Salicylic acid has a role in regulating gene expression during leaf senescence

Morris, Karl; Mackerness, Soheila A.-H.; Page, Tania; John, C. F.; Murphy, Alex M.; Carr, John P.; Buchanan‐Wollaston, Vicky

doi:10.1046/j.1365-313x.2000.00836.x

Cited by 491 publications

(388 citation statements)

References 51 publications

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“…Conversely, there are reports that an elevation of AsA results in a delay in senescence (Garg and Kapoor, 1972). Second, as mentioned above, SA levels have been shown to increase during senescence in Arabidopsis (Morris et al, 2000) and are also elevated in vtc1. It follows from this phenotype that SAG27, which is induced by SA (Quirino et al, 1999), is up-regulated in vtc1 (Fig.…”

Section: Ascorbate Deficiency In Vtc1 Is Associated With Promotion Ofmentioning

confidence: 91%

“…Furthermore, during senescence SA levels increase, resulting in the induction of defense-related genes (Quirino et al, 1999;Morris et al, 2000). To test whether leaves of vtc1 used for P. syringae infection are in an early stage of senescence, expression levels of several senescence-associated genes (SAGs) were tested using semiquantitative reverse transcription (RT)-PCR (Fig.…”

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

confidence: 99%

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

et al. 2004

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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.

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Section: Ascorbate Deficiency In Vtc1 Is Associated With Promotion Ofmentioning

confidence: 91%

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

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“…When the mutation did not lead to a change in a restriction site, we generated derived CAPS markers using the dCAPS web tool (Neff et al, 1998). The Etr1-1 (Hua and Meyerowitz, 1998), NahG (Morris et al, 2000), rar1-10 , sgt1b , coi1-1 (Xie et al, 1998), pad4-1 (Nishimura et al, 2003), and npr1-1 (Nishimura et al, 2003) primers have been described previously. See Supplemental Table 5 online for a listing of primers used in genotyping mutations.…”

Section: Double Mutant Constructionmentioning

confidence: 99%

ArabidopsisPEN3/PDR8, an ATP Binding Cassette Transporter, Contributes to Nonhost Resistance to Inappropriate Pathogens That Enter by Direct Penetration

et al. 2006

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Arabidopsis thaliana is a host to the powdery mildew Erysiphe cichoracearum and nonhost to Blumeria graminis f. sp hordei, the powdery mildew pathogenic on barley (Hordeum vulgare). Screening for Arabidopsis mutants deficient in resistance to barley powdery mildew identified PENETRATION3 (PEN3). pen3 plants permitted both increased invasion into epidermal cells and initiation of hyphae by B. g. hordei, suggesting that PEN3 contributes to defenses at the cell wall and intracellularly. pen3 mutants were compromised in resistance to the necrotroph Plectosphaerella cucumerina and to two additional inappropriate biotrophs, pea powdery mildew (Erysiphe pisi) and potato late blight (Phytophthora infestans). Unexpectedly, pen3 mutants were resistant to E. cichoracearum. This resistance was salicylic acid–dependent and correlated with chlorotic patches. Consistent with this observation, salicylic acid pathway genes were hyperinduced in pen3 relative to the wild type. The phenotypes conferred by pen3 result from the loss of function of PLEIOTROPIC DRUG RESISTANCE8 (PDR8), a highly expressed putative ATP binding cassette transporter. PEN3/PDR8 tagged with green fluorescent protein localized to the plasma membrane in uninfected cells. In infected leaves, the protein concentrated at infection sites. PEN3/PDR8 may be involved in exporting toxic materials to attempted invasion sites, and intracellular accumulation of these toxins in pen3 may secondarily activate the salicylic acid pathway.

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“…Cytokinins have been found to play a role in delaying leaf senescence (Gan and Amasino, 1995;McCabe et al, 2001;Kim et al, 2006), whereas ethylene, jasmonates (JAs), brassinosteroids, and salicylic acids are known to promote the process of senescence (Grbic and Bleecker, 1995;Oh et al, 1997;Morris et al, 2000;Jing et al, 2002;Yin et al, 2002). For example, JA could rapidly induce the expression of several SAGs (Park et al, 1998;Schenk et al, 2000).…”

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confidence: 99%

A Novel Nuclear-Localized CCCH-Type Zinc Finger Protein, OsDOS, Is Involved in Delaying Leaf Senescence in Rice

et al. 2006

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Leaf senescence is a developmentally programmed degeneration process, which is fine tuned by a complex regulatory network for plant fitness. However, molecular regulation of leaf senescence is poorly understood, especially in rice (Oryza sativa), an important staple crop for more than half of the world population. Here, we report a novel nuclear-localized CCCH-type zinc finger protein, Oryza sativa delay of the onset of senescence (OsDOS), involved in delaying leaf senescence in rice. The expression of OsDOS was down-regulated during natural leaf senescence, panicle development, and pollination, although its transcripts were accumulated in various organs. RNAi knockdown of OsDOS caused an accelerated age-dependent leaf senescence, whereas its overexpression produced a marked delay of leaf senescence, suggesting that it acts as a negative regulator for leaf senescence. A genome-wide expression analysis further confirmed its negative regulation for leaf senescence and revealed that, in particular, the jasmonate (JA) pathway was found to be hyperactive in the OsDOS RNAi transgenic lines but impaired in the OsDOS overexpressing transgenic lines, indicating that this pathway is likely involved in the OsDOS-mediated delaying of leaf senescence. Furthermore, methyl JA treatments of both seeds and detached leaves from the RNAi and the overexpressing transgenic lines showed hyperand hyporesponses, respectively, consistent with the negative regulation of the JA pathway by OsDOS. Together, these results indicate that OsDOS is a novel nuclear protein that delays leaf senescence likely, at least in part, by integrating developmental cues to the JA pathway.

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Salicylic acid has a role in regulating gene expression during leaf senescence

Cited by 491 publications

References 51 publications

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

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

ArabidopsisPEN3/PDR8, an ATP Binding Cassette Transporter, Contributes to Nonhost Resistance to Inappropriate Pathogens That Enter by Direct Penetration

A Novel Nuclear-Localized CCCH-Type Zinc Finger Protein, OsDOS, Is Involved in Delaying Leaf Senescence in Rice

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