A delayed leaf senescence mutant is defective in arginyl‐tRNA:protein arginyltransferase, a component of the N‐end rule pathway in <i>Arabidopsis</i>

Yoshida, Satoko; Ito, Masaki; Callis, Judy; Nishida, Ikuo; Watanabe, Akira

doi:10.1046/j.1365-313x.2002.01407.x

Cited by 138 publications

(127 citation statements)

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“…Another mutant (dLs1), defective in a gene encoding an arginyl-tRNA; proteinarginyl transferase (R-transferase) and involved in the N-end rule proteolytic pathway in yeast and mammals, exhibited delayed senescence. This observation suggests that the Nend rule pathway plays an important role in the progress of leaf senescence (Yoshida et al, 2002).…”

Section: Macromolecule Breakdown: Protein Degradation and Recyclingmentioning

confidence: 87%

Large‐scale identification of leaf senescence‐associated genes

et al. 2003

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SummaryLeaf senescence is a form of programmed cell death, and is believed to involve preferential expression of a speci®c set of`senescence-associated genes' (SAGs). To decipher the molecular mechanisms and the predicted complex network of regulatory pathways involved in the senescence program, we have carried out a large-scale gene identi®cation study in a reference plant, Arabidopsis thaliana. Using suppression subtractive hybridization, we isolated approximately 800 cDNA clones representing SAGs expressed in senescing leaves. Differential expression was con®rmed by Northern blot analysis for 130 non-redundant genes. Over 70 of the identi®ed genes have not previously been shown to participate in the senescence process. SAGencoded proteins are likely to participate in macromolecule degradation, detoxi®cation of oxidative metabolites, induction of defense mechanisms, and signaling and regulatory events. Temporal expression pro®les of selected genes displayed several distinct patterns, from expression at a very early stage, to the terminal phase of the senescence syndrome. Expression of some of the novel SAGs, in response to age, leaf detachment, darkness, and ethylene and cytokinin treatment was compared. The large repertoire of SAGs identi®ed here provides global insights about regulatory, biochemical and cellular events occurring during leaf senescence.

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Section: Macromolecule Breakdown: Protein Degradation and Recyclingmentioning

confidence: 87%

Large‐scale identification of leaf senescence‐associated genes

et al. 2003

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“…Arabidopsis contains 2 ATE genes, one of which (ATE1) has been implicated in leaf senescence (5). Model substrates starting with Asp or Glu were specifically stabilized in protoplasts of the ate1 mutant, confirming a biochemical role in the N-end rule pathway (5). Key to the formation of N-degrons is the activity of specific endopeptidases that expose primary, secondary, or tertiary destabilizing residues (Fig.…”

mentioning

confidence: 91%

The N-end rule pathway promotes seed germination and establishment through removal of ABA sensitivity in Arabidopsis

Holman

Jones²,

Russell

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

170

205

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The N-end rule pathway targets protein degradation through the identity of the amino-terminal residue of specific protein substrates. Two components of this pathway in Arabidopsis thaliana, PROTEOLYSIS6 (PRT6) and arginyl-tRNA:protein arginyltransferase (ATE), were shown to regulate seed after-ripening, seedling sugar sensitivity, seedling lipid breakdown, and abscisic acid (ABA) sensitivity of germination. Sensitivity of prt6 mutant seeds to ABA inhibition of endosperm rupture reduced with after-ripening time, suggesting that seeds display a previously undescribed window of sensitivity to ABA. Reduced root growth of prt6 alleles and the ate1 ate2 double mutant was rescued by exogenous sucrose, and the breakdown of lipid bodies and seed-derived triacylglycerol was impaired in mutant seedlings, implicating the N-end rule pathway in control of seed oil mobilization. Epistasis analysis indicated that PRT6 control of germination and establishment, as exemplified by ABA and sugar sensitivity, as well as storage oil mobilization, occurs at least in part via transcription factors ABI3 and ABI5. The N-end rule pathway of protein turnover is therefore postulated to inactivate as-yet unidentified key component(s) of ABA signaling to influence the seed-to-seedling transition.abscisic acid ͉ aminoacyl tRNA protein transferase ͉ lipid bodies ͉ targeted protein degradation

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“…The arginyl-tRNA:protein arginyltransferase ATE1, which is a component of the N-end rule pathway within the ubiquitin-dependent proteolytic system, also positively regulates senescence. Knockout of the ATE1 gene in delayed senescence1 mutant plants resulted in delayed leaf senescence (Yoshida et al, 2002). In contrast to ORE9 and ATE1, the RING-type ubiquitin ligase NITROGEN LIMITATION ADAPTATION (NLA) and the PLANT U-BOX (PUB)-ARMADILLO (ARM) E3 ubiquitin ligase SENESCENCE-ASSOCIATED UBIQUITIN LIGASE1 (SAUL1; At1g20780) are negative regulators of plant senescence (Peng et al, 2007;Raab et al, 2009).…”

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confidence: 99%

Early Senescence and Cell Death in Arabidopsis saul1 Mutants Involves the PAD4-Dependent Salicylic Acid Pathway

Vogelmann

Drechsel²,

Bergler³

et al. 2012

Plant Physiology

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Age-dependent leaf senescence and cell death in Arabidopsis (Arabidopsis thaliana) requires activation of the transcription factor ORESARA1 (ORE1) and is not initiated prior to a leaf age of 28 d. Here, we investigate the conditional execution of events that regulate early senescence and cell death in senescence-associated ubiquitin ligase1 (saul1) mutants, deficient in the PLANT U-BOX-ARMADILLO E3 ubiquitin ligase SAUL1. In saul1 mutants challenged with low light, the switch of age-dependent cell death was turned on prematurely, as indicated by the accumulation of ORE1 transcripts, induction of the senescence marker gene SENESCENCE-ASSOCIATED GENE12, and cell death. However, ORE1 accumulation by itself was not sufficient to cause saul1 phenotypes, as demonstrated by double mutant analysis. Exposure of saul1 mutants to low light for only 24 h did not result in visible symptoms of senescence; however, the senescence-promoting transcription factor genes WRKY53, WRKY6, and NAC-LIKE ACTIVATED BY AP3/PI were up-regulated, indicating that senescence in saul1 seedlings was already initiated. To resolve the time course of gene expression, microarray experiments were performed at narrow intervals. Differential expression of the genes involved in salicylic acid and defense mechanisms were the earliest events detected, suggesting a central role for salicylic acid in saul1 senescence and cell death. The salicylic acid content increased in low-light-treated saul1 mutants, and application of exogenous salicylic acid was indeed sufficient to trigger saul1 senescence in permissive light conditions. Double mutant analyses showed that PHYTOALEXIN DEFICIENT4 (PAD4) but not NONEXPRESSER OF PR GENES1 (NPR1) is essential for saul1 phenotypes. Our results indicate that saul1 senescence depends on the PAD4-dependent salicylic acid pathway but does not require NPR1 signaling.

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A delayed leaf senescence mutant is defective in arginyl‐tRNA:protein arginyltransferase, a component of the N‐end rule pathway in Arabidopsis

Cited by 138 publications

References 38 publications

Large‐scale identification of leaf senescence‐associated genes

Large‐scale identification of leaf senescence‐associated genes

The N-end rule pathway promotes seed germination and establishment through removal of ABA sensitivity in Arabidopsis

Early Senescence and Cell Death in Arabidopsis saul1 Mutants Involves the PAD4-Dependent Salicylic Acid Pathway

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