Leaf Senescence: Signals, Execution, and Regulation

Guo, Yongfeng; Gan, Susheng

doi:10.1016/s0070-2153(05)71003-6

Cited by 274 publications

(243 citation statements)

References 167 publications

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“…Taken together with our results from coi1, the contrasting controls of JA-related defense and senescence programming in cpr5 are proposed in Figure 7, but with enhanced senescence prevailing over any pathogen control exerted by enhanced defense gene expression. In addition to JA, the defense signal molecules SA and ET have also been implicated in senescence responses (Guo and Gan, 2005). We therefore screened mutants impaired in SA (NahG and eds5) and ET signaling (ein2 and etr1).…”

Section: Discussionmentioning

confidence: 99%

Fusarium oxysporum hijacks COI1‐mediated jasmonate signaling to promote disease development in Arabidopsis

Thatcher

Manners

Kazan³

2009

The Plant Journal

268

298

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SUMMARYAlthough defense responses mediated by the plant oxylipin jasmonic acid (JA) are often necessary for resistance against pathogens with necrotrophic lifestyles, in this report we demonstrate that jasmonate signaling mediated through COI1 in Arabidopsis thaliana is responsible for susceptibility to wilt disease caused by the root-infecting fungal pathogen Fusarium oxysporum. Despite compromised JA-dependent defense responses, the JA perception mutant coronatine insensitive 1 (coi1), but not JA biosynthesis mutants, exhibited a high level of resistance to wilt disease caused by F. oxysporum. This response was independent from salicylic acid-dependent defenses, as coi1/NahG plants showed similar disease resistance to coi1 plants. Inoculation of reciprocal grafts made between coi1 and wild-type plants revealed that coi1-mediated resistance occurred primarily through the coi1 rootstock tissues. Furthermore, microscopy and quantification of fungal DNA during infection indicated that coi1-mediated resistance was not associated with reduced fungal penetration and colonization until a late stage of infection, when leaf necrosis was highly developed in wild-type plants. In contrast to wild-type leaves, coi1 leaves showed no necrosis following the application of F. oxysporum culture filtrate, and showed reduced expression of senescence-associated genes during disease development, suggesting that coi1 resistance is most likely achieved through the inhibition of F. oxysporum-incited lesion development and plant senescence. Together, our results indicate that F. oxysporum hijacks non-defensive aspects of the JA-signaling pathway to cause wilt-disease symptoms that lead to plant death in Arabidopsis.

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Section: Discussionmentioning

confidence: 99%

Fusarium oxysporum hijacks COI1‐mediated jasmonate signaling to promote disease development in Arabidopsis

Thatcher

Manners

Kazan³

2009

The Plant Journal

268

298

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“…The senescence process is initiated by chloroplast degeneration (Gepstein, 2004), which is followed by the catabolism of macromolecules, such as nucleic acids, proteins, and lipids (Ulker et al, 2007), and degeneration of mitochondria and nuclei (Gan and Amasino, 1997;Lim et al, 2007a). The released nutrients are transferred to actively growing young leaves and developing fruits and seeds, leading to increased reproductive success (Gan and Amasino, 1997;Guo and Gan, 2005;Lim et al, 2007a).…”

Section: Introductionmentioning

confidence: 99%

ETHYLENE-INSENSITIVE3 Is a Senescence-Associated Gene That Accelerates Age-Dependent Leaf Senescence by Directly Repressing miR164 Transcription in Arabidopsis

et al. 2013

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Numerous endogenous and environmental signals regulate the intricate and highly orchestrated process of plant senescence. Ethylene is a well-known inducer of senescence, including fruit ripening and flower and leaf senescence. However, the underlying molecular mechanism of ethylene-induced leaf senescence remains to be elucidated. Here, we examine ETHYLENE-INSENSITIVE3 (EIN3), a key transcription factor in ethylene signaling, and find that EIN3 is a functional senescence-associated gene. Constitutive overexpression or temporary activation of EIN3 is sufficient to accelerate leaf senescence symptoms. Conversely, loss of EIN3 and EIN3-Like1 (its close homolog) function leads to a delay in agedependent and ethylene-, jasmonic acid-, or dark-induced leaf senescence. We further found that EIN3 acts downstream of ORESARA2 (ORE2)/ORE3/EIN2 to repress miR164 transcription and upregulate the transcript levels of ORE1/NAC2, a target gene of miR164. EIN3 directly binds to the promoters of microRNA164 (miR164), and this binding activity progressively increases during leaf ageing. Genetic analysis revealed that overexpression of miR164 or knockout of ORE1/NAC2 represses EIN3-induced early-senescence phenotypes. Collectively, our study defines a continuation of the signaling pathway involving EIN2-EIN3-miR164-NAC2 in regulating leaf senescence and provides a mechanistic insight into how ethylene promotes the progression of leaf senescence in Arabidopsis thaliana.

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“…Leaf senescence can also be initiated by internal signals, such as developmental cues and phytohormone balance. The internal or environmental cues that induce aging are perceived by plants, which then express senescence-associated genes (SAGs), resulting in dysfunctional developmental processes and, ultimately, the appearance of a senescence phenotype (Guo and Gan, 2005;Lim et al, 2007a). A large number of genes show enhanced or reduced expression during leaf senescence.…”

Section: Introductionmentioning

confidence: 99%

Overexpression of a LAM Domain Containing RNA-Binding Protein LARPIc Induces Precocious Leaf Senescence in Arabidopsis

Zhang

Jia

Yang

et al. 2012

Molecules and Cells

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Leaf senescence is the final stage of leaf life history, and it can be regulated by multiple internal and external cues. La-related proteins (LARPs), which contain a well-conserved La motif (LAM) domain and normally a canonical RNA recognition motif (RRM) or noncanonical RRM-like motif, are widely present in eukaryotes. Six LARP genes (LARP1a-1c and LARP6a-6c) are present in Arabidopsis, but their biological functions have not been studied previously. In this study, we investigated the biological roles of LARP1c from the LARP1 family. Constitutive or inducible overexpression of LARP1c caused premature leaf senescence. Expression levels of several senescence-associated genes and defense-related genes were elevated upon overexpression of LARP1c. The LARP1c null mutant 1c-1 impaired ABA-, SA-, and MeJA-induced leaf senescence in detached leaves. Gene expression profiles of LARP1c showed age-dependent expression in rosette leaves. Taken together, our results suggest LARP1c is involved in regulation of leaf senescence.

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Leaf Senescence: Signals, Execution, and Regulation

Cited by 274 publications

References 167 publications

Fusarium oxysporum hijacks COI1‐mediated jasmonate signaling to promote disease development in Arabidopsis

Fusarium oxysporum hijacks COI1‐mediated jasmonate signaling to promote disease development in Arabidopsis

ETHYLENE-INSENSITIVE3 Is a Senescence-Associated Gene That Accelerates Age-Dependent Leaf Senescence by Directly Repressing miR164 Transcription in Arabidopsis

Overexpression of a LAM Domain Containing RNA-Binding Protein LARPIc Induces Precocious Leaf Senescence in Arabidopsis

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