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PubMed2002

cag pathogenicity island of Helicobacter pylori in Korean children.

BACKGROUND: cag pathogenicity island is reported to be a major virulence factor of Helicobacter pylori. The aim of this study was to investigate the status of cag pathogenicity island genes and gastric histology in Korean children with H. pylori gastritis. METHODS: Helicobacter pylori DNA was extracted from antral biopsy specimens from 25 children with H. pylori gastritis. Specific polymerase chain reaction assays were used for four genes of cag pathogenicity island. The features of gastritis were scored in accordance with the updated Sydney System. RESULTS: cagA was present in 23 (92%) of 25 children, and cagE in 24 (96%). Twenty-two (88%) children were cagT positive and 19 (76%) virD4 positive. All of the selected genes of the cag pathogenicity island were present in 17 (68%) children and completely deleted in one child. There were no differences in neutrophil activity and chronic inflammation between children infected with intact cag pathogenicity island strains and those with partially or totally deleted-cag pathogenicity island strains. CONCLUSION: cag pathogenicity island is not a uniform, conserved entity in Korea. Completeness of cag pathogenicity island may not be the major factor to determine the severity of H. pylori gastritis in children.

Adolescent↗

PubMedDate not supplied

Broad-range PCR-TTGE for the first-line detection of bacterial pathogen DNA in ticks.

Ticks are known or suspected vectors for a wide range of bacterial pathogens. One of the first steps for tick-borne risk assessment is the detection of these pathogens in their vectors. In the present study, a broad-range PCR amplification of the eubacterial gene encoding the 16S rRNA gene combined with Temporal Temperature Gradient gel Electrophoresis (TTGE) was evaluated as a method allowing the one-step detection of bacterial pathogen DNA in ticks. Firstly, DNA extracts from bacteria known to be tick-borne pathogens, i.e., Borrelia burgdorferi lato sensu, Anaplasma phagocytophilum, Spotted Fever Group (SFG) Rickettsia spp., were used to establish a TTGE pathogen DNA reference marker. Secondly, we used broad-range PCR-TTGE to detect the presence of DNA from these three pathogens in 55 DNA extracts from pools of 10 nymphal Ixodes ricinus ticks, which have been previously shown to carry DNA from at least one of those bacteria by specific PCR. Among the 20 B. burgdorferi specific-PCR samples, 15 (75%) were also found to be positive using PCR-TTGE. Sixteen of the seventeen (94%) Rickettsia spp. PCR-specific samples were positive using PCR-TTGE detection and all PCR-specific positive extracts (11/11, 100%) for A. phagocytophilum were also positive using PCR-TTGE. Moreover, we identified unexpected bacterial sequences that were not related to any of the three pathogens such as a sequence related to Spiroplasma sp. Thus, broad-range PCR-TTGE allowed the single step detection of DNA from up to 3 pathogens in the same co-infected samples as well as detection of DNA from unexpected bacteria.

Anaplasma phagocytophilum↗

PubMed1999

Transgenic tobacco plants with reduced capability to detoxify reactive oxygen intermediates are hyperresponsive to pathogen infection.

Reactive oxygen intermediates (ROI) play a critical role in the defense of plants against invading pathogens. Produced during the "oxidative burst," they are thought to activate programmed cell death (PCD) and induce antimicrobial defenses such as pathogenesis-related proteins. It was shown recently that during the interaction of plants with pathogens, the expression of ROI-detoxifying enzymes such as ascorbate peroxidase (APX) and catalase (CAT) is suppressed. It was suggested that this suppression, occurring upon pathogen recognition and coinciding with an enhanced rate of ROI production, plays a key role in elevating cellular ROI levels, thereby potentiating the induction of PCD and other defenses. To examine the relationship between the suppression of antioxidative mechanisms and the induction of PCD and other defenses during pathogen attack, we studied the interaction between transgenic antisense tobacco plants with reduced APX or CAT and a bacterial pathogen that triggers the hypersensitive response. Transgenic plants with reduced capability to detoxify ROI (i.e., antisense APX or CAT) were found to be hyperresponsive to pathogen attack. They activated PCD in response to low amounts of pathogens that did not trigger the activation of PCD in control plants. Our findings support the hypothesis that suppression of ROI-scavenging enzymes during the hypersensitive response plays an important role in enhancing pathogen-induced PCD.

Apoptosis↗

PubMed2002

Control of morphogenesis in the human fungal pathogen Penicillium marneffei.

Fungal pathogens are an increasing threat to human health due to the increasing population of immunocompromised individuals and the increased incidence of treatment-derived infections. Penicillium marneffei is an emerging fungal pathogen endemic to South-east Asia, where it is AIDS defining. Like many other fungal pathogens, P. marneffei is capable of alternating between a filamentous and a yeast growth form, known as dimorphic switching, in response to environmental stimuli. P. marneffei grows in the filamentous form at 25 degrees C and in the yeast form at 37 degrees C. During filamentous growth and in response to environmental cues, P. marneffei undergoes asexual development to form complex multicellular structures from which the infectious agents, the conidia, are produced. At 37 degrees C, P. marneffei undergoes the dimorphic switching program to produce the pathogenic yeast cells. These yeast cells are found intracellularly in the mononuclear phagocyte system of the host and divide by fission, in contrast to the budding mode of division exhibited by most other fungal pathogens. In addition, P. marneffei is evolutionarily distinct from most other dimorphic fungal pathogens and is the only known Penicillium species which exhibits dimorphic growth. The unique evolutionary history of P. marneffei and the rapidly increasing incidence of infection, coupled with the presence of both complex asexual development and dimorphic switching programs in one organism, makes this system a valuable one for the study of morphogenesis and pathogenicity. Recent development of molecular genetic techniques for P. marneffei, including DNA-mediated transformation, have greatly facilitated the study of these two important morphogenetic programs, asexual development and dimorphic switching, and we are beginning to uncover important determinants which control these events. Understand these programs is providing insights into the biology of P. marneffei and its pathogenic capacity.

Cell Division↗

PubMed2005

Toward understanding the risk of secondary airborne infection: emission of respirable pathogens.

Certain respiratory tract infections are transmitted through air. Coughing and sneezing by an infected person can emit pathogen-containing particles with diameters less than 10 microm that can reach the alveolar region. Based on our analysis of the sparse literature on respiratory aerosols, we estimated that emitted particles quickly decrease in diameter due to water loss to one-half the initial values, and that in one cough the volume in particles with initial diameters less than 20 microm is 60 x 10(-8) mL. The pathogen emission rate from a source case depends on the frequency of expiratory events, the respirable particle volume, and the pathogen concentration in respiratory fluid. Viable airborne pathogens are removed by exhaust ventilation, particle settling, die-off, and air disinfection methods; each removal mechanism can be assigned a first-order rate constant. The pathogen concentration in well-mixed room air depends on the emission rate, the size distribution of respirable particles carrying pathogens, and the removal rate constants. The particle settling rate and the alveolar deposition fraction depend on particle size. Given these inputs plus a susceptible person's breathing rate and exposure duration to room air, an expected alveolar dosemicrois estimated. If the infectious dose is one organism, as appears to be true for tuberculosis, infection risk is estimated by the expression: R = 1-exp(-micro). Using published tuberculosis data concerning cough frequency, bacilli concentration in respiratory fluid, and die-off rate, we illustrate the model via a plausible scenario for a person visiting the room of a pulmonary tuberculosis case. We suggest that patients termed "superspreaders" or "dangerous disseminators" are those infrequently encountered persons with high values of cough and/or sneeze frequency, elevated pathogen concentration in respiratory fluid, and/or increased respirable aerosol volume per expiratory event such that their pathogen emission rate is much higher than average.

Aerosols↗

PubMed1999

An inhibitor of exported Mycobacterium tuberculosis glutamine synthetase selectively blocks the growth of pathogenic mycobacteria in axenic culture and in human monocytes: extracellular proteins as potential novel drug targets.

Mycobacterium tuberculosis and other pathogenic mycobacteria export abundant quantities of proteins into their extracellular milieu when growing either axenically or within phagosomes of host cells. One major extracellular protein, the enzyme glutamine synthetase, is of particular interest because of its link to pathogenicity. Pathogenic mycobacteria, but not nonpathogenic mycobacteria, export large amounts of this protein. Interestingly, export of the enzyme is associated with the presence of a poly-L-glutamate/glutamine structure in the mycobacterial cell wall. In this study, we investigated the influence of glutamine synthetase inhibitors on the growth of pathogenic and nonpathogenic mycobacteria and on the poly-L-glutamate/glutamine cell wall structure. The inhibitor L-methionine-S-sulfoximine rapidly inactivated purified M. tuberculosis glutamine synthetase, which was 100-fold more sensitive to this inhibitor than a representative mammalian glutamine synthetase. Added to cultures of pathogenic mycobacteria, L-methionine- S-sulfoximine rapidly inhibited extracellular glutamine synthetase in a concentration-dependent manner but had only a minimal effect on cellular glutamine synthetase, a finding consistent with failure of the drug to cross the mycobacterial cell wall. Remarkably, the inhibitor selectively blocked the growth of pathogenic mycobacteria, all of which release glutamine synthetase extracellularly, but had no effect on nonpathogenic mycobacteria or nonmycobacterial microorganisms, none of which release glutamine synthetase extracellularly. The inhibitor was also bacteriostatic for M. tuberculosis in human mononuclear phagocytes (THP-1 cells), the pathogen's primary host cells. Paralleling and perhaps underlying its bacteriostatic effect, the inhibitor markedly reduced the amount of poly-L-glutamate/glutamine cell wall structure in M. tuberculosis. Although it is possible that glutamine synthetase inhibitors interact with additional extracellular proteins or structures, our findings support the concept that extracellular proteins of M. tuberculosis and other pathogenic mycobacteria are worthy targets for new antibiotics. Such proteins constitute readily accessible targets of these relatively impermeable organisms, which are rapidly developing resistance to conventional antibiotics.

Aminobutyrates↗

PubMed1992

Predominant pathogens in hospital infections.

To determine the distribution of pathogens causing nosocomial infections in United States hospitals, we analysed data from the National Nosocomial Infections Surveillance (NNIS) System. From October 1986 to December 1990, amongst hospitals conducting hospital-wide surveillance, the five most commonly reported pathogens were Escherichia coli (13.7%), Staphylococcus aureus (11.2%), enterococci (10.7%), Pseudomonas aeruginosa (10.1%), and coagulase-negative staphylococci (9.7%). The commonest pathogens reported by site included, bloodstream: coagulase-negative staphylococci, S. aureus, enterococci, E. coli, and Candida spp.; lower respiratory tract infection: S. aureus, P. aeruginosa and Enterobacter spp.; surgical wound infection: S. aureus, enterococci and coagulase-negative staphylococci; and urinary tract infection: E. coli, enterococci, and P. aeruginosa. Among hospitals conducting intensive care unit (ICU) surveillance, the commonest pathogens were P. aeruginosa (12.4%), S. aureus (12.3%), coagulase-negative staphylococci (10.2%), Candida spp. (10.1%), Enterobacter spp. and enterococci (8.6% each). In the ICUs, the commonest pathogens found in the bloodstream were coagulase-negative staphylococci, S. aureus, and enterococci; in lower respiratory tract infections P. aeruginosa, S. aureus, and enterococci; in surgical wound infections enterococci, coagulase-negative staphylococci, and Enterobacter spp. and in urinary tract infections Candida spp., E. coli, enterococci, P. aeruginosa, and Enterobacter spp. These data show that S. aureus, E. coli and P. aeruginosa remain important nosocomial pathogens, that coagulase-negative staphylococci, enterococci and C. albicans are pathogens of increasing importance, and that the distribution of pathogens differs by site and hospital location.

Adult↗

PubMed2026

Frequency and clinical features of germline pathogenic variants in sarcoma: a case-control study.

BACKGROUND: Germline multigene panel testing is not yet integrated into standard care for patients with sarcoma. This study aimed to assess the frequency and distribution of germline pathogenic variants in patients with sarcoma compared with cancer-free controls and identify differences between patients with and without germline pathogenic variants. METHODS: This retrospective cohort included 488 sarcoma patients and 2440 cancer-free controls matched 1:5 by age, sex, and ethnicity. Multigene panel testing was performed between 2016 and 2024 at a single germline testing laboratory. The frequency of germline pathogenic variants in selected genes was compared using Fisher exact test with odds ratios (ORs) and 95% confidence intervals. Additionally, within the case-only cohort, clinical characteristics were evaluated to assess associations with the presence of germline pathogenic variants in any gene. RESULTS: Among 488 patients with sarcoma, 67.8% (n = 331) were female, with a median age at sarcoma diagnosis of 47 years (range = 0.5-87.5 years). Cases had a higher frequency of germline pathogenic variants compared with controls (26.2% vs 10.5%; OR = 3.05, P < .001). We observed a higher frequency of germline pathogenic variants in TP53, BRCA2, CHEK2, NF1, SDHA, BRIP1, POT1, RB1, and CDH1 among patients with sarcoma compared with controls. Age at sarcoma diagnosis did not differ between groups. CONCLUSIONS: This study confirms the high detection rate of germline pathogenic variants in patients with sarcoma and describes several associated genes. These findings indicate that age at sarcoma diagnosis may not reliably predict germline pathogenic variants. Expanding germline testing for patients with sarcoma would enhance personalized treatment strategies and familial risk assessment.

Humans↗

PubMed1992

Molecular evolution of the fungi: human pathogens.

The morphological, ecological, and clinical diversity among ascomycete fungi that are pathogenic to humans suggest that the potential for pathogenicity may have arisen multiple times within these higher fungi. We have obtained 18S ribosomal DNA sequences from a diverse group of human pathogenic fungi in order to determine their evolutionary origins. The fungi studied include a skin pathogen that is confined to humans (Trichophyton rubrum) and three systemic, facultative parasites that cause histoplasmosis (Histoplasma capsulatum), blastomycosis (Blastomyces dermatitidis) and coccidioidomycosis (Coccidioides immitis) in humans and other higher animals. Also included in our analysis are representatives of non-pathogenic fungi, as well as two opportunistic pathogens, Pneumocystis carinii and Candida albicans, that cause severe disease in immunocompromised individuals, especially those with AIDS. Two of the fungi we sequenced, T. rubrum and C. immitis, are limited to asexual modes of reproduction and therefore lack the sexual structures that are most useful for evolutionary comparison as well as being essential for classification among the higher fungi. Coccidioides immitis is particularly problematic owing to its contradictory and confusing asexual morphologies, which have caused it to be placed in three fungal classes and the protista. Our analysis shows that the specialized, superficial parasite and the systemic, facultative parasites, including C. immitis, are closely related ascomycetes, which clearly demonstrates the power of molecular characters to compensate for missing or confusing reproductive morphology. Analysis also shows that the opportunistic pathogens are more distantly related, with the likely explanation that pathogenicity has arisen more than once within the Ascomycetes.

Base Sequence↗

PubMed2005

Alternatives to antibiotics: chemical and physical antimicrobial interventions and foodborne pathogen response.

Successful control of foodborne pathogens requires placement of chemical and physical hurdles in the preharvest and postharvest food production sectors. Pathogens may also encounter indigenous antimicrobials in foods including certain botanical compounds that have historically been used for flavor enhancement as well as preservation. Chemical additives have traditionally included organic acids to control microbial contamination in foods and feeds. However, there is some concern that continuous application of certain chemical antimicrobials can lead to a buildup of microbial resistance. This creates problems if foodborne pathogens survive and develop resistance to a variety of environmental stressors encountered in pre- and postharvest animal production. To expand the diversity of potential antimicrobials that have practical application to food animal production requires exploring the interaction between the food matrix and foodborne pathogens. There is potential for isolating antimicrobial compounds that exhibit mechanisms unrelated to conventional antimicrobial compounds. However, understanding the potential for novel antimicrobial compounds in foods and feeds will require the physiological examination of foodborne pathogen response under experimental conditions comparable to the environment where the pathogen is most likely to occur. Research on foodborne Salmonella pathogenesis is extensive and should provide a model for detailed examination of the factors that influence antimicrobial effectiveness. Analysis of pathogen response to antimicrobials could yield clues for optimizing hurdle technologies to more effectively exploit vulnerabilities of Salmonella and other foodborne pathogens when administering antimicrobials during food and feed production.

Animal Feed↗

PubMed2006

Reducing the carriage of foodborne pathogens in livestock and poultry.

Several foodborne pathogens, including Salmonella species and campylobacters, are common contaminants in poultry and livestock. Typically, these pathogens are carried in the animal's intestinal tract asymptomatically; however, they can be shed in feces in large populations and be transmitted by other vectors from feces to animals, produce, or humans. A wide array of interventions has been developed to reduce the carriage of foodborne pathogens in poultry and livestock, including genetic selection of animals resistant to colonization, treatments to prevent vertical transmission of enteric pathogens, sanitation practices to prevent contamination on the farm and during transportation, elimination of pathogens from feed and water, feed and water additives that create an adverse environment for colonization by the pathogen, and biological treatments that directly or indirectly inactivate the pathogen within the host. To successfully reduce the carriage of foodborne pathogens, it is likely that a combination of intervention strategies will be required.

Animal Feed↗

PubMed2004

Immunomodulation and sepsis: impact of the pathogen.

Infection begins when microorganisms overcome host barriers and multiply within host tissues. To contain the infection, the host mounts an inflammatory response that mobilizes defense systems and kills the invading microorganisms. A focal inflammatory response is usually sufficient to eradicate the organisms. However, when it fails to contain the infection, the organisms, their toxins, and numerous host mediators are released into the bloodstream, producing a systemic inflammatory response and organ failure. Microorganisms have coevolved with their hosts, thereby acquiring means of overcoming host defense mechanisms or even taking advantage of innate host responses. Many pathogens avoid recognition by the host or dampen host immune responses via sophisticated pathogen-host interactions. Some pathogens benefit from the inflammatory response. According to current hypotheses regarding the pathogenesis of sepsis, the host generates both an innate immune response identical for all pathogens and an adaptive pathogen-specific response. Determining whether the innate response benefits the pathogen or the host is essential for understanding host-pathogen interactions. In this review, we discuss how pathogens interfere with innate and adaptive immune responses to escape eradication by the host.

Humans↗

PubMed2004

Transmission rates and adaptive evolution of pathogens in sympatric heterogeneous plant populations.

Diversification in agricultural cropping patterns is widely practised to delay the build-up of virulent races that can overcome host resistance in pathogen populations. This can lead to balanced polymorphism, but the long-term consequences of this strategy for the evolution of crop pathogen populations are still unclear. The widespread occurrence of sibling species and reproductively isolated sub-species among fungal and oomycete plant pathogens suggests that evolutionary divergence is common. This paper develops a mathematical model of host-pathogen interactions using a simple framework of two hosts to analyse the influences of sympatric host heterogeneity on the long-term evolutionary behaviour of plant pathogens. Using adaptive dynamics, which assumes that sequential mutations induce small changes in pathogen fitness, we show that evolutionary outcomes strongly depend on the shape of the trade-off curve between pathogen transmission on sympatric hosts. In particular, we determine the conditions under which the evolutionary branching of a monomorphic into a dimorphic population occurs, as well as the conditions that lead to the evolution of specialist (single host range) or generalist (multiple host range) pathogen populations.

Adaptation, Physiological↗

PubMed2006

Pathogen responses to host immunity: the impact of time delays and memory on the evolution of virulence.

Current analytical models of the mammalian immune system typically assume a specialist predator-prey relationship between invading pathogens and the active components of the immune response. However, in reality, the specific immune system is not immediately effective following invasion by a novel pathogen. First, there may be an explicit time delay between infection and immune initiation and, second, there may be a gradual build-up in immune efficacy (for instance, during the period of B-cell affinity maturation) during which the immune response develops, before reaching maximal specificity to the pathogen. Here, we use a novel theoretical approach to show that these processes, together with the presence of long-lived immune memory, decouple the immune response from current pathogen levels, greatly changing the dynamics of the pathogen-immune system interaction and the ability of the immune response to eliminate the pathogen. Furthermore, we use this model to show how distributed primary immune responses combine with immune memory to greatly affect the optimal virulence of the pathogen, potentially resulting in the evolution of highly virulent pathogens.

Animals↗

PubMed2001

The emergence of rabbit haemorrhagic disease virus: will a non-pathogenic strain protect the UK?

Rabbit haemorrhagic disease virus emerged in China in 1984, and has killed hundreds of millions of wild rabbits in Australia and Europe. In the UK there appears to be an endemic non-pathogenic strain, with high levels of seroprevalence being recorded, in the absence of associated mortality. Using a seasonal, age-structured model we examine the hypothesis that differences in rabbit population demography differentially affect the basic reproductive rates (R(0)) of the pathogenic and non-pathogenic strains, leading to each dominating in some populations and not others. The strain with the higher R(0) excluded the other, with the dynamics depending upon the ratio of the two R(0) values. When the non-pathogenic strain dominated, the pathogenic strain caused only transient mortality, although this could be significant when the two R(0) values were similar. When the pathogenic strain dominated, repeated epidemics led to host eradication. Seroprevalence data suggest that the non-pathogenic strain may be protecting some, but not all UK populations, with half being 'at risk' from invasion by the pathogenic strain and a fifth prone to significant transient mortality. We identify key questions for empirical research to test this prediction.

Animals↗

PubMed2002

Pseudomonas salomonii sp. nov., pathogenic on garlic, and Pseudomonas palleroniana sp. nov., isolated from rice.

A total of 26 strains, including 15 strains isolated from garlic plants with the typical symptoms of 'Café au lait' disease and 11 strains isolated from diseased or healthy rice seeds and sheaths infested by Pseudomonas fuscovaginae, were compared with 70 type or reference strains of oxidase-positive pathogenic or non-pathogenic fluorescent pseudomonads. The strains were characterized by using a polyphasic taxonomic approach. Numerical taxonomy of phenotypic characteristics showed that the garlic and rice strains were related to each other. However, they clustered into separate phenons, distinct from those of the other strains tested, and were different in several nutritional tests. On the basis of DNA-DNA hybridization, the garlic and rice strains constituted two distinct DNA hybridization groups, indicating that they belonged to separate species. The two groups of strains were also well differentiated by siderotyping. Garlic strains were pathogenic to garlic plants and either weakly pathogenic or non-pathogenic on rice; rice strains were either weakly pathogenic or non-pathogenic on rice and non-pathogenic on garlic. A phylogenetic analysis of 16S rRNA gene sequences confirmed that the two groups of strains belonged to the y-Proteobacteria and to the genus Pseudomonas. The names Pseudomonas salomonii sp. nov. and Pseudomonas palleroniana sp. nov. are respectively proposed for the garlic strains and the rice strains. The type strains are P. salomonii CFBP 2022(T) ( = ICMP 14252(T) = NCPPB 4277(T)) and P. palleroniana CFBP 4389(T) (= ICMP 14253(T) = NCPPB 4278(T)).

Base Composition↗

PubMed2003

A developmental response to pathogen infection in Arabidopsis.

We present evidence that susceptible Arabidopsis plants accelerate their reproductive development and alter their shoot architecture in response to three different pathogen species. We infected 2-week-old Arabidopsis seedlings with two bacterial pathogens, Pseudomonas syringae and Xanthomonas campestris, and an oomycete, Peronospora parasitica. Infection with each of the three pathogens reduced time to flowering and the number of aerial branches on the primary inflorescence. In the absence of competition, P. syringae and P. parasitica infection also increased basal branch development. Flowering time and branch responses were affected by the amount of pathogen present. Large amounts of pathogen caused the most dramatic changes in the number of branches on the primary inflorescence, but small amounts of P. syringae caused the fastest flowering and the production of the most basal branches. RPS2 resistance prevented large changes in development when it prevented visible disease symptoms but not at high pathogen doses and when substantial visible hypersensitive response occurred. These experiments indicate that phylogenetically disparate pathogens cause similar changes in the development of susceptible Arabidopsis. We propose that these changes in flowering time and branch architecture constitute a general developmental response to pathogen infection that may affect tolerance of and/or resistance to disease.

Arabidopsis↗

PubMed1996

Regulatory Genes Controlling MPG1 Expression and Pathogenicity in the Rice Blast Fungus Magnaporthe grisea.

MPG1, a pathogenicity gene of the rice blast fungus Magnaporthe grisea, is expressed during pathogenesis and in axenic culture during nitrogen or glucose limitation. We initiated a search for regulatory mutations that would impair nitrogen metabolism, MPG1 gene expression, and pathogenicity. First, we developed a pair of laboratory strains that were highly fertile and pathogenic toward barley. Using a combinatorial genetic screen, we identified mutants that failed to utilize a wide range of nitrogen sources (e.g., nitrate or amino acids) and then tested the effect of these mutations on pathogenicity. We identified five mutants and designated them Nr- (for nitrogen regulation defective). We show that two of these mutations define two genes, designated NPR1 and NPR2 (for nitrogen pathogenicity regulation), that are essential for pathogenicity and the utilization of many nitrogen sources. These genes are nonallelic to the major nitrogen regulatory gene in M. grisea and are required for expression of the pathogenicity gene MPG1. We propose that NPR1 and NPR2 are major regulators of pathogenicity in M. grisea and may be novel regulators of nitrogen metabolism in fungi.

Journal Article↗