Suppression and Restoration of Lesion Formation in Arabidopsis lsd Mutants

Weymann, Kris; Hunt, M. L.; Uknes, Scott; Neuenschwander, Urs; Lawton, Kay A.; Steiner, Henry-York; Ryals, John

doi:10.2307/3870147

Cited by 100 publications

(132 citation statements)

References 0 publications

Supporting

Mentioning

120

Contrasting

Unclassified

Order By: Relevance

“…In this pathway, formation of lesions leads to SA accumulation. To our knowledge, all lesion-mimic mutants that have been tested display elevated SA levels (Bowling et al, 1997;Greenberg et al, 1994;Shah et al, 1999;Weymann et al, 1995;Yu et al, 1998;Yu et al, 2000). Our data are consistent with the idea that production of SA in response to lesion formation is PAD4-independent.…”

Section: Analysis Ofsupporting

confidence: 88%

Constitutive salicylic acid‐dependent signaling in cpr1 and cpr6 mutants requires PAD4

Jirage¹,

Zhou²,

Cooper³

et al. 2001

The Plant Journal

127

View full text Add to dashboard Cite

SummarySalicylic acid (SA)-dependent signaling controls activation of a set of plant defense mechanisms that are important for resistance to a variety of microbial pathogens. Many Arabidopsis mutants that display altered SA-dependent signaling have been isolated. We used double mutant analysis to determine the relative positions of the pad4, cpr1, cpr5, cpr6, dnd1 and dnd2 mutations in the signal transduction network leading to SA-dependent activation of defense gene expression and disease resistance. The pad4 mutation causes failure of SA accumulation in response to infection by certain pathogens, while the other mutations cause constitutively high levels of SA, defense gene expression and resistance. The cpr1 pad4, cpr5 pad4, cpr6 pad4, dnd1 pad4 and dnd2 pad4 double mutants were constructed and assayed for stature, presence of spontaneous lesions, resistance to Pseudomonas syringae and Peronospora parasitica, SA levels, expression of PAD4, PR-1 and PDF1.2, and accumulation of camalexin. We found that the effects of the cpr1 and cpr6 mutations on SA-dependent gene expression are completely dependent on PAD4 function. In contrast, SA accumulation in the lesion-mimic mutant cpr5 is partially PAD4-independent, while in dnd1 and dnd2 mutants it is completely PAD4-independent. A model describing a possible arrangement of activities in the signal transduction network is presented.

show abstract

Section: Analysis Ofsupporting

confidence: 88%

Constitutive salicylic acid‐dependent signaling in cpr1 and cpr6 mutants requires PAD4

Jirage¹,

Zhou²,

Cooper³

et al. 2001

The Plant Journal

127

View full text Add to dashboard Cite

show abstract

“…The cet mutants resemble mutants that mimic this defense response (Dietrich et al, 1994;Greenberg et al, 1994;Hu et al, 1998). Some of the lesions occur independently of SA, while others require elevated levels of SA (Hunt et al, 1997;Weymann et al, 1995). The wildtype copies of the mutated genes had been thought to be involved in the genetic control of the HR response (Dietrich et al, 1994;Greenberg and Ausubel, 1993).…”

Section: Discussionmentioning

confidence: 99%

Isolation and characterization of signal transduction mutants of Arabidopsis thaliana that constitutively activate the octadecanoid pathway and form necrotic microlesions

et al. 2001

View full text Add to dashboard Cite

Summary Thionins are a group of antimicrobial polypeptides that form part of the plant's defense mechanism against pathogens. The Thi 2.1 thionin gene of Arabidopsis thaliana has been shown to be inducible by jasmonic acid (JA), an oxylipin‐like hormone derived from oxygenated linolenic acid and synthesized via the octadecanoid pathway. The JA‐dependent regulation of the Thi 2.1 gene has been exploited for setting up a genetic screen for the isolation of signal transduction mutants that constitutively express the Thi 2.1 gene. Ten cet‐mutants have been isolated which showed a constitutive expression of the thionin gene. Allelism tests revealed that they represent at least five different loci. Some mutants are dominant, others recessive, but all cet mutations behaved as monogenic traits when backcrossed with Thi 2.1‐GUS plants. Some of the mutants overproduce JA and its bioactive precursor 12‐oxophytodienoic acid (OPDA) up to 40‐fold while others have the same low levels as the control wildtype plants. Two of the mutants showed a strong induction of both the salicylic acid (SA)‐ and the JA‐dependent signaling pathways, while the majority seems to be affected only in the octadecanoid pathway. The Thi 2.1 thionin gene and the Pdf 1.2 defensin gene are activated independently, though both are regulated by JA. The cet‐mutants, except for one, also show a spontaneous leaf cell necrosis, a reaction often associated with the systemic acquired resistance (SAR) pathway.

show abstract

“…SA levels somewhat lower compared to vtc1 have been reported for the turnip crinkle virus-resistant Arabidopsis mutant Di-17, showing that low doses of SA are sufficient to induce certain defense genes (Dempsey et al, 1997). On the other hand, mutants, such as the constitutive expression of PR-1 (cep; Silva et al, 1999), the lesion simulating disease mutants lsd1, lsd6 and lsd7 (Weymann et al, 1995;Dietrich et al, 1997), as well as the accelerated cell death mutant acd2 (Mach et al, 2001), possess much higher levels of SA and also show increased disease resistance to virulent pathogens Table I. P. parasitica conidiophore production in 4-week-old wild-type, vtc1, and vtc2 plants Conidiophore production was assessed on leaves of the wild type as well as the AsA-deficient mutants vtc1 and vtc2 7 d after inoculation with P. parasitica pv Noco at 5 3 10 4 conidiophores mL 21 in water (replicate 1) or with 7 to 8 3 10 9 conidiophores mL 21 (replicate 2).…”

Section: A Subset Of Senescence-associated Gene Transcripts Is Elevatmentioning

confidence: 99%

The Timing of Senescence and Response to Pathogens Is Altered in the Ascorbate-Deficient Arabidopsis Mutant vitamin c-1

et al. 2004

View full text Add to dashboard Cite

The ozone-sensitive Arabidopsis mutant vitamin c-1 (vtc1) is deficient in l-ascorbic acid (AsA) due to a mutation in GDP-Man pyrophosphorylase (Conklin et al., 1999), an enzyme involved in the AsA biosynthetic pathway (Smirnoff et al., 2001). In this study, the physiology of this AsA deficiency was initially investigated in response to biotic (virulent pathogens) stress and subsequently with regards to the onset of senescence. Infection with either virulent Pseudomonas syringae or Peronospora parasitica resulted in largely reduced bacterial and hyphal growth in the vtc1 mutant in comparison to the wild type. When vitamin c-2 (vtc2), another AsA-deficient mutant, was challenged with P. parasitica, growth of the fungus was also reduced, indicating that the two AsA-deficient mutants are more resistant to these pathogens. Induction of pathogenesis-related proteins PR-1 and PR-5 is significantly higher in vtc1 than in the wild type when challenged with virulent P. syringae. In addition, the vtc1 mutant exhibits elevated levels of some senescence-associated gene (SAG) transcripts as well as heightened salicylic acid levels. Presumably, therefore, low AsA is causing vtc1 to enter at least some stage(s) of senescence prematurely with an accompanying increase in salicylic acid levels that results in a faster induction of defense responses.

show abstract

Suppression and Restoration of Lesion Formation in Arabidopsis lsd Mutants

Cited by 100 publications

References 0 publications

Constitutive salicylic acid‐dependent signaling in cpr1 and cpr6 mutants requires PAD4

Constitutive salicylic acid‐dependent signaling in cpr1 and cpr6 mutants requires PAD4

Isolation and characterization of signal transduction mutants of Arabidopsis thaliana that constitutively activate the octadecanoid pathway and form necrotic microlesions

The Timing of Senescence and Response to Pathogens Is Altered in the Ascorbate-Deficient Arabidopsis Mutant vitamin c-1

Contact Info

Product

Resources

About