Salt causes ion disequilibrium‐induced programmed cell death in yeast and plants

Huh, Gyung-Hye; Damsz, Barbara; Matsumoto, Tracie K.; Reddy, M. Venkat Ram; Rus, Ana; Ibeas, José I.; Narasimhan, Meena L.; Bressan, Ray A.; Hasegawa, Paul M.

doi:10.1046/j.0960-7412.2001.01247.x

Cited by 261 publications

(215 citation statements)

References 48 publications

Supporting

Mentioning

205

Contrasting

Unclassified

Order By: Relevance

“…This phenotype is unlike that of sos1 seedlings, for which salt/osmotic stress sensitivity is associated with the death of root meristematic cells (Huh et al, 2002). Instead, the salt/osmotic stress-responsive phenotype of stt3a seedlings resembles the phenotype caused by the mutation to the RSW3 locus ( rsw3-1 ) that encodes ␣ -glucosidase II (Burn et al, 2002).…”

Section: Isolation Of the Salt/osmotic Stress-sensitive Stt3a Mutantsmentioning

confidence: 67%

The STT3a Subunit Isoform of the Arabidopsis Oligosaccharyltransferase Controls Adaptive Responses to Salt/Osmotic Stress

Koiwa¹

2003

THE PLANT CELL ONLINE

191

287

View full text Add to dashboard Cite

Arabidopsis stt3a-1 and stt3a-2 mutations cause NaCl/osmotic sensitivity that is characterized by reduced cell division in the root meristem. Sequence comparison of the STT3a gene identified a yeast ortholog, STT3 , which encodes an essential subunit of the oligosaccharyltransferase complex that is involved in protein N -glycosylation. NaCl induces the unfolded protein response in the endoplasmic reticulum (ER) and cell cycle arrest in root tip cells of stt3a seedlings, as determined by expression profiling of ER stress-responsive chaperone ( BiP -GUS ) and cell division ( CycB1;1 -GUS ) genes, respectively. Together, these results indicate that plant salt stress adaptation involves ER stress signal regulation of cell cycle progression. Interestingly, a mutation ( stt3b-1 ) in another Arabidopsis STT3 isogene ( STT3b ) does not cause NaCl sensitivity. However, the stt3a-1 stt3b-1 double mutation is gametophytic lethal. Apparently, STT3a and STT3b have overlapping and essential functions in plant growth and developmental processes, but the pivotal and specific protein glycosylation that is a necessary for recovery from the unfolded protein response and for cell cycle progression during salt/osmotic stress recovery is associated uniquely with the function of the STT3a isoform.

show abstract

Section: Isolation Of the Salt/osmotic Stress-sensitive Stt3a Mutantsmentioning

confidence: 67%

The STT3a Subunit Isoform of the Arabidopsis Oligosaccharyltransferase Controls Adaptive Responses to Salt/Osmotic Stress

Koiwa¹

2003

THE PLANT CELL ONLINE

191

287

View full text Add to dashboard Cite

show abstract

“…52 Abiotic stresses, including temperature, salinity, drought, light, ROS, and ozone, are now often regarded not as toxins, but rather as elicitors of PCD, when plant cells are chronically exposed to physiological levels of these stresses. 41,[73][74][75][76][77] However, necrosis, which represents an uncontrolled form of cell death, does occur in plant cells when they are exposed to high levels of abiotic stress that the plant cannot override with their tolerance mechanisms. ROS are pivotal mediators of PCD in plants.…”

Section: Discussionmentioning

confidence: 99%

AtBAG6, a novel calmodulin-binding protein, induces programmed cell death in yeast and plants

et al. 2005

View full text Add to dashboard Cite

Calmodulin (CaM) influences many cellular processes by interacting with various proteins. Here, we isolated AtBAG6, an Arabidopsis CaM-binding protein that contains a central BCL-2-associated athanogene (BAG) domain. In yeast and plants, overexpression of AtBAG6 induced cell death phenotypes consistent with programmed cell death (PCD). Recombinant AtBAG6 had higher affinity for CaM in the absence of free Ca 2 þ than in its presence. An IQ motif (IQXXXRGXXXR, where X denotes any amino-acid) was required for Ca 2 þ -independent CaM complex formation and single amino-acid changes within this motif abrogated both AtBAG6-activated CaM-binding and cell death in yeast and plants. A 134-amino-acid stretch, encompassing both the IQ motif and BAG domain, was sufficient to induce cell death. Agents generating oxygen radicals, which are known to be involved in plant PCD, specifically induced the AtBAG6 transcript. Collectively, these results suggest that AtBAG6 is a stress-upregulated CaM-binding protein involved in plant PCD.

show abstract

“…Next to its role in age-dependent cell death, ORE1/ANAC092 has been shown to mediate salt-induced senescence and cell death, too. Compared with the wild type, anac092-1 mutants were more tolerant to salt (Huh et al, 2002;Balazadeh et al, 2010). To study whether SAUL1 is also involved in the salt response, wild-type and saul1-1 mutant seedlings were grown in permissive light conditions for 5 d, transferred to agar plates containing 0 or 150 mM NaCl, and kept in permissive light.…”

Section: Resultsmentioning

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

View full text Add to dashboard Cite

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.

show abstract

Salt causes ion disequilibrium‐induced programmed cell death in yeast and plants

Cited by 261 publications

References 48 publications

The STT3a Subunit Isoform of the Arabidopsis Oligosaccharyltransferase Controls Adaptive Responses to Salt/Osmotic Stress

The STT3a Subunit Isoform of the Arabidopsis Oligosaccharyltransferase Controls Adaptive Responses to Salt/Osmotic Stress

AtBAG6, a novel calmodulin-binding protein, induces programmed cell death in yeast and plants

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

Contact Info

Product

Resources

About