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1.
Plants have evolved a powerful immune system to defend against infection by most microbial organisms. However, successful pathogens, such as Pseudomonas syringae, have developed countermeasures and inject virulence proteins into the host plant cell to suppress immunity and cause devastating diseases. Despite intensive research efforts, the molecular targets of bacterial virulence proteins that are important for plant disease development have remained obscure. Here, we show that a conserved P. syringae virulence protein, HopM1, targets an immunity-associated protein, AtMIN7, in Arabidopsis thaliana. HopM1 mediates the destruction of AtMIN7 via the host proteasome. Our results illustrate a strategy by which a bacterial pathogen exploits the host proteasome to subvert host immunity and causes infection in plants. 相似文献
2.
Allen RL Bittner-Eddy PD Grenville-Briggs LJ Meitz JC Rehmany AP Rose LE Beynon JL 《Science (New York, N.Y.)》2004,306(5703):1957-1960
Plants are constantly exposed to attack by an array of diverse pathogens but lack a somatically adaptive immune system. In spite of this, natural plant populations do not often suffer destructive disease epidemics. Elucidating how allelic diversity within plant genes that function to detect pathogens (resistance genes) counteracts changing structures of pathogen genes required for host invasion (pathogenicity effectors) is critical to our understanding of the dynamics of natural plant populations. The RPP13 resistance gene is the most polymorphic gene analyzed to date in the model plant Arabidopsis thaliana. Here we report the cloning of the avirulence gene, ATR13, that triggers RPP13-mediated resistance, and we show that it too exhibits extreme levels of amino acid polymorphism. Evidence of diversifying selection visible in both components suggests that the host and pathogen may be locked in a coevolutionary conflict at these loci, where attempts to evade host resistance by the pathogen are matched by the development of new detection capabilities by the host. 相似文献
3.
Plant resistance proteins detect the presence of specific pathogen effectors and initiate effector-triggered immunity. Few immune regulators downstream of resistance proteins have been identified, none of which are known virulence targets of effectors. We show that Arabidopsis ENHANCED DISEASE SUSCEPTIBILITY1 (EDS1), a positive regulator of basal resistance and of effector-triggered immunity specifically mediated by Toll-interleukin-1 receptor-nucleotide binding-leucine-rich repeat (TIR-NB-LRR) resistance proteins, forms protein complexes with the TIR-NB-LRR disease resistance proteins RPS4 and RPS6 and with the negative immune regulator SRFR1 at a cytoplasmic membrane. Further, the cognate bacterial effectors AvrRps4 and HopA1 disrupt these EDS1 complexes. Tight association of EDS1 with TIR-NB-LRR-mediated immunity may therefore derive mainly from being guarded by TIR-NB-LRR proteins, and activation of this branch of effector-triggered immunity may directly connect to the basal resistance signaling pathway via EDS1. 相似文献
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5.
Schirawski J Mannhaupt G Münch K Brefort T Schipper K Doehlemann G Di Stasio M Rössel N Mendoza-Mendoza A Pester D Müller O Winterberg B Meyer E Ghareeb H Wollenberg T Münsterkötter M Wong P Walter M Stukenbrock E Güldener U Kahmann R 《Science (New York, N.Y.)》2010,330(6010):1546-1548
Biotrophic pathogens, such as the related maize pathogenic fungi Ustilago maydis and Sporisorium reilianum, establish an intimate relationship with their hosts by secreting protein effectors. Because secreted effectors interacting with plant proteins should rapidly evolve, we identified variable genomic regions by sequencing the genome of S. reilianum and comparing it with the U. maydis genome. We detected 43 regions of low sequence conservation in otherwise well-conserved syntenic genomes. These regions primarily encode secreted effectors and include previously identified virulence clusters. By deletion analysis in U. maydis, we demonstrate a role in virulence for four previously unknown diversity regions. This highlights the power of comparative genomics of closely related species for identification of virulence determinants. 相似文献
6.
真菌无毒基因克隆与抗性蛋白互作研究 总被引：1，自引：0，他引：1
无毒基因（avirulence genes, Avr）是病原物遗传因子,能诱发寄主植物产生抗病性。真菌Avr基因的克隆、编码产物结构和功能分析,以及与寄主抗性蛋白的互作机制等方面的研究对于深入了解植物的抗真菌病害分子机理具有重要意义。其编码AVR蛋白（又可以称为效应子,effector）通常富含半胱氨酸,效应子通过吸器或侵入丝被分泌到寄主细胞内促发抗性反应。在抗性反应过程中,效应子能直接或间接地被植物细胞相应的抗性蛋白识别,这种识别机制与效应子和抗性蛋白的区段相关。以几个真菌病害为例,综述了近年来有关无毒基因克隆、表达、以及与抗性蛋白的互作机制等方面的主要研究进展,以期为相关研究的深入提供参考。 相似文献
7.
Guttman DS Vinatzer BA Sarkar SF Ranall MV Kettler G Greenberg JT 《Science (New York, N.Y.)》2002,295(5560):1722-1726
Type III secreted "effector" proteins of bacterial pathogens play central roles in virulence, yet are notoriously difficult to identify. We used an in vivo genetic screen to identify 13 effectors secreted by the type III apparatus (called Hrp, for "hypersensitive response and pathogenicity") of the plant pathogen Pseudomonas syringae. Although sharing little overall homology, the amino-terminal regions of these effectors had strikingly similar amino acid compositions. This feature facilitated the bioinformatic prediction of 38 P. syringae effectors, including 15 previously unknown proteins. The secretion of two of these putative effectors was shown to be type III--dependent. Effectors showed high interstrain variation, supporting a role for some effectors in adaptation to different hosts. 相似文献
8.
Wu L Estrada O Zaborina O Bains M Shen L Kohler JE Patel N Musch MW Chang EB Fu YX Jacobs MA Nishimura MI Hancock RE Turner JR Alverdy JC 《Science (New York, N.Y.)》2005,309(5735):774-777
It is generally reasoned that lethal infections caused by opportunistic pathogens develop permissively by invading a host that is both physiologically stressed and immunologically compromised. However, an alternative hypothesis might be that opportunistic pathogens actively sense alterations in host immune function and respond by enhancing their virulence phenotype. We demonstrate that interferon-gamma binds to an outer membrane protein in Pseudomonas aeruginosa, OprF, resulting in the expression of a quorum-sensing dependent virulence determinant, the PA-I lectin. These observations provide details of the mechanisms by which prokaryotic organisms are directly signaled by immune activation in their eukaryotic host. 相似文献
9.
Signatures of adaptation to obligate biotrophy in the Hyaloperonospora arabidopsidis genome 总被引：2，自引：0，他引：2
Baxter L Tripathy S Ishaque N Boot N Cabral A Kemen E Thines M Ah-Fong A Anderson R Badejoko W Bittner-Eddy P Boore JL Chibucos MC Coates M Dehal P Delehaunty K Dong S Downton P Dumas B Fabro G Fronick C Fuerstenberg SI Fulton L Gaulin E Govers F Hughes L Humphray S Jiang RH Judelson H Kamoun S Kyung K Meijer H Minx P Morris P Nelson J Phuntumart V Qutob D Rehmany A Rougon-Cardoso A Ryden P Torto-Alalibo T Studholme D Wang Y Win J Wood J Clifton SW Rogers J Van den Ackerveken G Jones JD 《Science (New York, N.Y.)》2010,330(6010):1549-1551
Many oomycete and fungal plant pathogens are obligate biotrophs, which extract nutrients only from living plant tissue and cannot grow apart from their hosts. Although these pathogens cause substantial crop losses, little is known about the molecular basis or evolution of obligate biotrophy. Here, we report the genome sequence of the oomycete Hyaloperonospora arabidopsidis (Hpa), an obligate biotroph and natural pathogen of Arabidopsis thaliana. In comparison with genomes of related, hemibiotrophic Phytophthora species, the Hpa genome exhibits dramatic reductions in genes encoding (i) RXLR effectors and other secreted pathogenicity proteins, (ii) enzymes for assimilation of inorganic nitrogen and sulfur, and (iii) proteins associated with zoospore formation and motility. These attributes comprise a genomic signature of evolution toward obligate biotrophy. 相似文献
10.
In a wild plant-pathogen system, host resistance and pathogen virulence varied markedly among local populations. Broadly virulent pathogens occurred more frequently in highly resistant host populations, whereas avirulent pathogens dominated susceptible populations. Experimental inoculations indicated a negative trade-off between spore production and virulence. The nonrandom spatial distribution of pathogens, maintained through time despite high pathogen mobility, implies that selection favors virulent strains of Melampsora lini in resistant Linum marginale populations and avirulent strains in susceptible populations. These results are consistent with gene-for-gene models of host-pathogen coevolution that require trade-offs to prevent pathogen virulence increasing until host resistance becomes selectively neutral. 相似文献
11.
病原菌和植物相互作用时分泌效应蛋白（effectors）抑制植物的防卫反应。枯萎病是由尖孢镰刀菌引起的真菌病害,尖孢镰刀菌和寄主相互作用时分泌几个特定的富含半胱氨酸的小分子量蛋白（15.8～29.9 kD）进入木质部启动致病力,称为SIX（secreted in xylem）蛋白,其中,SIX6蛋白是一个效应蛋白。西瓜枯萎病是由西瓜专化型尖孢镰刀菌（Fusarium oxysporum f. sp.Niveurn,Fon）引起的真菌病害。为了明确FonSIX6在侵染西瓜时的作用,克隆了该基因的上下游序列,以潮霉素为筛选标记构建了该基因的缺失突变体载体pDH\|SIX6;将构建好的基因缺失载体转入农杆菌AGL\|1中,通过农杆菌介导的遗传转化和转化子的筛选获得了FonSIX6基因的缺失突变体。 相似文献
12.
Lebreton A Lakisic G Job V Fritsch L Tham TN Camejo A Matteï PJ Regnault B Nahori MA Cabanes D Gautreau A Ait-Si-Ali S Dessen A Cossart P Bierne H 《Science (New York, N.Y.)》2011,331(6022):1319-1321
Intracellular pathogens such as Listeria monocytogenes subvert cellular functions through the interaction of bacterial effectors with host components. Here we found that a secreted listerial virulence factor, LntA, could target the chromatin repressor BAHD1 in the host cell nucleus to activate interferon (IFN)-stimulated genes (ISGs). IFN-λ expression was induced in response to infection of epithelial cells with bacteria lacking LntA; however, the BAHD1-chromatin associated complex repressed downstream ISGs. In contrast, in cells infected with lntA-expressing bacteria, LntA prevented BAHD1 recruitment to ISGs and stimulated their expression. Murine listeriosis decreased in BAHD1(+/-) mice or when lntA was constitutively expressed. Thus, the LntA-BAHD1 interplay may modulate IFN-λ-mediated immune response to control bacterial colonization of the host. 相似文献
13.
在面对病原微生物的侵袭时,植物用2类先天性免疫系统对侵染做出免疫应答,第一类内免疫系统能识别很多种类微生物的共有分子并对其做出应答,第二类是对病原体分泌的毒力效应因子产生应答反应。该文根据最近的研究发现对植物免疫病原微生物的作用机理及研究进展进行了综述。 相似文献
14.
Orth K Xu Z Mudgett MB Bao ZQ Palmer LE Bliska JB Mangel WF Staskawicz B Dixon JE 《Science (New York, N.Y.)》2000,290(5496):1594-1597
Homologs of the Yersinia virulence effector YopJ are found in both plant and animal bacterial pathogens, as well as plant symbionts. These YopJ family members were shown to act as cysteine proteases. The catalytic triad of the protease was required for inhibition of the mitogen-activated protein kinase (MAPK) and nuclear factor kappaB (NF-kappaB) signaling in animal cells and for induction of localized cell death in plants. The substrates for YopJ were shown to be highly conserved ubiquitin-like molecules, which are covalently added to numerous regulatory proteins. YopJ family members exert their pathogenic effect on cells by disrupting this posttranslational modification. 相似文献
15.
利用酵母双杂交系统筛选感病番茄中蔬四号与无毒蛋白AvrPto、AvrPtoB互作的蛋白 总被引：1，自引：0，他引：1
【目的】利用酵母双杂交系统在感病番茄中蔬四号中筛选分别与AvrPto、AvrPtoB互作的蛋白,研究AvrPto、AvrPtoB作为毒性因子在感病番茄中的作用通路。【方法】提取感病番茄中蔬四号的总RNA,合成中蔬四号cDNA文库,分别构建AvrPto和AvrPtoB的诱饵载体,从中蔬四号cDNA文库中筛选分别与AvrPto、AvrPtoB互作的蛋白,并对阳性克隆进行分析和鉴定。【结果】最终筛选到7个与AvrPto互作的蛋白,2个与AvrPtoB互作的蛋白,核酮糖-1,5-二磷酸（RuBP）羧化酶/加氧酶小亚基和AvrPto、AvrPtoB都能够互作,说明AvrPto、AvrPtoB参与破坏植物的光合作用;另外与AvrPto互作的蛋白质还包括叶绿体原卟啉原氧化酶、叶绿体醛缩酶、叶绿体延伸因子TufA、翻译延伸因子等参与植物光合作用蛋白。【结论】分析筛选到的蛋白主要是参与植物光合作用的蛋白,推测AvrPto、AvrPtoB通过与植物光合作用有关的蛋白互作,或者影响卡尔文循环,或者影响叶绿素和相关蛋白质的合成,从而破坏植物光合作用,促进侵袭位点叶肉细胞衰老、死亡,进而引起坏死症状。 相似文献
17.
A secreted serine-threonine kinase determines virulence in the eukaryotic pathogen Toxoplasma gondii
Taylor S Barragan A Su C Fux B Fentress SJ Tang K Beatty WL Hajj HE Jerome M Behnke MS White M Wootton JC Sibley LD 《Science (New York, N.Y.)》2006,314(5806):1776-1780
Toxoplasma gondii strains differ dramatically in virulence despite being genetically very similar. Genetic mapping revealed two closely adjacent quantitative trait loci on parasite chromosome VIIa that control the extreme virulence of the type I lineage. Positional cloning identified the candidate virulence gene ROP18, a highly polymorphic serine-threonine kinase that was secreted into the host cell during parasite invasion. Transfection of the virulent ROP18 allele into a nonpathogenic type III strain increased growth and enhanced mortality by 4 to 5 logs. These attributes of ROP18 required kinase activity, which revealed that secretion of effectors is a major component of parasite virulence. 相似文献
18.
根瘤农杆菌T-DNA结合蛋白VirD2和VirE2在水稻中的亚细胞定位研究 总被引：1，自引：0，他引：1
根瘤农杆菌侵染植物过程中,至少有5种毒性蛋白（Vir）进入宿主细胞发挥作用,而其中VirD2与VirE2的作用最为关键,研究二者在水稻中的亚细胞定位,对农杆菌介导的水稻遗传转化机制的阐明具有重要意义。利用水稻叶鞘原生质体瞬时表达系统,发现3种冠瘿碱型的VirD2均只定位于细胞核中,与在拟南芥中相同;而3种冠瘿碱型的VirE2均主要定位于细胞核中,但在细胞质中仍有较多分布,与在拟南芥中的定位不同。因此,推测不同冠瘿碱型的农杆菌对水稻侵染能力的差异与VirD2和VirE2亚细胞定位的关系不大;同时表明根瘤农杆菌介导的拟南芥及水稻遗传转化机制存在相似性,但也有不同之处。 相似文献
19.
Antagonistic control of disease resistance protein stability in the plant immune system 总被引：1，自引：0，他引：1
Pathogen recognition by the plant immune system is governed by structurally related, polymorphic products of disease resistance (R) genes. RAR1 and/or SGT1b mediate the function of many R proteins. RAR1 controls preactivation R protein accumulation by an unknown mechanism. We demonstrate that Arabidopsis SGT1b has two distinct, genetically separable functions in the plant immune system: SGT1b antagonizes RAR1 to negatively regulate R protein accumulation before infection, and SGT1b has a RAR1-independent function that regulates programmed cell death during infection. The balanced activities of RAR1 and SGT1, in concert with cytosolic HSP90, modulate preactivation R protein accumulation and signaling competence. 相似文献
