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At least 1,531 records · Page 85Linked to original sources
PubMed1999

The Arabidopsis ssi1 mutation restores pathogenesis-related gene expression in npr1 plants and renders defensin gene expression salicylic acid dependent.

The Arabidopsis NPR1 gene was previously shown to be required for the salicylic acid (SA)- and benzothiadiazole (BTH)-induced expression of pathogenesis-related (PR) genes and systemic acquired resistance. The dominant ssi1 (for suppressor of SA insensitivity) mutation characterized in this study defines a new component of the SA signal transduction pathway that bypasses the requirement of NPR1 for expression of the PR genes and disease resistance. The ssi1 mutation caused PR (PR-1, BGL2 [PR-2], and PR-5) genes to be constitutively expressed and restored resistance to an avirulent strain of Pseudomonas syringae pv tomato in npr1-5 (previously called sai1) mutant plants. In addition, ssi1 plants were small, spontaneously developed hypersensitive response-like lesions, accumulated elevated levels of SA, and constitutively expressed the antimicrobial defensin gene PDF1.2. The phenotypes of the ssi1 mutant are SA dependent. When SA accumulation was prevented in ssi1 npr1-5 plants by expressing the SA-degrading salicylate hydroxylase (nahG) gene, all of the phenotypes associated with the ssi1 mutation were suppressed. However, lesion formation and expression of the PR genes were restored in these plants by the application of BTH. Interestingly, expression of PDF1.2, which previously has been shown to be SA independent but jasmonic acid and ethylene dependent, was also suppressed in ssi1 npr1-5 plants by the nahG gene. Furthermore, exogenous application of BTH restored PDF1.2 expression in these plants. Our results suggest that SSI1 may function as a switch modulating cross-talk between the SA- and jasmonic acid/ethylene-mediated defense signal transduction pathways.

Arabidopsis↗
PubMed1999

The involvement of cysteine proteases and protease inhibitor genes in the regulation of programmed cell death in plants.

Programmed cell death (PCD) is a process by which cells in many organisms die. The basic morphological and biochemical features of PCD are conserved between the animal and plant kingdoms. Cysteine proteases have emerged as key enzymes in the regulation of animal PCD. Here, we show that in soybean cells, PCD-activating oxidative stress induced a set of cysteine proteases. The activation of one or more of the cysteine proteases was instrumental in the PCD of soybean cells. Inhibition of the cysteine proteases by ectopic expression of cystatin, an endogenous cysteine protease inhibitor gene, inhibited induced cysteine protease activity and blocked PCD triggered either by an avirulent strain of Pseudomonas syringae pv glycinea or directly by oxidative stress. Similar expression of serine protease inhibitors was ineffective. A glutathione S-transferase-cystatin fusion protein was used to purify and characterize the induced proteases. Taken together, our results suggest that plant PCD can be regulated by activity poised between the cysteine proteases and the cysteine protease inhibitors. We also propose a new role for proteinase inhibitor genes as modulators of PCD in plants.

Amino Acid Sequence↗
PubMed1999

Salicylic acid induction-deficient mutants of Arabidopsis express PR-2 and PR-5 and accumulate high levels of camalexin after pathogen inoculation.

In Arabidopsis, systemic acquired resistance against pathogens has been associated with the accumulation of salicylic acid (SA) and the expression of the pathogenesis-related proteins PR-1, PR-2, and PR-5. We report here the isolation of two nonallelic mutants impaired in the pathway leading to SA biosynthesis. These SA induction-deficient (sid) mutants do not accumulate SA after pathogen inoculation and are more susceptible to both virulent and avirulent forms of Pseudomonas syringae and Peronospora parasitica. However, sid mutants are not as susceptible to these pathogens as are transgenic plants expressing the nahG gene encoding an SA hydroxylase that degrades SA to catechol. In contrast to NahG plants, only the expression of PR-1 is strongly reduced in sid mutants, whereas PR-2 and PR-5 are still expressed after pathogen attack. Furthermore, the accumulation of the phytoalexin camalexin is normal. These results indicate that SA-independent compensation pathways that do not operate in NahG plants are active in sid mutants. One of the mutants is allelic to eds5 (for enhanced disease susceptibility), whereas the other mutant has not been described previously.

Alleles↗
PubMed2000

Simulation of fungal-mediated cell death by fumonisin B1 and selection of fumonisin B1-resistant (fbr) Arabidopsis mutants.

Fumonisin B1 (FB1), a programmed cell death-eliciting toxin produced by the necrotrophic fungal plant pathogen Fusarium moniliforme, was used to simulate pathogen infection in Arabidopsis. Plants infiltrated with 10 microM FB1 and seedlings transferred to agar media containing 1 microM FB1 develop lesions reminiscent of the hypersensitive response, including generation of reactive oxygen intermediates, deposition of phenolic compounds and callose, accumulation of phytoalexin, and expression of pathogenesis-related (PR) genes. Arabidopsis FB1-resistant (fbr) mutants were selected directly by sowing seeds on agar containing 1 microM FB1, on which wild-type seedlings fail to develop. Two mutants chosen for further analyses, fbr1 and fbr2, had altered PR gene expression in response to FB1. fbr1 and fbr2 do not exhibit differential resistance to the avirulent bacterial pathogen Pseudomonas syringae pv maculicola (ES4326) expressing the avirulence gene avrRpt2 but do display enhanced resistance to a virulent isogenic strain that lacks the avirulence gene. Our results demonstrate the utility of FB1 for high-throughput isolation of Arabidopsis defense-related mutants and suggest that pathogen-elicited programmed cell death of host cells may be an important feature of compatible plant-pathogen interactions.

Arabidopsis↗
PubMed2000

Arabidopsis dth9 mutation identifies a gene involved in regulating disease susceptibility without affecting salicylic acid-dependent responses.

To determine which components of the plant defense response make important contributions to limiting pathogen attack, an M(2) mutagenized population of a transgenic Arabidopsis line was screened for mutants showing constitutive expression of beta-glucuronidase activity driven by the promoter region of the CEVI-1 gene. The CEVI-1 gene originally was isolated from tomato plants and has been shown to be induced in susceptible varieties of tomato plants by virus infection in a salicylic acid-independent manner. We report here the characterization of a recessive mutant, detachment9 (dth9). This mutant is more susceptible to both virulent and avirulent forms of the oomycete Peronospora and also exhibits increased susceptibility to the moderately virulent bacterial pathogen Pseudomonas syringae pv maculicola ES4326. However, this mutant is not affected in salicylic acid metabolism and shows normal expression of pathogenesis-related (PR) genes after pathogen attack. Furthermore, after inoculation with avirulent pathogens, the dth9 mutant shows a compromised systemic acquired resistance response that cannot be complemented by exogenous application of salicylic acid, although this molecule is able to promote normal activation of PR genes. Therefore, the dth9 mutation defines a regulator of disease susceptibility that operates upstream or independently of salicylic acid. Pleiotropy is also evident in the dth9 mutant in the sense that the shoots of dth9 plants are insensitive to the exogenously applied auxin analog 2,4-dichlorophenoxyacetic acid.

Arabidopsis↗
PubMed2000

The pseudomonas AvrPto protein is differentially recognized by tomato and tobacco and is localized to the plant plasma membrane.

The avrPto gene of Pseudomonas syringae pv tomato triggers race-specific resistance in tomato plants carrying Pto, a resistance gene encoding a protein kinase. When introduced into P. s. tabaci, avrPto triggers resistance in tobacco W38 plants that carry the corresponding R gene. The AvrPto protein is believed to be secreted into host cells through the bacterial type III secretion pathway, where it activates disease resistance in tomato by interacting with Pto. We report here the identification of two distinct regions in AvrPto that determine the recognition specificity of this protein in tomato and tobacco. Point mutations in the central region disrupted the avirulence activity in tomato but not in tobacco. Conversely, point mutations in the C-terminal region abolished the avirulence in tobacco but not in tomato. We further report that AvrPto was localized to the plasma membrane of plant cells. Disrupting the membrane association by mutating a putative myristoylation motif of AvrPto abolished the avirulence activity in both tomato and tobacco. These findings demonstrate that AvrPto is recognized differently by the R genes in tomato and tobacco and that the recognition of AvrPto probably is associated with the plasma membrane.

Bacterial Proteins↗
PubMed2000

Mutational analysis of the Arabidopsis nucleotide binding site-leucine-rich repeat resistance gene RPS2.

Disease resistance proteins containing a nucleotide binding site (NBS) and a leucine-rich repeat (LRR) region compose the largest class of disease resistance proteins. These so-called NBS-LRR proteins confer resistance against a wide variety of phytopathogens. To help elucidate the mechanism by which NBS-LRR proteins recognize and transmit pathogen-derived signals, we analyzed mutant versions of the Arabidopsis NBS-LRR protein RPS2. The RPS2 gene confers resistance against Pseudomonas syringae strains carrying the avirulence gene avrRpt2. The activity of RPS2 derivatives in response to AvrRpt2 was measured by using a functional transient expression assay or by expressing the mutant proteins in transgenic plants. Directed mutagenesis revealed that the NBS and an N-terminal leucine zipper (LZ) motif were critical for RPS2 function. Mutations near the N terminus, including an LZ mutation, resulted in proteins that exhibited a dominant negative effect on wild-type RPS2. Scanning the RPS2 molecule with a small in-frame internal deletion demonstrated that RPS2 does not have a large dispensable region. Overexpression of RPS2 in the transient assay in the absence of avrRpt2 also led to an apparent resistant response, presumably a consequence of a low basal activity of RPS2. The NBS and LZ were essential for this overdose effect, whereas the entire LRR was dispensable. RPS2 interaction with a 75-kD protein (p75) required an N-terminal portion of RPS2 that is smaller than the region required for the overdose effect. These findings illuminate the pathogen recognition mechanisms common among NBS-LRR proteins.

Amino Acid Sequence↗
PubMed2000

Pti4 is induced by ethylene and salicylic acid, and its product is phosphorylated by the Pto kinase.

The tomato Pti4 gene encodes a transcription factor that was identified on the basis of its specific interaction with the product of the Pto disease resistance gene in a yeast two-hybrid system. We show here that the Pti4 protein specifically binds the GCC-box cis element, which is present in the promoter region of many pathogenesis-related (PR) genes. Expression of the Pti4 gene in tomato leaves was rapidly induced by ethylene and by infection with Pseudomonas syringae pv tomato, and this induction preceded expression of GCC-box-containing PR genes. Although salicylic acid also induced Pti4 gene expression, it did not induce GCC-box PR genes. Rather, salicylic acid antagonized ethylene-mediated expression of GCC-box PR genes. We demonstrate that the Pti4 protein is specifically phosphorylated by the Pto kinase and that this phosphorylation enhances binding of Pti4 to the GCC box. In addition, induced overexpression of Pto and Pti4 in tomato leaves resulted in a concomitant increase in GCC-box PR genes. Our results support a model in which phosphorylation of the Pti4 protein by the Pto kinase enhances the ability of Pti4 to activate expression of GCC-box PR genes in tomato.

Cycloheximide↗
PubMed2001

A harpin binding site in tobacco plasma membranes mediates activation of the pathogenesis-related gene HIN1 independent of extracellular calcium but dependent on mitogen-activated protein kinase activity.

Harpin from the bean halo-blight pathogen Pseudomonas syringae pv phaseolicola (harpin(Psph)) elicits the hypersensitive response and the accumulation of pathogenesis-related gene transcripts in the nonhost plant tobacco. Here, we report the characterization of a nonproteinaceous binding site for harpin(Psph) in tobacco plasma membranes, which is assumed to mediate the activation of plant defense responses in a receptor-like manner. Binding of 125I-harpin(Psph) to tobacco microsomal membranes (dissociation constant = 425 nM) and protoplasts (dissociation constant = 380 nM) was specific, reversible, and saturable. A close correlation was found between the abilities of harpin(Psph) fragments to elicit the transcript accumulation of the pathogenesis-related tobacco gene HIN1 and to compete for binding of 125I-harpin(Psph) to its binding site. Another elicitor of the hypersensitive response and HIN1 induction in tobacco, the Phytophthora megasperma-derived beta-elicitin beta-megaspermin, failed to bind to the putative harpin(Psph) receptor. In contrast to activation by beta-megaspermin, harpin(Psph)-induced activation of the 48-kD salicylic acid-responsive mitogen-activated protein kinase (MAPK) and HIN1 transcript accumulation were independent of extracellular calcium. Moreover, use of the MAPK kinase inhibitor U0126 revealed that MAPK activity was essential for pathogenesis-related gene expression in harpin(Psph)-treated tobacco cells. Thus, a receptor-mediated MAPK-dependent signaling pathway may mediate the activation of plant defense responses induced by harpin(Psph).

Bacterial Outer Membrane Proteins↗
PubMed1992

Functional homologs of the Arabidopsis RPM1 disease resistance gene in bean and pea.

We showed that a bacterial avirulence (avr) gene function, avrPpiA1, from the pea pathogen Pseudomonas syringae pv pisi, is recognized by some, but not all, genotypes of Arabidopsis. Thus, an avr gene functionally defined on a crop species is also an avr gene on Arabidopsis. The activity of avrPpiA1 on a series of Arabidopsis genotypes is identical to that of the avrRpm1 gene from P.s. pv maculicola previously defined using Arabidopsis. The two avr genes are homologous and encode nearly identical predicted products. Moreover, this conserved avr function is also recognized by some bean and pea cultivars in what has been shown to be a gene-for-gene manner. We further demonstrated that the Arabidopsis disease resistance locus, RPM1, conditioning resistance to avrRpm1, also conditions resistance to bacterial strains carrying avrPpiA1. Therefore, bean, pea, and conceivably other crop species contain functional and potentially molecular homologs of RPM1.

Amino Acid Sequence↗
PubMed1993

Generalized Induction of Defense Responses in Bean Is Not Correlated with the Induction of the Hypersensitive Reaction.

Transcripts for phenylalanine ammonia-lyase, chalcone synthase, chalcone isomerase, and chitinase accumulated in common bean after infiltration with the Pseudomonas syringae pv tabaci Hrp- mutant Pt11528::Hrp1, even though a hypersensitive reaction did not occur. The temporal pattern of this transcript accumulation was similar to that seen after infiltration with wild-type P. s. tabaci Pt11528, which resulted in a hypersensitive reaction. Escherichia coli DH5[alpha], P. fluorescens Pf101, heat-killed Pt11528 cells, and Pt11528 cells treated with protein synthesis inhibitors also induced accumulation of defense transcripts but not a hypersensitive reaction. In contrast, these transcripts were not detected in plants infiltrated with water or P.s. pv phaseolicola NPS3121, a compatible pathogen that causes halo blight. Phytoalexins were produced in bean after infiltration with Pt11528, Pt11528::Hrp1, Pt11528 cells treated with neomycin, or Pf101, but not in plants infiltrated with NPS3121 or water. These results suggest that there are unique biochemical events associated with the expression of a hypersensitive reaction which are distinct from other plant defense responses such as phytoalexin biosynthesis. In addition, our results support the hypothesis that there is a general, nonspecific mechanism for the induction of defense transcripts and phytoalexins by pathogenic and saprophytic bacteria that is distinct from the more specific mechanism associated with the induction of the hypersensitive reaction.

Journal Article↗
PubMed1994

A member of the tomato Pto gene family confers sensitivity to fenthion resulting in rapid cell death.

Leaves of tomato cultivars that contain the Pto bacterial resistance locus develop small necrotic lesions within 24 hr after exposure to fenthion, an organophosphorous insecticide. Recently, the Pto gene was isolated and shown to be a putative serine/threonine protein kinase. Pto is one member of a multigene family that is clustered within a 400-kb region on chromosome 5. Here, we report that another member of this gene family, termed Fen, is responsible for the sensitivity to fenthion. Fen was isolated by map-based cloning using closely linked DNA markers to identify a yeast artificial chromosome clone that spanned the Pto region. After transformation with the Fen gene under control of the cauliflower mosaic virus (CaMV) 35S promoter, tomato plants that are normally insensitive to fenthion rapidly developed extensive necrotic lesions upon exposure to fenthion. Two related insecticides, fensulfothion and fenitrothion, also elicited necrotic lesions specifically on Fen-transformed plants. Transgenic tomato plants harboring integrated copies of the Pto gene under control of the CaMV 35S promoter displayed sensitivity to fenthion but to a lesser extent than did wild-type fenthion-sensitive plants. The Fen protein shares 80% identity (87% similarity) with Pto but does not confer resistance to Pseudomonas syringae pv tomato. These results suggest that Pto and Fen participate in the same signal transduction pathway.

Amino Acid Sequence↗
PubMed1994

Characterization of an Arabidopsis Mutant That Is Nonresponsive to Inducers of Systemic Acquired Resistance.

Systemic acquired resistance (SAR) is a general defense response in plants that is characterized by the expression of pathogenesis-related (PR) genes. SAR can be induced after a hypersensitive response to an avirulent pathogen or by treatment with either salicylic acid (SA) or 2,6-dichloroisonicotinic acid (INA). To dissect the signal transduction pathway of SAR, we isolated an Arabidopsis mutant that lacks the expression of an SA-, INA-, and pathogen-responsive chimeric reporter gene composed of the 5[prime] untranslated region of an Arabidopsis PR gene, [beta]-1,3-glucanase (BGL2), and the coding region of [beta]-glucuronidase (GUS). This mutant, npr1 (nonexpresser of PR genes), carries a single recessive mutation that abolishes the SAR-responsive expression of other PR genes as well. While SA-, INA-, or avirulent pathogen-induced SAR protects wild-type plants from Pseudomonas syringae infection, the mutant cannot be protected by pretreatment with these inducers. The insensitivity of npr1 to SA, INA, and avirulent pathogens in SAR induction indicates that these inducers share a common signal transduction pathway. Moreover, in npr1, the localized expression of PR genes induced by a virulent Pseudomonas pathogen is disrupted, and the lesion formed is less confined. These results suggest a role for PR genes in preventing the proximal spread of pathogens in addition to their suggested role in SAR.

Journal Article↗
PubMed1994

Function of Oxidative Cross-Linking of Cell Wall Structural Proteins in Plant Disease Resistance.

Elicitation of soybean cells causes a rapid insolubilization of two cell wall structural proteins, p33 and p100. Likewise, a short elicitation of 30 min rendered cell walls more refractory to enzyme digestion as assayed by the yield of protoplasts released. This effect could be ascribed to protein cross-linking because of its insensitivity to inhibitors of transcription (actinomycin D) and translation (cycloheximide) and its induction by exogenous H2O2. Moreover, the induced loss of protoplasts could be prevented by preincubation with DTT, which also blocks peroxidase-mediated oxidative cross-linking. The operation of protein insolubilization in plant defense was also demonstrated by its occurrence in the incompatible interaction but not in the compatible interaction between soybean and Pseudomonas syringae pv glycinea. Likewise, protein insolubilization was observed in bean during non-host hypersensitive resistance to the tobacco pathogen P. s. pv tabaci mediated by the hypersensitive resistance and pathogenicity (Hrp) gene cluster. Our data strongly suggest that rapid protein insolubilization leads to a strengthened cell wall, and this mechanism functions as a rapid defense in the initial stages of the hypersensitive response prior to deployment of transcription-dependent defenses.

Journal Article↗
PubMed1994

A mutation in Arabidopsis that leads to constitutive expression of systemic acquired resistance.

Systemic acquired resistance (SAR) is a nonspecific defense response in plants that is associated with an increase in the endogenous level of salicylic acid (SA) and elevated expression of pathogenesis-related (PR) genes. To identify mutants involved in the regulation of PR genes and the onset of SAR, we transformed Arabidopsis with a reporter gene containing the promoter of a beta-1,3-glucanase-encoding PR gene (BGL2) and the coding region of beta-glucuronidase (GUS). The resulting transgenic line (BGL2-GUS) was mutagenized, and the M2 progeny were scored for constitutive GUS activity. We report the characterization of one mutant, cpr1 (constitutive expressor of PR genes), that was identified in this screen and shown by RNA gel blot analysis also to have elevated expression of the endogenous PR genes BGL2, PR-1, and PR-5. Genetic analyses indicated that the phenotype conferred by cpr1 is caused by a single, recessive nuclear mutation and is suppressed in plants producing a bacterial salicylate hydroxylase, which inactivates SA. Furthermore, biochemical analysis showed that the endogenous level of SA is elevated in the mutant. Finally, the cpr1 plants were found to be resistant to the fungal pathogen Peronospora parasitica NOCO2 and the bacterial pathogen Pseudomonas syringae pv maculicola ES4326, which are virulent in wild-type BGL2-GUS plants. Because the cpr1 mutation is recessive and associated with an elevated endogenous level of SA, we propose that the CPR1 gene product acts upstream of SA as a negative regulator of SAR.

Arabidopsis↗
PubMed1994

Tomato mutants altered in bacterial disease resistance provide evidence for a new locus controlling pathogen recognition.

We have employed a genetic approach to study the resistance of tomato to the phytopathogenic bacterium Pseudomonas syringae pv tomato. Resistance to P. s. tomato depends upon expression of the Pto locus in tomato, which encodes a protein with similarity to serine/threonine protein kinases and recognizes pathogen strains expressing the avirulence gene avrPto. Eleven tomato mutants were isolated with altered resistance to P. s. tomato strains expressing avrPto. We identified mutations both in the Pto resistance locus and in a new locus designated Prf (for Pseudomonas resistance and fenthion sensitivity). The genetic approach allowed us to dissect the roles of these loci in signal transduction in response to pathogen attack. Lines carrying mutations in the Pto locus vary 200-fold in the degree to which they are susceptible to P. s. tomato strains expressing avrPto. The pto mutants retain sensitivity to the organophosphate insecticide fenthion; this trait segregates with Pto in genetic crosses. This result suggested that contrary to previous hypotheses, the Pto locus controls pathogen recognition but not fenthion sensitivity. Interestingly, mutations in the prf locus result in both complete susceptibility to P. s. tomato and insensitivity to fenthion, suggesting that Prf plays a role in tomato signaling in response to both pathogen elicitors and fenthion. Because pto and prf mutations do not alter recognition of Xanthomonas campestris strains expressing avrBsP, an avirulence gene recognized by all tested tomato cultivars, Prf does not play a general role in disease resistance but possibly functions specifically in resistance against P. s. tomato. Genetic analysis of F2 populations from crosses of pto and prf homozygotes indicated that the Pto and Prf loci are tightly linked.

Crosses, Genetic↗
PubMed1994

Arabidopsis Mutants Selected for Resistance to the Phytotoxin Coronatine Are Male Sterile, Insensitive to Methyl Jasmonate, and Resistant to a Bacterial Pathogen.

The phytotoxin coronatine and the plant growth regulator methyl jasmonate (MeJA) caused similar growth-inhibitory effects on Arabidopsis seedlings. To test whether these two compounds have similar action, 14 independent coi1 (coronatine-insensitive) mutants of Arabidopsis were selected. The mutants segregated as single recessive Mendelian markers, and all were alleles at the coi1 locus. All coi1 mutants were also insensitive to MeJA and were male sterile. Both coronatine and MeJA inhibited root growth, stimulated anthocyanin accumulation, and increased the level of two proteins of ~31 and ~29 kD detected in SDS-polyacrylamide gels of wild-type Arabidopsis but caused none of these effects in the coi1 mutant. Coronatine and MeJA also induced the systemic appearance of proteinase inhibitor activity in tomato. The male-sterile flowers of the coi1 mutant produced abnormal pollen and had reduced level of an ~31-kD protein, which was abundant in the wild-type flowers. A coronatine-producing strain of Pseudomonas syringae grew in leaves of wild-type Arabidopsis to a population more than 100 times greater than it reached in the coi1 mutant. We conclude that coronatine mimics the action of MeJA and that coi1 controls a step in MeJA perception/response and in flower development.

Journal Article↗
PubMed1995

Intergeneric transfer and functional expression of the tomato disease resistance gene Pto.

Plant disease resistance loci have been used successfully in breeding programs to transfer traits from resistant germplasm to susceptible plant cultivars. The molecular cloning of plant disease resistance genes now permits the transfer of such traits across species boundaries by genetic transformation of recipient hosts. The tomato disease resistance gene Pto confers resistance to strains of the bacterial pathogen Pseudomonas syringae pv tomato expressing the avirulence gene avrPto. Transformation of Nicotiana benthamiana with Pto results in specific resistance to P. s. pv tabaci strains carrying avrPto. The resistant phenotype is manifested by a strong inhibition of bacterial growth and the ability to exhibit a hypersensitive response. Resistance cosegregates with the Pto gene in transgene selfings and testcrosses. Our results demonstrate the conservation of disease resistance functions across genus boundaries and suggest that the utility of host-specific resistance genes can be extended by intergeneric transfer.

Base Sequence↗