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dc.contributor.author Lee, Il Hwan -
dc.contributor.author Lee, In Chul -
dc.contributor.author Kim, Jeongsik -
dc.contributor.author Kim, Jin Hee -
dc.contributor.author Chung, Eui-Hwan -
dc.contributor.author Kim, Hyo Jung -
dc.contributor.author Park, Su Jin -
dc.contributor.author Kim, Yong Min -
dc.contributor.author Kang, Sin Kyu -
dc.contributor.author Nam, Hong Gil -
dc.contributor.author Woo, Hye Ryun -
dc.contributor.author Lim, Pyung Ok -
dc.date.available 2018-01-25T01:07:36Z -
dc.date.created 2017-04-10 -
dc.date.issued 2016-10 -
dc.identifier.issn 0031-9317 -
dc.identifier.uri http://hdl.handle.net/20.500.11750/5075 -
dc.description.abstract Leaf senescence is not only primarily governed by developmental age but also influenced by various internal and external factors. Although some genes that control leaf senescence have been identified, the detailed regulatory mechanisms underlying integration of diverse senescence-associated signals into the senescence programs remain to be elucidated. To dissect the regulatory pathways involved in leaf senescence, we isolated the not oresara1-1 (nore1-1) mutant showing accelerated leaf senescence phenotypes from an EMS-mutagenized Arabidopsis thaliana population. We found that altered transcriptional programs in defense response-related processes were associated with the accelerated leaf senescence phenotypes observed in nore1-1 through microarray analysis. The nore1-1 mutation activated defense program, leading to enhanced disease resistance. Intriguingly, high ambient temperature effectively suppresses the early senescence and death phenotypes of nore1-1. The gene responsible for the phenotypes of nore1-1 contains a missense mutation in SENESCENCE-ASSOCIATED E3 UBIQUITIN LIGASE 1 (SAUL1), which was reported as a negative regulator of premature senescence in the light intensity- and PHYTOALEXIN DEFICIENT 4 (PAD4)-dependent manner. Through extensive double mutant analyses, we recently identified suppressor of the G2 Allele of SKP1b (SGT1b), one of the positive regulators for disease resistance conferred by many resistance (R) proteins, as a downstream signaling component in NORE1-mediated senescence and cell death pathways. In conclusion, NORE1/SAUL1 is a key factor integrating signals from temperature-dependent defense programs and leaf senescence in Arabidopsis. These findings provide a new insight that plants might utilize defense response program in regulating leaf senescence process, possibly through recruiting the related genes during the evolution of the leaf senescence program. © 2016 Scandinavian Plant Physiology Society -
dc.language English -
dc.publisher Wiley Blackwell -
dc.title NORE1/SAUL1 integrates temperature-dependent defense programs involving SGT1b and PAD4 pathways and leaf senescence in Arabidopsis -
dc.type Article -
dc.identifier.doi 10.1111/ppl.12434 -
dc.identifier.scopusid 2-s2.0-85027930593 -
dc.identifier.bibliographicCitation Physiologia Plantarum, v.158, no.2, pp.180 - 199 -
dc.description.isOpenAccess FALSE -
dc.subject.keywordPlus AGE-RELATED RESISTANCE -
dc.subject.keywordPlus CELL-DEATH -
dc.subject.keywordPlus Disease Resistance -
dc.subject.keywordPlus E3 UBIQUITIN LIGASE -
dc.subject.keywordPlus F-BOX PROTEIN -
dc.subject.keywordPlus HYPERSENSITIVE RESPONSE -
dc.subject.keywordPlus PLANT INNATE IMMUNITY -
dc.subject.keywordPlus SALICYLIC-ACID -
dc.subject.keywordPlus SYSTemIC ACQUIRED-RESISTANCE -
dc.subject.keywordPlus Transcription Factor -
dc.citation.endPage 199 -
dc.citation.number 2 -
dc.citation.startPage 180 -
dc.citation.title Physiologia Plantarum -
dc.citation.volume 158 -

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