的GroEL蛋白的分子系统树可以用于分析物种间的进化关系。氨基酸序列比较表明：烟粉虱内共生菌GroEL具有原核GroEL的保守氨基酸、ATP酶活性位点、多肽结合位点和GroES连接位点,为典型的hsp60。不同来源烟粉虱内共生菌GroEL有少数几个保守氨基酸发生了置换,可能不是GroEL功能的重要位点。说明在容易变异的细菌基因组中,groEL基因为了维持其正常重要的生理功能,会通过保持功能位点的稳定性来应对不同生态因素的影响。     

刺吸式昆虫次生内共生菌的研究进展

蚜虫作为典型的刺吸式昆虫,需要以取食植物韧皮部汁液来补充营养,几乎所有蚜虫均带有一种能为其提供植物韧皮部缺失营养物质的初生共生菌Buchnera aphidicola。此外,蚜虫还可携带一种或多种次生内共生菌。在众多共生菌—寄主系统中,蚜虫与其所带内共生菌间的互作研究最为透彻。虽然次生内共生菌对寄主的存活和生殖影响并不显著,但其在寄主对环境耐受力、天敌防御能力等方面作用明显。本文在查阅大量蚜虫次生内共生菌相关文献的基础上,着重对蚜虫次生内共生菌的种类及传播规律、次生内共生菌对蚜虫表型的影响、蚜虫次生内共生菌基因组学等方面的研究现状进行综述,以求为刺吸式昆虫次生内共生菌的研究提供参考。     

The role of fever in the infected host

Sepsis is a highly lethal clinical syndrome characterized by a systemic inflammatory response to infection. Fever, a non-specific acute-phase response, has been associated with improved survival and shortened disease duration in non-life-threatening infections. However, the influence of fever and the effects of antipyresis in patients with sepsis has not been prospectively studied in humans. This paper reviews the state of our knowledge concerning the biological effects of fever in infected hosts and the influence of fever and antipyretic therapy on survival during sepsis in experimental models and in man.     

The constraints of selecting for insect resistance in plantation trees

• 1 High productivity in plantations of exotic tree species is achieved by management for fast growth in the absence of the full complex of co‐evolved insect herbivores. In the case of Eucalyptus, silvicultural selection for desirable wood traits is concomitant with a trade‐off against defence and a reduction of chemical and genetic diversity. These factors, combined with accidental introductions, rapid insect evolution and the emergence of new pests, increase the likelihood that future plantations will need insect pest management to maintain productivity.
• 2 Forestry researchers have suggested that selecting for resistant genotypes may be beneficial in insect control. There are, however, significant differences between long‐lived trees and annual crops that make this approach unlikely to be successful. This is illustrated using several examples of research into resistance to insect herbivores in trees.
• 3 Selection for resistance to insects in trees requires an assessment of trial plantations for heritable variation in insect damage and then a determination of the effect of variation in resistance on insect population parameters. Identifying rare resistant genotypes using markers is difficult because many factors interact to produce a resistant phenotype, and phytophagous insects have less intimate relationships with their host than pathogens, resulting in weak associations with genetic loci.
• 4 If resistant genotypes are identified, their widespread deployment in plantations might not provide satisfactory management of insect pests when the use of extensive monocultures is continued. In this paper, experiments are suggested that would explore the effectiveness of polycultures or chemotype mixtures with respect to ameliorating the damage of insects on plantation productivity. In addition, mitigating the effects of some insects on plantation productivity by maintaining vigour of fast‐growing eucalypts should be considered.

     

Knockdown of specific host factors protects against influenza virus-induced cell death

Cell death is a characteristic consequence of cellular infection by influenza virus. Mounting evidence indicates the critical involvement of host-mediated cellular death pathways in promoting efficient influenza virus replication. Furthermore, it appears that many signaling pathways, such as NF-κB, formerly suspected to solely promote cell survival, can also be manipulated to induce cell death. Current understanding of the cell death pathways involved in influenza virus-mediated cytopathology and in virus replication is limited. This study was designed to identify host genes that are required for influenza-induced cell death. The approach was to perform genome-wide lentiviral-mediated human gene silencing in A549 cells and determine which genes could be silenced to provide resistance to influenza-induced cell death. The assay proved to be highly reproducible with 138 genes being identified in independent screens. The results were independently validated using siRNA to each of these candidates. Graded protection was observed in this screen with the silencing of any of 19 genes, each providing >85% protection. Three gene products, TNFSF13 (APRIL), TNFSF12-TNFSF13 (TWE-PRIL) and USP47, were selected because of the high levels of protection conferred by their silencing. Protein and mRNA silencing and protection from influenza-induced cell death was confirmed using multiple shRNA clones and siRNA, indicating the specificity of the effects. USP47 knockdown prevented proper viral entry into the host cell, whereas TNFSF12-13/TNFSF13 knockdown blocked a late stage in viral replication. This screening approach offers the means to identify a large number of potential candidates for the analysis of viral-induced cell death. These results may also have much broader applicability in defining regulatory mechanisms involved in cell survival.