PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Plant Immunity”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 289 records · Page 16Linked to original sources

Involvement of specific calmodulin isoforms in salicylic acid-independent activation of plant disease resistance responses.

The Ca2+ signal is essential for the activation of plant defense responses, but downstream components of the signaling pathway are still poorly defined. Here we demonstrate that specific calmodulin (CaM) isoforms are activated by infection or pathogen-derived elicitors and participate in Ca2+-mediated induction of plant disease resistance responses. Soybean CaM (SCaM)-4 and SCaM-5 genes, which encode for divergent CaM isoforms, were induced within 30 min by a fungal elicitor or pathogen, whereas other SCaM genes encoding highly conserved CaM isoforms did not show such response. This pathogen-triggered induction of these genes specifically depended on the increase of intracellular Ca2+ level. Constitutive expression of SCaM-4 and SCaM-5 in transgenic tobacco plants triggered spontaneous induction of lesions and induces an array of systemic acquired resistance (SAR)-associated genes. Surprisingly, these transgenic plants have normal levels of endogenous salicylic acid (SA). Furthermore, coexpression of nahG gene did not block the induction of SAR-associated genes in these transgenic plants, indicating that SA is not involved in the SAR gene induction mediated by SCaM-4 or SCaM-5. The transgenic plants exhibit enhanced resistance to a wide spectrum of virulent and avirulent pathogens, including bacteria, fungi, and virus. These results suggest that specific CaM isoforms are components of a SA-independent signal transduction chain leading to disease resistance.

Calcium↗

Essential role of the small GTPase Rac in disease resistance of rice.

Production of reactive oxygen intermediates (ROI) and a form of programmed cell death called hypersensitive response (HR) are often associated with disease resistance of plants. We have previously shown that the Rac homolog of rice, OsRac1, is a regulator of ROI production and cell death in rice. Here we show that the constitutively active OsRac1 (i) causes HR-like responses and greatly reduces disease lesions against a virulent race of the rice blast fungus; (ii) causes resistance against a virulent race of bacterial blight; and (iii) causes enhanced production of a phytoalexin and alters expression of defense-related genes. The dominant-negative OsRac1 suppresses elicitor-induced ROI production in transgenic cell cultures, and in plants suppresses the HR induced by the avirulent race of the fungus. Taken together, our findings strongly suggest that OsRac1 has a general role in disease resistance of rice.

Agrobacterium tumefaciens↗

Characterization of susceptibility and resistance responses to potato cyst nematode (Globodera spp.) infection of tomato lines in the absence and presence of the broad-spectrum nematode resistance Hero gene.

The tomato Hero A gene is the only member of a multigene family that confers a high level (>80%) of resistance to all the economically important pathotypes of potato cyst nematode (PCN) species Globodera rostochiensis and G. pallida. Although the resistance levels of transgenic tomato lines were similar to those of the tomato line LA1792 containing the introgressed Hero multigene family, transgenic potato plants expressing the tomato Hero A gene are not resistant to PCNs. Comparative microscopy studies of in vitro infected roots of PCN-susceptible tomato cv. Money Maker, the resistant breeding line LA1792, and transgenic line L10 with Ro1 pathotype have revealed no statistically significant difference in the number of juveniles invading roots. However, syncytia (specialized feeding cells) induced in LA1792 and L10 roots mostly were found to have degenerated a few days after their induction, and a few surviving syncytia were able to support only the development of males rather than females. Thus, the ratio between males and females was biased towards males on LA1792 and L10 roots. A series of changes occur in resistant plants leading to formation of a layer of necrotic cells separating the syncytium from stellar conductive tissues and this is followed by degradation of the syncytium. Although the Hero A gene is expressed in all tissues, including roots, stems, leaves, and flower buds, its expression is upregulated in roots in response to PCN infection. Moreover, the expression profiles of the Hero A correlates with the timing of death of the syncytium.

Animals↗

Arabidopsis mutations at the RPS2 locus result in loss of resistance to Pseudomonas syringae strains expressing the avirulence gene avrRpt2.

We isolated and characterized two Arabidopsis thaliana mutants that fail to mount a hypersensitive defense response (HR) when infiltrated with phytopathogenic Pseudomonas strains carrying the avirulence (avr) gene avrRpt2 but still mount an HR when infiltrated with strains carrying other avr genes. One of these mutants was isolated using a method we developed that enriches for Arabidopsis seedlings that survive vacuum-infiltration with a bacterial strain carrying an avr gene. Genetic analysis showed that the phenotypes of both mutants resulted from mutations at a single locus, RPS2. In contrast to the wild type, both rps2 mutants failed to limit the growth of Pseudomonas strains carrying avrRpt2. Heterozygous RPS2/rps2 plants displayed a phenotype intermediate between those of RPS2/RPS2 and rps2/rps2 homozygotes. These experiments show that the wild-type allele at the rps2 locus, RPS2, encodes a component of a signal transduction pathway that responds to a signal generated by avrRpt2 and that RPS2 is required for the elicitation of an HR. RPS2 was mapped near the restriction fragment length polymorphism marker PG11 on chromosome IV.

Arabidopsis↗

Fusarium solani DNase is a signal for increasing expression of nonhost disease resistance response genes, hypersensitivity, and pisatin production.

The inoculation of pea endocarp tissue with the bean pathogen Fusarium solani f. sp. phaseoli results in a non-host resistance response causing a complete cessation of fungal growth within 6 to 8 h. In addition to previously reported elicitation by chitosan, we now report that components of this response are also induced by a DNase released from this fungus. A single band of protein corresponding with DNase activity elicits phytoalexin production and the accumulation of RnA homologous with the pathogenesis-related (PR) genes DRR49, DRR206, and DRR230. Both the enzyme activity and the eliciting potential of the Fusarium DNase (Fsp DNase) are heat stable but susceptible to digestion by proteinase K. Fsp DNase mimics the intact fungus in inducing resistance against F. solani f. sp. pisi. Also, Fsp DNase causes similar cytologically detectable changes in pea tissue, such as increasing hypersensitive discoloration and diminishing fluorescence of Hoechst 33342-stained nuclei and fluorescein diacetate stained cells.

Benzopyrans↗

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↗

Overexpression of the tomato Asc-1 gene mediates high insensitivity to AAL toxins and fumonisin B1 in tomato hairy roots and confers resistance to Alternaria alternata f. sp. lycopersici in Nicotiana umbratica plants.

The sphinganine-analog mycotoxins (SAMs) fumonisin B1 and AAL toxins are inhibitors of eukaryotic sphinganine N-acyltransferase in vitro. Treatment of eukaryotes with SAMs generally results in an accumulation of sphingoid base precursors and a depletion of complex sphingolipids. The asc,asc genotypes of tomato (Lycopersicon esculentum) and Nicotiana umbratica are sensitive to SAMs and host of the AAL toxin-producing fungus Alternaria alternata f. sp. lycopersici. Codominant insensitivity to SAMs in tomato is mediated by the Asc-1 gene, and sensitivity is associated with a frame-shift mutation present in asc-1. We investigated the function of Asc-1 in mediating insensitivity to SAMs and resistance to the fungus by overexpression of asc-1 and Asc-1. In this study, it is shown that overexpression of these genes did not lead to visual symptoms in tomato hairy roots and N. umbratica plants. Overexpression of asc-1 did not influence the (in)sensitivity to SAMs. Overexpression of Asc-1 in SAM-sensitive hairy roots and N. umbratica plants, however, mediated a high insensitivity to SAMs and resistance to plant infection by Alternaria alternata f. sp. lycopersici.

Alternaria↗

Constitutive activation of jasmonate signaling in an Arabidopsis mutant correlates with enhanced resistance to Erysiphe cichoracearum, Pseudomonas syringae, and Myzus persicae.

In Arabidopsis spp., the jasmonate (JA) response pathway generally is required for defenses against necrotrophic pathogens and chewing insects, while the salicylic acid (SA) response pathway is generally required for specific, resistance (R) gene-mediated defenses against both biotrophic and necrotrophic pathogens. For example, SA-dependent defenses are required for resistance to the biotrophic fungal pathogen Erysiphe cichoracearum UCSC1 and the bacterial pathogen Pseudomonas syringae pv. maculicola, and also are expressed during response to the green peach aphid Myzus persicae. However, recent evidence indicates that the expression of JA-dependent defenses also may confer resistance to E. cichoracearum. To confirm and to extend this observation, we have compared the disease and pest resistance of wild-type Arabidopsis plants with that of the mutants coil, which is insensitive to JA, and cev1, which has constitutive JA signaling. Measurements of the colonization of these plants by E. cichoracearum, P. syringae pv. maculicola, and M. persicae indicated that activation of the JA signal pathway enhanced resistance, and was associated with the activation of JA-dependent defense genes and the suppression of SA-dependent defense genes. We conclude that JA and SA induce alternative defense pathways that can confer resistance to the same pathogens and pests.

Animals↗

Ectopic expression of Tsi1 in transgenic hot pepper plants enhances host resistance to viral, bacterial, and oomycete pathogens.

In many plants, including hot pepper plants, productivity is greatly affected by pathogen attack. We reported previously that tobacco stress-induced gene 1 (Tsi1) may play an important role in regulating stress responsive genes and pathogenesis-related (PR) genes. In this study, we demonstrated that overexpression of Tsi1 gene in transgenic hot pepper plants induced constitutive expression of several PR genes in the absence of stress or pathogen treatment. The transgenic hot pepper plants expressing Tsi1 exhibited resistance to Pepper mild mottle virus (PMMV) and Cucumber mosaic virus (CMV). Furthermore, these transgenic plants showed increased resistance to a bacterial pathogen, Xanthomonas campestris pv. vesicatoria and also an oomycete pathogen, Phytophthora capsici. These results suggested that ectopic expression of Tsi1 in transgenic hot pepper plants enhanced the resistance of the plants to various pathogens, including viruses, bacteria, and oomycete. These results suggest that using transcriptional regulatory protein genes may contribute to developing broad-spectrum resistance in crop plants.

Bacteria↗

Tobacco transgenic for the flax rust resistance gene L expresses allele-specific activation of defense responses.

Tobacco was transformed with three different alleles (L2, L6, and L10) of the flax rust resistance gene L, a member of the toll interleukin-1 receptor, nucleotide-binding site, leucine-rich repeat (TIR-NBS-LRR) class of plant disease resistance genes. L6 transgenics had a stunted phenotype, expressed several defense response genes constitutively, and had increased resistance to the fungus Cercospora nicotianae and the oomycete Phytophthora parasitica pv. nicotianae. L2 and L10 transgenics, with one exception for L10, did not express these phenotypes, indicating that the activation of tobacco defense responses is L6 allele-specific. The phenotype of the exceptional L10 transgenic plant was associated with the presence of a truncated L10 gene resulting from an aberrant T-DNA integration. The truncated gene consisted of the promoter, the complete TIR region, and 39 codons of the NBS domain fused inframe to a tobacco retrotransposon-like sequence. A similar truncated L10 gene, constructed in vitro, was transiently expressed in tobacco leaves and gave rise to a strong localized necrotic reaction. Together, these results suggest that defense signaling properties of resistance genes can be expressed in an allele-specific and pathogen-independent manner when transferred between plant genera.

Ascomycota↗

Developmental regulation of Mi-mediated aphid resistance is independent of Mi-1.2 transcript levels.

Mi-1.2, a member of the intracellular, nucleotide-binding site-leucine-rich repeat family of resistance genes, confers resistance in tomato (Lycopersicon esculentum) against both root-feeding nematodes and leaf-feeding aphids. Nematode resistance is effective in all life stages of the plant; in contrast, Mi-mediated aphid resistance is developmentally regulated, and protects mature plants but not seedlings against aphid infestation. To determine if the onset of aphid resistance is regulated by Mi-1.2 transcript abundance, we compared aphid resistance and Mi-1.2 transcript levels in seedlings and flowering plants. Paired bioassays and RNase protection assays revealed that Mi-1.2 is transcribed in the leaves prior to the onset of aphid resistance, and that transcript levels are comparable in seedlings and flowering life stages. Furthermore, constitutive overexpression of Mi-1.2 in transgenic plants did not hasten the onset of aphid resistance in seedlings, or boost the level of resistance observed in flowering plants. These data demonstrate that Mi-1.2 transcript levels do not modulate the degree of aphid resistance in tomato leaves, or control the differences in regulation between aphid and nematode resistance.

Animals↗

Gene expression signatures from three genetically separable resistance gene signaling pathways for downy mildew resistance.

Resistance gene-dependent disease resistance to pathogenic microorganisms is mediated by genetically separable regulatory pathways. Using the GeneChip Arabidopsis genome array, we compared the expression profiles of approximately 8,000 Arabidopsis genes following activation of three RPP genes directed against the pathogenic oomycete Peronospora parasitica. Judicious choice of P. parasitica isolates and loss of resistance plant mutants allowed us to compare the responses controlled by three genetically distinct resistance gene-mediated signaling pathways. We found that all three pathways can converge, leading to up-regulation of common sets of target genes. At least two temporal patterns of gene activation are triggered by two of the pathways examined. Many genes defined by their early and transient increases in expression encode proteins that execute defense biochemistry, while genes exhibiting a sustained or delayed expression increase predominantly encode putative signaling proteins. Previously defined and novel sequence motifs were found to be enriched in the promoters of genes coregulated by the local defense-signaling network. These putative promoter elements may operate downstream from signal convergence points.

Arabidopsis↗

A key role for ALD1 in activation of local and systemic defenses in Arabidopsis.

The Arabidopsis thaliana agd2-like defense response protein1 (ald1) mutant was previously found to be hypersusceptible to the virulent bacterial pathogen Pseudomonas syringae and had reduced accumulation of the defense signal salicylic acid (SA). ALD1 was shown to possess aminotransferase activity in vitro, suggesting it generates an amino acid-derived defense signal. We now find ALD1 to be a key defense component that acts in multiple contexts and partially requires the PHYTOALEXIN DEFICIENT4 (PAD4) defense regulatory gene for its expression in response to infection. ald1 plants have increased susceptibility to avirulent P. syringae strains, are unable to activate systemic acquired resistance and are compromised for resistance to the oomycete pathogen Peronospora parasitica in mutants with constitutively active defenses. ALD1 and PAD4 can act additively to control SA, PATHOGENESIS RELATED GENE1 (PR1) transcript and camalexin (an antimicrobial metabolite) accumulation as well as disease resistance. Finally, ALD1 and PAD4 can mutually affect each other's expression in a constitutive defense mutant, suggesting that these two genes can act in a signal amplification loop.

Arabidopsis↗

Signaling requirements and role of salicylic acid in HRT- and rrt-mediated resistance to turnip crinkle virus in Arabidopsis.

Inoculation of turnip crinkle virus (TCV) on the resistant Arabidopsis ecotype Di-17 elicits a hypersensitive response (HR), which is accompanied by increased expression of pathogenesis-related (PR) genes. Previous genetic analyses revealed that the HR to TCV is conferred by HRT, which encodes a coiled-coil (CC), nucleotide-binding site (NBS) and leucine-rich repeat (LRR) class resistance (R) protein. In contrast to the HR, resistance to TCV requires both HRT and a recessive allele at a second locus designated rrt. Here, we demonstrate that unlike most CC-NBS-LRR R genes, HRT/rrt-mediated resistance is dependent on EDS1 and independent of NDR1. Resistance is also independent of RAR1 and SGT1. HRT/rrt-mediated resistance is compromised in plants with reduced salicylic acid (SA) content as a consequence of mutations eds5, pad4, or sid2. By contrast, HR is not affected by mutations in eds1, eds5, pad4, sid2, ndr1, rar1, or sgt1b. Resistance to TCV is restored in both SA-deficient Di-17 plants expressing the nahG transgene and mutants containing the eds1, eds5, or sid2 mutations by exogenous application of SA or the SA analog benzo(1,2,3)thiadiazole-7-carbothioic acid (BTH). In contrast, SA/BTH treatment failed to enhance resistance in HRT pad4, Col-0, or hrt homozygous progeny of a cross between Di-17 and Col-0. Thus, HRT and PAD4 are required for SA-induced resistance. Exogenously supplied SA or high endogenous levels of SA, due to the ssi2 mutation, overcame the suppressive effects of RRT and enhanced resistance to TCV, provided the HRT allele was present. High levels of SA upregulate HRT expression via a PAD4-dependent pathway. As Col-0 transgenic lines expressing high levels of HRT were resistant to TCV, but lines expressing moderate to low levels of HRT were not, we conclude that SA enhances resistance in the RRT background by upregulating HRT expression. These data suggest that the HRT-TCV interaction is unable to generate sufficient amounts of SA required for a stable resistance phenotype, and the presence of rrt possibly corrects this deficiency.

Arabidopsis↗

Genome-wide transcriptional analysis of the Arabidopsis thaliana interaction with the plant pathogen Pseudomonas syringae pv. tomato DC3000 and the human pathogen Escherichia coli O157:H7.

Pseudomonas syringae pv. tomato DC3000 (Pst) is a virulent pathogen that causes disease on tomato and Arabidopsis. The type III secretion system (TTSS) plays a key role in pathogenesis by translocating virulence effectors from the bacteria into the plant host cell, while the phytotoxin coronatine (COR) contributes to virulence and disease symptom development. Recent studies suggest that both the TTSS and COR are involved in the suppression of host basal defenses. However, little is known about the interplay between the host gene expression changes associated with basal defenses and the virulence activities of the TTSS and COR during infection. In this study, we used the Affymetrix full genome chip to determine the Arabidopsis transcriptome associated with basal defense to Pst DC3000 hrp mutants and the human pathogenic bacterium Escherichia coli O157:H7. We then used Pst DC3000 virulence mutants to characterize Arabidopsis transcriptional responses to the action of hrp-regulated virulence factors (e.g. TTSS and COR) during bacterial infection. Additionally, we used bacterial fliC mutants to assess the role of the pathogen-associated molecular pattern flagellin in induction of basal defense-associated transcriptional responses. In total, our global gene expression analysis identified 2800 Arabidopsis genes that are reproducibly regulated in response to bacterial pathogen inoculation. Regulation of these genes provides a molecular signature for Arabidopsis basal defense to plant and human pathogenic bacteria, and illustrates both common and distinct global virulence effects of the TTSS, COR, and possibly other hrp-regulated virulence factors during Pst DC3000 infection.

Abscisic Acid↗

Use of RNA interference to dissect defense-signaling pathways in rice.

The RNA interference (RNAi) technique is a powerful tool to suppress gene expression and has been widely used for functional discovery of eukaryotic genes. To dissect defense-signaling pathways in rice, it is important to generate a series of rice mutant lines deficient in or insensitive to major signal molecules such as jasmonic acid and ethylene. Here we describe an RNAi protocol for generating and characterizing transgenic gene-silencing lines defective in rice jasmonic acid signaling. The RNAi technique should be useful for effective suppression of host genes encoding signaling components and facilitating the dissection of defense signal pathways in rice.

Cyclopentanes↗