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PubMedDate not supplied

Identification and DNA sequence of a pathogenicity gene of Xanthomonas campestris pv. campestris.

A region of Xanthomonas campestris pv. campestris DNA containing at least two pathogenicity genes was identified. Mutants in one gene were clearly reduced in pathogenicity while mutants in the other were only moderately reduced. Both classes of mutants were prototrophic and motile, and had wild-type levels of extracellular enzymes and extracellular polysaccharide. They also grew in vitro and in planta at the same rate as the wild type. Experiments involving one of the clear pathogenicity mutants indicated that the recovery of mutant cells from turnip seedlings 24 hr after inoculation was lower than for the wild type. This may be due to cell death as a result of action by some preformed or induced plant factor. From DNA sequencing an open reading frame was identified that encompassed the site of the mutations giving a clear reduction in pathogenicity. The predicted protein sequence had no homology with other proteins in the computer data base.

Amino Acid Sequence↗
PubMed1997

Identification of a pathogenicity locus, rpfA, in Erwinia carotovora subsp. carotovora subsp. carotovora that encodes a two-component sensor-regulator protein.

A mutant of Erwinia carotovora subsp. carotovora, AH2552, created by a Mud1 insertion was found to be reduced in plant pathogenicity and deficient in extracellular protease and cellulase activity, although it produced normal levels of pectate lyase and polygalacturonase. A cosmid clone, pEC462, was isolated from a wild-type E. carotovora subsp. carotovora DNA library that concomitantly restored pathogenicity and protease and cellulase activities of AH2552 to wild-type levels when present in trans. The genetic locus that was disrupted in AH2552 by insertion of Mud1 has been designated rpfA, for regulator of pathogenicity factors. Sequencing of the rpfA region identified an open reading frame of 2,787 bp, and the predicted 929-amino acid polypeptide shared high identity with several two-component sensor-regulator proteins: BarA from Escherichia coli, ApdA from Pseudomonas fluorescens, PheN from P. tolaasii, RepA from P. viridiflava, LemA from P. syringae pv. syringae, and RpfC from Xanthomonas campestris pv. campestris. The RpfA locus described in this study encodes a putative sensor kinase protein that is involved in both extracellular protease and cellulase production and the pathogenicity of E. carotovora subsp. carotovora on potato tubers.

Aconitate Hydratase↗
PubMed1998

Activation of hsr203, a plant gene expressed during incompatible plant-pathogen interactions, is correlated with programmed cell death.

hsr203J is a tobacco gene whose activation is rapid, highly localized, and specific for incompatible interactions between tobacco and the bacterial pathogen Ralstonia solanacearum. The effect of other hypersensitive response (HR)-inducing pathogens and elicitors has been tested with transgenic plants containing the hsr203J promoter-GUS reporter gene fusion, and confirms the generality of the preferential inducibility of the hsr203J gene promoter during incompatible interactions: bacterial and viral pathogens inducing an HR in tobacco were able to induce the promoter fusion, as were inducers of HR-like responses such as harpin, elicitins, and PopA1 proteins. A tomato hsr203 homologous cDNA was isolated (Lehsr203) and used to examine the effect of avr gene products on the expression of such genes. Lehsr203 was shown to be rapidly and transiently induced in leaves of the tomato Cf-9 line, following Avr9 product infiltration, but not in those of the Cf-0 line. Among potential effectors of HR or resistance such as H2O2, salicylic acid, methyl jasmonate, and 2,6-dichloro-isonicotinic acid (INA), none is able to induce a significant increase in promoter activation. In contrast, heavy metals that cause leaf necrosis can trigger such an activation. In addition, hsr203-GUS fusion expression is detected in transgenic tobacco lines expressing the bO gene and exhibiting spontaneous HR-like lesions. Taken together, these results demonstrate a strong correlation between hsr203 and genetically controlled cell death in tobacco and tomato. The expression of this gene should be a useful marker for programmed cell death occurring in response not only to diverse pathogens, but also to diverse death-triggering extracellular agents.

Amino Acid Sequence↗
PubMed1998

A pathogenicity gene isolated from the pPATH plasmid of Erwinia herbicola pv. gypsophilae determines host specificity.

The host range of the gall-forming bacterium Erwinia herbicola pv. gypsophilae (Ehg) is restricted to the gypsophila plant whereas E. herbicola pv. betae (Ehb) incites galls on beet as well as gypsophila. The pathogenicity of Ehg and Ehb was previously shown to be dependent on a plasmid (pPATH). Transposon mutagenesis was used to generate mutants on the cosmid pLA150 of the pPATH from Ehg824-1. A cluster of nonpathogenic mutations flanked by two IS1327 elements was identified on a 3.2-kb NdeI DNA fragment. All mutants were restored to pathogenicity by complementation in trans with the wild-type Ehg DNA. DNA sequence analysis of the 3.2-kb NdeI fragment revealed a single open reading frame (ORF) of 2 kb as well as a potential ribosome binding site and a putative hrp box upstream to the ORF. The ORF had no significant homology to known genes. Southern analysis also revealed the presence of DNA sequences that hybridized to the ORF in the beet pathovar Ehb4188. This gene was isolated and sequenced. Marker exchange mutants generated in the ORF of Ehb eliminated the pathogenicity of Ehb on gypsophila but fully retained its pathogenicity on beet. Since the putative gene appeared to encode a host-specific virulence factor for gypsophila it was designated as hsvG.

Amino Acid Sequence↗
PubMed1999

Identification of an ancestral resistance gene cluster involved in the coevolution process between Phaseolus vulgaris and its fungal pathogen Colletotrichum lindemuthianum.

The recent cloning of plant resistance (R) genes and the sequencing of resistance gene clusters have shed light on the molecular evolution of R genes. However, up to now, no attempt has been made to correlate this molecular evolution with the host-pathogen coevolution process at the population level. Cross-inoculations were carried out between 26 strains of the fungal pathogen Colletotrichum lindemuthianum and 48 Phaseolus vulgaris plants collected in the three centers of diversity of the host species. A high level of diversity for resistance against the pathogen was revealed. Most of the resistance specificities were overcome in sympatric situations, indicating an adaptation of the pathogen to the local host. In contrast, plants were generally resistant to allopatric strains, suggesting that R genes that were efficient against exotic strains but had been overcome locally were maintained in the plant genome. These results indicated that coevolution processes between the two protagonists led to a differentiation for resistance in the three centers of diversity of the host. To improve our understanding of the molecular evolution of these different specificities, a recombinant inbred (RI) population derived from two representative genotypes of the Andean (JaloEEP558) and Mesoamerican (BAT93) gene pools was used to map anthracnose specificities. A gene cluster comprising both Andean (Co-y; Co-z) and Mesoamerican (Co-9) host resistance specificities was identified, suggesting that this locus existed prior to the separation of the two major gene pools of P. vulgaris. Molecular analysis revealed a high level of complexity at this locus. It harbors 11 restriction fragment length polymorphisms when R gene analog (RGA) clones are used. The relationship between the coevolution process and diversification of resistance specificities at resistance gene clusters is discussed.

Amino Acid Sequence↗
PubMed2000

Restriction enzyme-mediated integration used to produce pathogenicity mutants of Colletotrichum graminicola.

We have developed a restriction enzyme-mediated insertional mutagenesis (REMI) system for the maize pathogen Colletotrichum graminicola. In this report, we demonstrate the utility of a REMI-based mutagenesis approach to identify novel pathogenicity genes. Use of REMI increased transformation efficiency by as much as 27-fold over transformations with linearized plasmid alone. Ninety-nine transformants were examined by Southern analysis, and 51% contained simple integrations consisting of one copy of the vector integrated at a single site in the genome. All appeared to have a plasmid integration at a unique site. Sequencing across the integration sites of six transformants demonstrated that in all cases the plasmid integration occurred at the corresponding restriction enzyme-recognition site. We used an in vitro bioassay to identify two pathogenicity mutants among 660 transformants. Genomic DNA flanking the plasmid integration sites was used to identify corresponding cosmids in a wild-type genomic library. The pathogenicity of one of the mutants was restored when it was transformed with the cosmids.

Blotting, Southern↗
PubMed2001

Overexpression of Pti5 in tomato potentiates pathogen-induced defense gene expression and enhances disease resistance to Pseudomonas syringae pv. tomato.

The tomato Pti5 gene encodes a pathogen-inducible ethylene response element-binding protein-like transcription factor that interacts with the disease resistance gene product Pto. Overexpression of Pti5 or Pti5-VP16, a translational fusion with a constitutive transcriptional activation domain, in tomato enhanced resistance to Pseudomonas syringae pv. tomato. Constitutive expression of Pti5 or Pti5-VP16 did not affect the basal level of pathogenesis-related gene expression, but it accelerated pathogen-induced expression of GluB and Catalase. The results demonstrate a positive role of Pti5 in defense gene regulation and disease resistance and suggest that a pathogen-activated posttranscriptional regulatory step is necessary for the pathogen induction of the defense gene expression.

DNA-Binding Proteins↗
PubMed2002

Ethylene insensitivity impairs resistance to soilborne pathogens in tobacco and Arabidopsis thaliana.

Transgenic ethylene-insensitive tobacco (Tetr) plants spontaneously develop symptoms of wilting and stem necrosis when grown in nonautoclaved soil. Fusarium oxysporum, F. solani, Thielaviopsis basicola, Rhizopus stolonifer, and two Pythium spp. were isolated from these diseased Tetr plants and demonstrated to be causal agents of the disease symptoms. Pathogenicity of the two Pythium isolates and four additional Pythium spp. was tested on ethylene-insensitive tobacco and Arabidopsis seedlings. In both plant species, ethylene insensitivity enhanced susceptibility to the Pythium spp., as evidenced by both a higher disease index and a higher percentage of diseased plants. Based on the use of a DNA probe specific for Pythium spp., Tetr plants exhibited more pathogen growth in stem and leaf tissue than similarly diseased control plants. These results demonstrate that ethylene signaling is required for resistance to different root pathogens and contributes to limiting growth and systemic spread of the pathogen.

Arabidopsis↗
PubMed2002

Constitutive expression of hrap gene in transgenic tobacco plant enhances resistance against virulent bacterial pathogens by induction of a hypersensitive response.

Hypersensitive response-assisting protein (HRAP) has been previously reported as an amphipathic plant protein isolated from sweet pepper that intensifies the harpin(Pss)-mediated hypersensitive response (HR). The hrap gene has no appreciable similarity to any other known sequences, and its activity can be rapidly induced by incompatible pathogen infection. To assess the function of the hrap gene in plant disease resistance, the CaMV 35S promoter was used to express sweet pepper hrap in transgenic tobacco. Compared with wild-type tobacco, transgenic tobacco plants exhibit more sensitivity to harpin(Pss) and show resistance to virulent pathogens (Pseudomonas syringae pv. tabaci and Erwinia carotovora subsp. carotovora). This disease resistance of transgenic tobacco does not originate from a constitutive HR, because endogenous level of salicylic acid and hsr203J mRNA showed similarities in transgenic and wildtype tobacco under noninfected conditions. However, following a virulent pathogen infection in hrap transgenic tobacco, hsr203J was rapidly induced and a micro-HR necrosis was visualized by trypan blue staining in the infiltration area. Consequently, we suggest that the disease resistance of transgenic plants may result from the induction of a HR by a virulent pathogen infection.

Base Sequence↗
PubMed2003

Analysis of gene expression in two growth states of Xylella fastidiosa and its relationship with pathogenicity.

Xylella fastidiosa is a plant pathogen responsible for diseases of economically important crops. Although there is considerable disagreement about its mechanism of pathogenicity, blockage of the vessels is one of the most accepted hypotheses. Loss of virulence by this bacterium was observed after serial passages in axenic culture. To confirm the loss of pathogenicity of X. fastidiosa, the causing agent of citrus variegated chlorosis (CVC), freshly-isolated bacteria (first passage [FP] condition) as well as bacteria obtained after 46 passages in axenic culture (several passage [SP] condition) were inoculated into sweet orange and periwinkle plants. Using real time quantitative polymerase chain reaction, we verified that the colonization of FP cells was more efficient for both hosts. The sequence of the complete X. fastidiosa genome allowed the construction of a DNA microarray that was used to investigate the total changes in gene expression associated with the FP condition. Most genes found to be induced in the FP condition were associated with adhesion and probably with adaptation to the host environment. This report represents the first study of the transcriptome of this pathogen, which has recently gained more importance, since the genome of several strains has been either partially or entirely sequenced.

Base Sequence↗
PubMed2004

Pseudomonas Type III effector AvrPto suppresses the programmed cell death induced by two nonhost pathogens in Nicotiana benthamiana and tomato.

Many gram-negative bacterial pathogens rely on a type III secretion system to deliver a number of effector proteins into the host cell. Though a number of these effectors have been shown to contribute to bacterial pathogenicity, their functions remain elusive. Here we report that AvrPto, an effector known for its ability to interact with Pto and induce Pto-mediated disease resistance, inhibited the hypersensitive response (HR) induced by nonhost pathogen interactions. Pseudomonas syringae pv. tomato T1 causes an HR-like cell death on Nicotiana benthamiana. This rapid cell death was delayed significantly in plants inoculated with P. syringae pv. tomato expressing avrPto. In addition, P. syringae pv. tabaci expressing avrPto suppressed nonhost HR on tomato prf3 and ptoS lines. Transient expression of avrPto in both N. benthamiana and tomato prf3 plants also was able to suppress nonhost HR. Interestingly, AvrPto failed to suppress cell death caused by other elicitors and nonhost pathogens. AvrPto also failed to suppress cell death caused by certain gene-for-gene disease resistance interactions. Experiments with avrPto mutants revealed several residues important for the suppression effects. AvrPto mutants G2A, G99V, P146L, and a 12-amino-acid C-terminal deletion mutant partially lost the suppression ability, whereas S94P and 196T enhanced suppression of cell death in N. benthamiana. These results, together with other discoveries, demonstrated that suppression of host-programmed cell death may serve as one of the strategies bacterial pathoens use for successful invasion.

Agrobacterium tumefaciens↗
PubMed1990

Pathogenic idiotypes of autoantibodies in autoimmunity: lessons from new experimental models of SLE.

Systemic lupus erythematosus (SLE) is considered a classical autoimmune disease that involves many biological systems. Similar to other autoimmune conditions, its etiology is multifactorial entailing genetic, environmental, hormonal, and immunologic factors. In this review we demonstrate that by using a pathogenic idiotype of anti-DNA autoantibodies, it is possible to explain some of the pathogenesis and diversity of clinical and serological manifestations reported by SLE patients. The 16/6 idiotype (Id) is a representative pathogenic idiotype of anti-DNA autoantibodies. The serum titers of 16/6 Id in SLE patients correlate with clinical activity of the disease, and are deposited in afflicted tissues in SLE patients. SLE was experimentally induced in naive mice after immunization with 1 microgram of the Id. The disease is characterized clinically (proteinuria), serologically (e.g., anti-dsDNA, anti-Sm antibodies), and by pathological findings (e.g., deposition of 16/6 Id in the kidneys). The condition can be induced by other human and mouse antibodies carrying the 16/6 Id, as well as by mouse antimonoclonal-16/6 Id and by T cell lines and clones specifically reactive with 16/6 Id. There are strain-dependent differences in susceptibility to the induction of systemic lupus erythematosus (SLE). Induction of SLE is directly correlated with the ability to respond to the 16/6 idiotype (or 16/6 Id)2 by anti-Id antibody production. It is easier to induce the disease in females, and it can be modulated by manipulation of sex hormones. Being able to identify the pathogenic idiotype allowed us to generate T suppressor (Ts) cells specific for the 16/6 Id. Treatment of mice with these T cells abrogated the disease. Our studies point to the importance of pathogenic idiotypes of autoantibodies in autoimmunity, which suggests that SLE may represent a dysregulation of a functional network of idiotypes-anti-idiotypes interactions among autoreactive B cells, T helper cells, and T suppressor cells.

Animals↗
PubMed2003

Human metapneumovirus: a newly emerging respiratory pathogen.

PURPOSE OF REVIEW: The present review focuses on the recent discovery, and clinical and epidemiological features of a virus associated with respiratory tract infections. RECENT FINDINGS: In June 2001, researchers in The Netherlands reported the discovery of a virus associated with respiratory tract disease in infants and children. Genetic studies of this newly discovered viral pathogen revealed that it was a paramyxovirus. This virus is the first human pathogen in the Genus Metapneumovirus and was called human metapneumovirus (hMPV). hMPV may be a common respiratory virus. Seroepidemiologic studies in The Netherlands suggested that, by age 5 years, nearly all individuals have been exposed to hMPV. The results of several studies suggest that hMPV may account for about 10% of respiratory tract infections in which a common respiratory virus, such as respiratory syncytial virus, or influenza or parainfluenza viruses, could not be detected. hMPV has been detected in patients with either upper or lower respiratory tract disease, or both. Symptoms associated with hMPV include cough, dyspnea, wheeze, and hypoxia. This newly recognized pathogen has been detected in children and adults. Epidemiological findings suggest that it may circulate worldwide and may have a seasonal distribution. SUMMARY: hMPV is a newly emerging respiratory pathogen and may be the cause of a significant proportion of both upper and lower respiratory tract infection in infants, children, and adults.

Adolescent↗
PubMed2001

Conserved CXCR4 usage and enhanced replicative capacity of HIV-2/287, an isolate highly pathogenic in Macaca nemestrina.

OBJECTIVE: To investigate viral properties that contribute to the pathogenic potential of HIV-2 in macaques. DESIGN: We compared HIV-2/287, a virus highly pathogenic in Macaca nemestrina, with its non-pathogenic progenitor HIV-2 EHO, for coreceptor usage and ability to infect human and macaque peripheral blood mononuclear cells (PBMC). METHODS: Coreceptor usage was determined in GHOST cells expressing known coreceptors, and in PBMC with coreceptor-specific inhibitors. Infectivity in PBMC was determined by virus titration and p27 antigen production. Early and late products of reverse transcription were measured by PCR with primers specific for the long terminal repeat (LTR), or the gag region, respectively. RESULTS: Both viruses preferentially infect HOS-CD4 cells expressing CXCR4. Inhibition by CXCR4-specific peptide TW70 and monoclonal antibody 12G5 indicated that both viruses use predominantly CXCR4 to infect macaque and human PBMC. HIV-2/287 showed greater infectivity than HIV-2 EHO in macaque cells, but the situation was reversed in human cells. Kinetic analysis of reverse transcription products revealed no restriction in reverse transcription following HIV-2 EHO infection of macaque PBMC. However, comparison of the level of newly initiated HIV-2 EHO DNA in macaque and human PBMC indicated that there is an early restriction, prior to the initiation of reverse transcription. CONCLUSIONS: Results indicate that the adaptation of HIV-2 EHO in M. nemestrina to a highly pathogenic virus HIV-2/287 is not correlated with a shift in or an expansion of coreceptor usage, but with the acquisition of an ability to overcome restrictions for growth in macaque PBMC.

Animals↗
PubMedDate not supplied

Interleukin-18 and host defense against infectious pathogens.

Host defense to infectious pathogens is largely mediated by neutrophil-, cellular, or humoral immunity or eosinophil-dependent mechanism. Each mechanism preferentially acts against extracellular or intracellular microbial pathogens, viruses, or helminthes. These host defense responses are strictly regulated by two different categories of cytokines, T helper (Th)1 and Th2 cytokines. Interleukin-18, originally found as interferon-gamma-inducing factor, has now been identified to be involved in the development of Th1 and Th2 cells, which suggests the considerable involvement of this cytokine in the protective immune responses against infection. This review focuses on the role of interleukin-18 in the development and regulation of host resistance to infectious pathogens, with an emphasis on the infection with Cryptococcus neoformans, an intracellular fungal pathogen, as determined by recent studies from our laboratory.

Animals↗
PubMed1997

Incidence, etiologic pathogens, and diagnostic testing of community-acquired pneumonia.

Determination of the etiologic pathogens of community-acquired pneumonia has been problematic because of the lack of reliable rapid laboratory diagnostic tools as well as the controversy concerning diagnostic criteria. In the studies reviewed here, a specific pathogen was identified in 39% to 88% of patients. Streptococcus pneumoniae remains the most common cause of community-acquired pneumonia. Depending on the demographics of the study, between 2% to 43% of cases have been attributed to legionella or Chlamydia pneumoniae. More recently, other pathogens have emerged, including respiratory syncytial virus in adults, hantavirus, and possibly legionella-like amoebal pathogens and Streptococcus milleri group. Treatment guidelines published by various societies of experts have been helpful, but they cannot replace the need for better and rapid diagnostic techniques.

AIDS-Related Opportunistic Infections↗
PubMed1997

Atypical pathogen pneumonia.

The term atypical pathogens has been applied in recent years to Chlamydia pneumoniae, Mycoplasma pneumoniae, and the various species of Legionella. The incidence of pneumonia caused by these pathogens has increased with the development of specific diagnostic techniques. Atypical pathogen community-acquired pneumonia demonstrates a broad spectrum of severity from a mild disease not requiring hospitalization to adult respiratory distress syndrome necessitating mechanical ventilation. The clinical, radiological, and laboratory manifestations of the disease are similar to those of community-acquired pneumonia caused by other pathogens, and reliable etiological differentiation cannot be based on these factors alone. The possibility of shortening treatment time, at least in some patients, by antibiotic therapy with the new macrolides has been added to standard therapeutic regimens with erythromycin, tetracyclines, or quinolones.

Chlamydia Infections↗
PubMed2001

Pathogenic determinants of the mucosally transmissible CXCR4-specific SHIV(SF33A2) map to env region.

Infection of rhesus macaques with chimeric simian-human immunodeficiency viruses (SHIV) is an established method to study AIDS pathogenesis and is increasingly used to assess the efficacy of vaccine and antiviral candidates. For these reasons, a detailed understanding of those molecular determinants, which confer pathogenic potential to SHIV viruses, should assist in both rational experimental design and interpretation of results. In this report, we describe the development and in vivo characterization of a pathogenic molecular clone, SHIVSF33A2, which contains an envelope sequence derived from the CXCR4-dependent isolate, HIV-1SF33. Proviral DNA, amplified from a rhesus macaque infected with the pathogenic isolate SHIVSF33A, was substituted into the corresponding region of the parental, nonpathogenic SHIVSF33 genome creating the molecular clone SHIVSF33A2. Coreceptor specificity of SHIVSF33A2 was determined to be CXCR4 specific. Naive rhesus macaques were productively infected after a single exposure to cell-free SHIVSF33A2 by either the intravenous (IV) or intravaginal (IVAG) routes. Animals infected with SHIVSF33A2 suffered a severe loss of peripheral CD4+ T cells and high acute plasma viremia with development of simian AIDS 9 months after inoculation. Sequence analysis identified 25 discreet amino acid changes within the V1-V5 regions of the envelope protein when compared with the nonpathogenic parental virus. These data indicate that domains within the HIV-1 envelope protein are sufficient to define pathogenic potential in the context of the SIVmac239 genome.

Amino Acid Sequence↗