Jasmonate signalling network in <i>Arabidopsis thaliana</i>: crucial regulatory nodes and new physiological scenarios

Balbi, Virginia; Devoto, Alessandra

doi:10.1111/j.1469-8137.2007.02292.x

Cited by 349 publications

(261 citation statements)

References 230 publications

(353 reference statements)

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“…Plant microarray studies have revealed that JA signaling alters gene expression and that genes induced by MeJA generally required COI1 in Arabidopsis (for review, see Balbi and Devoto, 2008;Acosta and Farmer, 2010;Avanci et al, 2010). We dissected here MeJA-dependent global transcriptional regulation during leaf development using the Arabidopsis ATH1 full-genome DNA arrays (Affymetrix; NASCARRAY-568/573).…”

Section: Molecular Understanding Of the Action Of Meja On Cell Cycle mentioning

confidence: 99%

“…In plants, jasmonates (JAs) form a group of oxylipins (oxygenated fatty acids) produced via the octadecanoid pathway (for review, see Balbi and Devoto, 2008;Schaller and Stintzi, 2009;Wasternack and Kombrink, 2010). The volatile phytohormone methyl jasmonate (MeJA), produced through the activity of JA carboxyl methyltransferase (Seo et al, 2001), is an easy-tohandle JA conjugate extensively used in biological assays (Staswick et al, 1992;Pauwels et al, 2008).…”

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confidence: 99%

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Jasmonate Controls Leaf Growth by Repressing Cell Proliferation and the Onset of Endoreduplication while Maintaining a Potential Stand-By Mode

et al. 2013

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Phytohormones regulate plant growth from cell division to organ development. Jasmonates (JAs) are signaling molecules that have been implicated in stress-induced responses. However, they have also been shown to inhibit plant growth, but the mechanisms are not well understood. The effects of methyl jasmonate (MeJA) on leaf growth regulation were investigated in Arabidopsis (Arabidopsis thaliana) mutants altered in JA synthesis and perception, allene oxide synthase and coi1-16B (for coronatine insensitive1), respectively. We show that MeJA inhibits leaf growth through the JA receptor COI1 by reducing both cell number and size. Further investigations using flow cytometry analyses allowed us to evaluate ploidy levels and to monitor cell cycle progression in leaves and cotyledons of Arabidopsis and/or Nicotiana benthamiana at different stages of development. Additionally, a novel global transcription profiling analysis involving continuous treatment with MeJA was carried out to identify the molecular players whose expression is regulated during leaf development by this hormone and COI1. The results of these studies revealed that MeJA delays the switch from the mitotic cell cycle to the endoreduplication cycle, which accompanies cell expansion, in a COI1-dependent manner and inhibits the mitotic cycle itself, arresting cells in G1 phase prior to the S-phase transition. Significantly, we show that MeJA activates critical regulators of endoreduplication and affects the expression of key determinants of DNA replication. Our discoveries also suggest that MeJA may contribute to the maintenance of a cellular "stand-by mode" by keeping the expression of ribosomal genes at an elevated level. Finally, we propose a novel model for MeJA-regulated COI1-dependent leaf growth inhibition.

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Section: Molecular Understanding Of the Action Of Meja On Cell Cycle mentioning

confidence: 99%

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confidence: 99%

Jasmonate Controls Leaf Growth by Repressing Cell Proliferation and the Onset of Endoreduplication while Maintaining a Potential Stand-By Mode

et al. 2013

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“…Plants perceive exogenous and endogenous stimuli, decode them, and alter their gene expression patterns via various plant hormonal signal transduction pathways. Jasmonates (JAs) are lipid-derived hormones that regulate plant responses to stresses such as wounding and herbivore attack and also act in various developmental processes, including male fertility (Devoto and Turner, 2003;Wasternack, 2007;Balbi and Devoto, 2008). JA negatively regulates plant growth and is considered to modulate the distribution of energy to defense responses (Yan et al, 2007;Zhang and Turner, 2008;Yang et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

A bHLH-Type Transcription Factor, ABA-INDUCIBLE BHLH-TYPE TRANSCRIPTION FACTOR/JA-ASSOCIATED MYC2-LIKE1, Acts as a Repressor to Negatively Regulate Jasmonate Signaling inArabidopsis

et al. 2013

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Jasmonates (JAs) are plant hormones that regulate the balance between plant growth and responses to biotic and abiotic stresses. Although recent studies have uncovered the mechanisms for JA-induced responses in Arabidopsis thaliana, the mechanisms by which plants attenuate the JA-induced responses remain elusive. Here, we report that a basic helix-loophelix-type transcription factor, ABA-INDUCIBLE BHLH-TYPE TRANSCRIPTION FACTOR/JA-ASSOCIATED MYC2-LIKE1 (JAM1), acts as a transcriptional repressor and negatively regulates JA signaling. Gain-of-function transgenic plants expressing the chimeric repressor for JAM1 exhibited substantial reduction of JA responses, including JA-induced inhibition of root growth, accumulation of anthocyanin, and male fertility. These plants were also compromised in resistance to attack by the insect herbivore Spodoptera exigua. Conversely, jam1 loss-of-function mutants showed enhanced JA responsiveness, including increased resistance to insect attack. JAM1 and MYC2 competitively bind to the target sequence of MYC2, which likely provides the mechanism for negative regulation of JA signaling and suppression of MYC2 functions by JAM1. These results indicate that JAM1 negatively regulates JA signaling, thereby playing a pivotal role in fine-tuning of JA-mediated stress responses and plant growth.

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“…The JA signal is perceived by the F-box protein COI1, which plays a key role in JA signaling (Katsir et al, 2008a), and is required for the majority of the JA-mediated responses analyzed to date (Feys et al, 1994;Xie et al, 1998;Wasternack, 2007;Balbi and Devoto, 2008). The coi1 mutant was first identified for its insensitivity to the bacterial toxin coronatine (COR), but it also displays male sterility, altered senescence, and increased susceptibility to several necrotrophic pathogens and insect pests (reviewed in Browse, 2005;Wasternack, 2007;Balbi and Devoto, 2008).…”

Section: Introductionmentioning

confidence: 99%

“…The coi1 mutant was first identified for its insensitivity to the bacterial toxin coronatine (COR), but it also displays male sterility, altered senescence, and increased susceptibility to several necrotrophic pathogens and insect pests (reviewed in Browse, 2005;Wasternack, 2007;Balbi and Devoto, 2008). COI1 forms an integral part of a highly conserved multiprotein complex called the Skp1-Cullin-F-box (SCF) E3 ubiquitin ligase complex SCF coi1 .…”

Section: Introductionmentioning

confidence: 99%

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

Thatcher

Manners

Kazan³

2009

The Plant Journal

261

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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Jasmonate signalling network in Arabidopsis thaliana: crucial regulatory nodes and new physiological scenarios

Cited by 349 publications

References 230 publications

Jasmonate Controls Leaf Growth by Repressing Cell Proliferation and the Onset of Endoreduplication while Maintaining a Potential Stand-By Mode

Jasmonate Controls Leaf Growth by Repressing Cell Proliferation and the Onset of Endoreduplication while Maintaining a Potential Stand-By Mode

A bHLH-Type Transcription Factor, ABA-INDUCIBLE BHLH-TYPE TRANSCRIPTION FACTOR/JA-ASSOCIATED MYC2-LIKE1, Acts as a Repressor to Negatively Regulate Jasmonate Signaling inArabidopsis

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

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