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PubMed2026

ReGAIN: a bioinformatics platform for assessing probabilistic co-occurrence between resistance genes in bacterial pathogens.

MOTIVATION: Multidrug-resistant bacterial pathogens continue to rise globally, yet scalable methods are needed to infer how resistance determinants co-occur across pathogen populations and to quantify conditional dependencies underlying co-occurrence and shared genetic context. RESULTS: We present ReGAIN (Resistance Gene Association and Inference Network), an open-source platform that applies Bayesian network structure learning to infer probabilistic, conditional dependency relationships among antibiotic resistance, heavy metal tolerance, stress response, and virulence determinants in bacteria. In contrast to pairwise co-occurrence analyses, ReGAIN reports conditional probabilities, relative risks, and absolute risk differences with confidence intervals to prioritize candidate relationships for downstream prioritization. Applied across ESKAPEE pathogens, ReGAIN recapitulated established resistance gene relationships and identified additional candidate patterns consistent with co-selection and shared genetic context. Together, these results support scalable, reproducible population-wide analysis of resistance networks for surveillance, comparative genomics and epidemiology. AVAILABILITY: ReGAIN analyses are performed using Python v3.11.5 and R v4.4.1 and is available as open-source software through Bioconda at {https://anaconda.org/bioconda/regain-cli}. Source code and documentation can be found at {https://github.com/ERBringHorvath/regain_CLI}. All genomes used in this publication were downloaded from the National Center for Biotechnology Information database. Large supplementary tables and results data from the ESKAPEE pathogen example network analyses can be downloaded from https://figshare.com/articles/dataset/ReGAIN_command_line_software_and_supplemental_figures_/28959431.

Computational Biology↗
PubMed2004

Support vector machines for separation of mixed plant-pathogen EST collections based on codon usage.

MOTIVATION: Discovery of host and pathogen genes expressed at the plant-pathogen interface often requires the construction of mixed libraries that contain sequences from both genomes. Sequence identification requires high-throughput and reliable classification of genome origin. When using single-pass cDNA sequences difficulties arise from the short sequence length, the lack of sufficient taxonomically relevant sequence data in public databases and ambiguous sequence homology between plant and pathogen genes. RESULTS: A novel method is described, which is independent of the availability of homologous genes and relies on subtle differences in codon usage between plant and fungal genes. We used support vector machines (SVMs) to identify the probable origin of sequences. SVMs were compared to several other machine learning techniques and to a probabilistic algorithm (PF-IND) for expressed sequence tag (EST) classification also based on codon bias differences. Our software (Eclat) has achieved a classification accuracy of 93.1% on a test set of 3217 EST sequences from Hordeum vulgare and Blumeria graminis, which is a significant improvement compared to PF-IND (prediction accuracy of 81.2% on the same test set). EST sequences with at least 50 nt of coding sequence can be classified using Eclat with high confidence. Eclat allows training of classifiers for any host-pathogen combination for which there are sufficient classified training sequences. AVAILABILITY: Eclat is freely available on the Internet (http://mips.gsf.de/proj/est) or on request as a standalone version. CONTACT: friedel@informatik.uni-muenchen.de.

Algorithms↗
PubMedDate not supplied

Occurrence and pathogenicity of the Streptococcus milleri group.

Streptococci of the milleri group are part of the normal flora of human mucous membranes. These streptococci have also been reported to be significant pathogens. Like other mucosal streptococci, they may cause infective endocarditis; unlike other mucosal streptococci, however, they have also been repeatedly associated (more frequently in men than in women) with serious suppurative infections. Evidence for the pathogenicity of the Streptococcus milleri group is scattered and mainly circumstantial. Although the organisms are found in a high proportion of certain suppurative infections, other bacteria are often present as well. Successful treatment of these infections with surgery and broad-spectrum antibiotics is not indicative of any specific etiology. Only a few attempts at the induction of experimental infections other than endocarditis have been effective. Further investigation is required to establish the pathogenicity and pathogenic mechanisms of the S. milleri group.

Digestive System↗
PubMed1993

Corynebacterium striatum: a diphtheroid with pathogenic potential.

Although nondiphtherial corynebacteria are ubiquitous in nature and commonly colonize the skin and mucous membranes of humans, they rarely account for clinical infection. Corynebacterium striatum has rarely been reported to be a pathogen, causing pleuropulmonary infections and bacteremia in only immunocompromised or anatomically altered patients. We noted C. striatum to be the infecting pathogen or copathogen in six patients. To our knowledge, this report describes the first cases of C. striatum causing infection of exist sites of central venous catheters, thrombophlebitis associated with central venous catheters, conjunctivitis, and chorioamnionitis as well as a possible pathogen contributing to peritonitis and pyogenic granuloma. Unlike Corynebacterium jeikeium, which is highly resistant to beta-lactam agents, aminoglycosides, and quinolones, all strains of C. striatum isolated from the patients described in this report were susceptible to vancomycin and aminoglycosides, and all strains except one were susceptible to penicillin G, imipenem, and ciprofloxacin. C. striatum should be recognized as a potential pathogen in both immunocompromised and normal hosts in the appropriate circumstances, and appropriate antimicrobial therapy can quickly lead to resolution of infection.

Adult↗
PubMed2005

Prediction of pathogenic mutations in mitochondrially encoded human tRNAs.

Some mutations in human mitochondrial tRNAs are severely pathogenic. The available computational methods have a poor record of predicting the impact of a tRNA mutation on the phenotype and fitness. Here patterns of evolution at tRNA sites that harbor pathogenic mutations and at sites that harbor phenotypically cryptic polymorphisms were compared. Mutations that are pathogenic to humans occupy more conservative sites, are only rarely fixed in closely related species, and, when located in stem structures, often disrupt Watson-Crick pairing and display signs of compensatory evolution. These observations make it possible to classify approximately 90% of all known pathogenic mutations as deleterious together with only approximately 30% of polymorphisms. These polymorphisms segregate at frequencies that are more than two times lower than frequencies of polymorphisms classified as benign, indicating that at least approximately 30% of known polymorphisms in mitochondrial tRNAs affect fitness negatively.

Base Sequence↗
PubMed1981

Selective antimicrobial modulation of human microbial flora: infection prevention in patients with decreased host defense mechanisms by selective elimination of potentially pathogenic bacteria.

To reduce the frequency and severity of bacterial infection, selective antimicrobial modulation (SAM) was applied in 39 patients with severely decreased host defense mechanisms. The objective was to eliminate potentially pathogenic aerobic microorganisms with minimal disturbance of the normal anaerobic bacterial flora. Elimination of potentially pathogenic aerobic microorganisms was easily accomplished in patients not infected at hospitalization. The anaerobic flora seemed to be undisturbed, and selection of or overgrowth with resistant microorganisms did not occur. The microbiologic results of the SAM regimen correlated with the incidence of infection. Only three major infections occurred in 23 patients who were free of potentially pathogenic microorganisms; 10 major infections occurred in 16 patients who were not free of potential pathogens. Seven of these 10 infections were present at hospitalization. The incidence of major infections was 47% in the patients on the SAM regimen and 82% in a group of control patients with a similar risk of infection.

Adolescent↗
PubMed1995

Pathogen antigen- and superantigen-reactive synovial fluid T cells in reactive arthritis.

Analysis of pathogen-reactive T cell clones (CD3+4+8-TCR alpha beta +), isolated from the synovial fluid of 2 HLA-B27-positive patients with Yersinia enterocolitica-triggered reactive arthritis, has provided important information about the cellular immune response to this disease-inciting pathogen. This study demonstrates that the proteins secreted by Y. enterocolitica, including a protein with tyrosine phosphatase activity (YopH), are potent immunogens stimulating CD4+ cells within the inflamed joint. The pathogen-reactive T cell clones preferentially utilized a limited set of T cell receptor variable region gene segments. A purified Yersinia superantigen triggered a proliferative response in most of the antigen-reactive T cell clones tested. These results suggest that the activity of this pathogen's superantigen influences the cellular immune response to its antigens.

Adult↗
PubMed1999

Characteristics and pathogenic role of anti-beta2-glycoprotein I single-chain Fv domains: induction of experimental antiphospholipid syndrome.

Antiphospholipid syndrome is characterized by the presence of high titers of anti-beta(2)-glycoprotein I (beta(2)GPI) antibodies, lupus anticoagulant associated with thromboembolic phenomena, thrombocytopenia and recurrent fetal loss. Single-chain Fv (scFv) were prepared from four anti-beta(2)GPI mAb, CAM, CAL, CAR and 2C4C2, and one anti-ssDNA. All five scFv showed the same antigen binding properties as the original mAb. Replacement of the pathogenic CAM V(H) domain with the non-pathogenic CAL V(H) or anti-ssDNA V(H) decreased the binding affinity of the scFv to beta(2)GPI and completely abrogated the anticoagulant activity. Exchanging the CAM V(H) with anti-DNA V(H) resulted in a shift from anti-beta(2)GPI to anti-ssDNA binding of the scFv. Replacement of the CAM V(L) with CAL V(L) did not affect the binding and activity. BALB/c mice were immunized with the anti-beta(2)GPI scFv, and the scFv resulting from the substitution of the heavy (H) and light (L) chains. The mice which were immunized with CAM, 2C4C2 and CAR scFv developed clinical manifestations of experimental anti-phospholipid syndrome. Elevated titers of mouse anti-cardiolipin (aCL), anti-beta(2)GPI, associated with lupus anticoagulant activity, thrombocytopenia, prolonged activated partial thromboplastin time and a high percentage of fetal resorptions were detected, in the CAM scFv group and in the scFv composed of CAM V(H) groups. High titers of aCL, anti-beta(2)GPI, anti-ss/dsDNA and anti-histone associated with lupus findings were observed in the sera of the 2C4C2 scFv-immunized mice. Immunization with CAL scFv did not lead to any clinical findings. The current study shows that scFv of pathogenic antibodies are capable of inducing the same clinical manifestations as the whole antibody molecule upon active immunization. Replacement of H/L chains point to the importance of the V(H) domains in the pathogenic potential of anti-beta(2)GPI.

Animals↗
PubMed1990

Selective strain distribution pattern of a germline VH gene for a pathogenic anti-DNA autoantibody family.

Autoimmune NZB mice rarely develop nephritis, but the SNF1, progeny of Crosses between NZB and the normal SWR strain uniformly develop severe lupus nephritis, indicating that the normal SWR strain makes a genetic contribution to the development of nephritis. The SNF1 mice produce a select population of cationic IgG anti-DNA autoantibodies that share a recurrent cross-reactive idiotype called Id564 and these autoantibodies play a prominent role in the development of nephritis. These pathogenic autoantibodies of SNF1 possess the IgCH allotype of the SWR, indicating their origin from the normal parent. The leader-VH sequences of these Id564+ pathogenic anti-DNA autoantibodies are highly homologous and they are also related by 95% homology to a germline gene of normal C57BL/6 mice, called VH-23, that is a member of an anti-NP antibody gene family. Herein, we cloned the flanking and coding regions of the expressed VHDJH genes of the anti-DNA mAb 564, the prototype member of the pathogenic Id564 family. By restriction analysis and partial sequencing, we found that the VH564 gene is related but distinct in its 5' flanking region from all of the known anti-NP VH genes of C57BL/6 and BALB/c mice. Hybridization with four probes complementary to different segments of the flanking and coding regions of the expressed VH564 gene indicated that the germline gene for VH564 is contained in an approximately 5.2 kb EcoRI fragment of SWR genomic DNA. Moreover, high stringency hybridization with oligonucleotide probes complementary to unique CDR2 and 5' flanking sequences of the expressed VH564 gene revealed that the 'approximately 5.2 kb' germline allele for VH564 that is possessed by the normal SWR parental strain is lacking in the NZB parental strain. C57BL/6 mice also lack this allele of the anti-DNA VH564 germline gene, although this strain possesses the highly homologous, anti-NP-related VH-23 germline gene. Thus germline VH genes for certain pathogenic autoantibodies may have a selective strain distribution pattern.

Alleles↗
PubMed1990

Monoclonal anti-erythrocyte autoantibodies derived from NZB mice cause autoimmune hemolytic anemia by two distinct pathogenic mechanisms.

In vivo pathological manifestations of eight monoclonal anti-mouse red blood cell (MRBC) autoantibodies obtained from unmanipulated NZB mice were determined in BALB/c mice. Three (two IgG1 and one IgG2a) of four IgG monoclonal antibodies (mAb) and two of four IgM mAb were able to induce anemia following their i.p. injection. All five pathogenic anti-MRBC mAbs reacted only with MRBC, whereas non-pathogenic anti-MRBC mAbs showed binding to different species of RBC. Competition studies suggested the presence of at least two distinct epitopes recognized by our pathogenic anti-MRBC mAb. Histological examinations revealed that anemia resulted from either marked sequestration of agglutinated MRBC in spleens and livers or erythrophagocytosis, most remarkably by Kupffer cells in livers. This difference was correlated with the ability of each mAb to mediate Fc receptor-dependent phagocytosis by macrophages. The absence of complement-mediated hemolysis in vitro and the development of anemia in C5-deficient or C3-depleted mice indicated a minor role, if any, for complement-mediated lysis in the anemia induced by our anti-MRBC mAb. Our results suggest that (i) at least two different pathogenic epitopes are implicated in autoimmune hemolytic anemia; and (ii) sequestration of agglutinated MRBC in spleens and livers and Fc receptor-dependent phagocytosis, but not complement-mediated hemolysis, are the major mechanisms for the development of autoimmune hemolytic anemia.

Anemia, Hemolytic, Autoimmune↗
PubMed1990

Changes in the antibiotic sensitivities of urinary pathogens, 1971-1989.

All urinary pathogens from general practice and hospital have been tested for sensitivity to a range of antimicrobial agents for the last 19 years. There have been marked changes during that time. In general practice there has been a considerable increase in the proportion of staphylococcal infections from 5.1% to a peak of 14.8% in 1982 and a more recent decline to 3.4%. There has also been a decrease in the proportion caused by Proteus mirabilis, from 9.2% to 5.0%. Similar, but smaller changes have been observed in the proportions of hospital urinary tract infections (UTI) caused by these organisms, while the proportion of hospital infections due to Klebsiella spp. and Enterobacter spp. has fallen from 16.8% to 9.2%. These and other changes have been reflected in changing patterns of sensitivity to antibiotics. In particular, sensitivity of urinary pathogens to ampicillin/amoxycillin has continued to fall both in general practice and in hospital. Nalidixic acid resistance is becoming more important as the proportion of Gram-positive urinary pathogens (especially enterococci) increases. More organisms were sensitive to ciprofloxacin than the other drugs tested, with no evidence of increasing resistance over a six-year period. Over the same time there has been a reduction of overall sensitivity of urinary pathogens to trimethoprim from 90.8% to 82.5% in general practice, with no significant change in isolates from hospital practice.

Anti-Infective Agents, Urinary↗
PubMed2002

Dynamics of nasopharyngeal colonization by potential respiratory pathogens.

Studies have shown that colonization of the nasopharynx by potential respiratory pathogens Streptococcus pneumoniae, Haemophilus influenzae and Moraxella catarrhalis is established early in childhood, although rates vary greatly according to locality, sampling frequency, individual and social factors. Factors influencing colonization and elimination are not as yet fully understood, but adhesion to mucosal receptors and immune responses are implicated in addition to bacterial properties and colonization resistance dynamics. Colonization in children and adults has been intensively studied in various localities. Potential pathogens are more likely to colonize the nasopharynx of children prone to recurrent otitis media, where impaired local immunity and repeated exposure to respiratory pathogens are additional risk factors. Adults with chronic respiratory tract disease also have higher carriage rates. The factors contributing to increased risk of carriage of potential respiratory pathogens, as well as to clinical infection and antimicrobial resistance, are summarized in this review.

Animals↗
PubMed2006

The effect of vitamin A supplementation on the intestinal immune response in Mexican children is modified by pathogen infections and diarrhea.

Vitamin A supplementation has consistently reduced infant mortality and the severity of pathogen-induced diarrhea. The mechanism by which vitamin A modulates the mucosal immune response to produce these effects remains poorly defined. To address this issue, stools collected during the summer months from 127 Mexican children 5-15 mo old enrolled in a larger, randomized, double-blind, placebo-controlled, vitamin A supplementation trial were screened for interleukin (IL)-4, IL-6, interferon-gamma (IFN-gamma), and gastrointestinal pathogens. Fecal cytokine values were categorized into 3 levels (undetectable, or =median). Multinomial regression models were used to determine the probability that vitamin A-supplemented children had higher categorical values of a cytokine than children in the placebo group. Differences in categorical values were also analyzed after stratification by gastrointestinal pathogen infections and diarrheal symptoms. Overall, fecal cytokine categorical levels did not differ between children randomized to the 2 arms. Vitamin A-supplemented children infected with enteropathogenic E. coli (EPEC) had reduced IL-4 and IFN-gamma levels [odds ratio (OR) = 0.3, 95% CI 0.13-0.67 and OR = 0.34, 95% CI 0.14-0.83, respectively] compared with children in the placebo group. Vitamin A-supplemented children had increased IL-4 levels when infected with A. lumbricoides (OR = 12.06, 95% CI 0.95-153.85). In contrast, IL-4 levels increased (OR = 2.14, 95% CI 0.94-4.87) and IFN-gamma levels decreased (OR = 0.51, 95% CI 0.26-0.99) among vitamin A-supplemented children with diarrhea compared with children in the placebo group. These findings suggest that the regulation of the mucosal immune response by vitamin A may depend on the type of enteric pathogen infecting the child and the presence of clinical symptoms.

Animals↗
PubMed2004

Positive directional selection in the proline-rich antigen (PRA) gene among the human pathogenic fungi Coccidioides immitis, C. posadasii and their closest relatives.

In this study, we investigate the possibility of selection acting on the proline-rich antigen (PRA) gene in natural populations of the two human pathogens, Coccidioides immitis and Coccidioides posadasii, and three of their close relatives, Chrysosporium lucknowense, Chrysosporium queenslandicum, and Uncinocarpus reesii. We addressed the following questions: Is diversifying selection acting on PRA in the pathogenic species as a result of avoidance of the host's immune system, and has adaptation to a pathogenic life style lead to positive directional selection and increased rate of evolution in PRA between the species? For these purposes, we amplified and sequenced from 40 individuals belonging to the five species, the entire coding region of the PRA gene, as well as partial sequences from the coding region of each of the three housekeeping genes glyderaldehyde-3-phosphate dehydrogenase, glutamine synthetase A, and hexokinase A. We used likelihood-based methods to compare models of different types of selective pressure among codons to analyze the mode of evolution of the genes and found that the PRA gene evolves under positive selection, but the investigated parts of the housekeeping genes evolve primarily under purifying selection. We found a very low level of intraspecific variability and no evidence of diversifying selection, suggesting that the increased rate of evolution in the PRA gene is not a result of avoidance of the host's immune system. Neither did likelihood-based analyses suggest that selection was stronger on the branch separating pathogenic and nonpathogenic species. Instead, we suggest that positive selection act on PRA as a consequence of spore cell-wall morphogenesis unique to each species.

Amino Acid Sequence↗
PubMed2001

Gene genealogies, cryptic species, and molecular evolution in the human pathogen Coccidioides immitis and relatives (Ascomycota, Onygenales).

Previous genealogical analyses of population structure in Coccidioides immitis revealed the presence of two cryptic and sexual species in this pathogenic fungus but did not clarify their origin and relationships with respect to other taxa. By combining the C. immitis data with those of two of its closest relatives, the free-living saprophytes Auxarthron zuffianum and Uncinocarpus reesii, we show that the C. immitis species complex is monophyletic, indicating a single origin of pathogenicity. Cryptic species also were found in both A. zuffianum and U. reesii, indicating that they can be found in both pathogenic and free-living fungi. Our study, together with a few others, indicates that the current list of known fungal species might be augmented by a factor of at least two. However, at least in the C. immitis, A. zuffianum, and U. reesii complexes, cryptic species represent subdivisions at the tips of deep monophyletic clades and thus well within the existing framework of generic classification. An analysis of silent and expressed divergence and polymorphism values between and within the taxa identified by genealogical concordance did not reveal faster evolution in C. immitis as a consequence of adaptation to the pathogenic habit, nor did it show positive Darwinian evolution in a region of a dioxygenase gene (tcrP gene coding for 4-HPPD) known to cause antigenic responses in humans. Instead, the data suggested relative stasis, indicative of purifying selection against mostly deleterious mutations. Two introns in the same gene fragment were considerably more divergent than exons and were unalignable between species complexes but had very low polymorphism within taxa.

4-Hydroxyphenylpyruvate Dioxygenase↗
PubMed1999

Molecular evolution and mosaic structure of alpha, beta, and gamma intimins of pathogenic Escherichia coli.

Two types of pathogenic Escherichia coli, enteropathogenic E. coli (EPEC) and enterohemorrhagic E. coli (EHEC), cause diarrheal disease by disrupting the intestinal environment through the intimate attachment of the bacteria to the intestinal epithelium. This process is mediated by intimin, an outer membrane protein that is homologous to the invasins of pathogenic Yersinia. The intimin (eae) gene is part of a pathogenicity island, a 35-kb segment of DNA that has been acquired independently in different groups of pathogens. Nucleotide sequences of eae of three EPEC and four EHEC strains representing distinct clonal lineages revealed an exceptionally high level of divergence (15%) in the amino acid sequences of alpha, beta, and gamma intimin molecules, most of which is concentrated in the C-terminal region. The gamma intimin sequences from E. coli strains with serotypes O157:H7, O55:H7, and O157:H- are virtually identical, supporting the hypothesis that these bacteria belong to a single clonal lineage. Sequences of beta intimin of EPEC strains of serotypes O111:H2 and O128:H2 show substantial differences from alpha and gamma intimins, indicating that these strains have evolved independently. Strong nonrandom clustering of polymorphic sites indicates that the intimin genes are mosaics, suggesting that protein divergence has been accelerated by recombination and diversifying selection.

Adhesins, Bacterial↗
PubMed2004

New TAXI-type xylanase inhibitor genes are inducible by pathogens and wounding in hexaploid wheat.

TAXI-I (Triticum aestivum xylanase inhibitor I) is a wheat grain protein that inhibits arabinoxylan fragmentation by microbial endo-beta-1,4-xylanases used in the food industry. Although TAXI was speculated to be involved in counterattack against pathogens, there is actually no evidence to support this hypothesis. We have now demonstrated the presence of TAXI family members with isolation of two mRNA species, Taxi-III and Taxi-IV. At the nucleotide sequence level, Taxi-III and Taxi-IV were 91.7% and 92.0% identical, respectively, to Taxi-I, and Taxi-III and Taxi-IV were 96.8% identical. Accumulation of Taxi-III/IV transcripts was most evident in roots and older leaves where transcripts of Taxi-I were negligible. When challenged by fungal pathogens Fusarium graminearum and Erysiphe graminis, the concentrations of Taxi-III/IV transcripts increased significantly. In contrast, the increases in Taxi-I transcripts in response to these pathogens were rather limited. Both Taxi-I and Taxi-III/IV were strongly expressed in wounded leaves. The upstream region of Taxi-III contained W boxes and GCC boxes, which are sufficient to confer pathogen and wound inducibility on promoters. Recombinant TAXI-III protein inhibited Aspergillus niger and Trichoderma sp. xylanases: it was also active against some spelt xylan-induced xylanases of F. graminearum. These features suggest that some, but not all, TAXI-type xylanase inhibitors have a role in plant defense.

Amino Acid Sequence↗
PubMed2006

Loss of AtPDR8, a plasma membrane ABC transporter of Arabidopsis thaliana, causes hypersensitive cell death upon pathogen infection.

Plants contain a large number of ATP-binding cassette (ABC) transporters belonging to different subclasses. AtPDR8 is the only member of the pleiotropic drug resistance (PDR) ABC transporter subclass in Arabidopsis that is constitutively highly expressed. In transgenic Arabidopsis plants harboring the AtPDR8 promoter fused to beta-glucuronidase (GUS), reporter expression was shown to be strong in the stomata and hydathode. In the stomata, transcripts of AtPDR8 were particularly frequent in the cells surrounding air spaces. Subcellular fractionation and immunochemical analysis showed that AtPDR8 was localized in the plasma membrane. When a knockout mutant of AtPDR8 (atpdr8) was infected with bacterial and oomycete pathogens, the plants exhibited chlorotic lesions and a hypersensitive response (HR)-like cell death. Cell death was detected in the atpdr8 mutants within 10 h of infection with the virulent bacterial pathogen, Pseudomonas syringae. As a result, the growth of P. syringae in the leaves of the atpdr8 mutant was reduced to 1% of that in the wild type. The defense response genes, PR-1, PR-2, PR-5, VPEgamma, AtrbohD and AtrbohF were highly expressed when the mutant plants were grown under non-sterile conditions. The expression of the AtPDR8 gene was enhanced by infection of virulent and avirulent bacterial pathogens. Our results indicate that AtPDR8 is a key factor controlling the extent of cell death in the defense response and suggest that AtPDR8 transports some substance(s) which is closely related to the response of plants to pathogens.

ATP-Binding Cassette Transporters↗