A light-dependent molecular link between competition cues and defence responses in plants

Fernández-Milmanda, Guadalupe L; Crocco, Carlos Daniel; Reichelt, Michael; Mazza, Carmen; Köllner, Tobias G.; Zhang, Tong; Cargnel, Miriam D.; Lichy, Micaela Z.; Fiorucci, Anne-Sophie; Fankhauser, Christian; Koo, Abraham J.; Austin, Amy T.; Gershenzon, Jonathan; Ballaré, Carlos L.

doi:10.1038/s41477-020-0604-8

Cited by 113 publications

(114 citation statements)

References 63 publications

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“…DELLA removal in low R:FR therefore releases JAZ proteins that in turn sequester MYC transcription factors, thereby preventing the activation of JA-associated defense gene expression (Chico et al, 2014;Leone et al, 2014;Pieterse et al, 2014). In addition, low R:FR conditions were also shown to reduce the pool of bioactive JAs available in Arabidopsis plant tissue upon exogenous MeJA treatment and was associated with increased susceptibility to B. cinerea (Fernández-Milmanda et al, 2020).…”

Section: Introductionmentioning

confidence: 99%

Far‐red light promotes Botrytis cinerea disease development in tomato leaves via jasmonate‐dependent modulation of soluble sugars

Courbier

Grevink

Sluijs

et al. 2020

Plant Cell & Environment

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Plants experience a decrease in the red:far-red light ratio (R:FR) when grown at high planting density. In addition to eliciting the shade avoidance response, low R:FR also enhances plant susceptibility to pathogens via modulation of defense hormonemediated responses. However, other mechanisms, also affected by low R:FR, have not been considered as potential components in FR-induced susceptibility. Here, we identify FR-induced accumulation of leaf soluble sugars as a novel component of FRinduced susceptibility. We observed that phytochrome inactivation by FR or phytochrome B mutation was associated with elevated leaf glucose and fructose levels and enhanced disease severity caused by Botrytis cinerea. By experimentally manipulating internal leaf sugar levels, we found that the FR-induced susceptibility in tomato was partly sugar-dependent. Further analysis revealed that the observed sugar accumulation in supplemental FR occurred in a jasmonic acid (JA)-dependent manner, and the JA biosynthesis mutant def1 also displayed elevated soluble sugar levels, which was rescued by exogenous methyl jasmonate (MeJA) application. We propose that the reduced JA responsiveness under low R:FR promotes disease symptoms not only via dampened induction of defense responses, but also via increased levels of soluble sugars that supports pathogen growth in tomato leaves.

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Section: Introductionmentioning

confidence: 99%

Far‐red light promotes Botrytis cinerea disease development in tomato leaves via jasmonate‐dependent modulation of soluble sugars

Courbier

Grevink

Sluijs

et al. 2020

Plant Cell & Environment

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“…Specifically, leaf and petiole growth restriction was strongly attenuated in the JA-synthesis mutant allene oxide synthase (aos; Yan et al, 2007) and in a JA-signaling mutant (Zhang and Turner, 2008). Therefore, a key function of JA pathway-activating signals produced in damaged organs is to travel to apical tissues to reprogram future growth, allowing plants to optimize their defense strategies (Huot et al, 2014;Guo et al, 2018;Ballaré and Austin, 2019;Fernández-Milmanda et al, 2020). Importantly, the activation of JA signaling after wounding requires the de novo synthesis of JA (Browse, 2009;Chini et al, 2016;Howe et al, 2018).…”

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confidence: 99%

Jasmonate Precursor Biosynthetic Enzymes LOX3 and LOX4 Control Wound-Response Growth Restriction

et al. 2020

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Wound-response plant growth restriction requires the synthesis of potent mediators called jasmonates (JAs). Four 13-lipoxygenases (13-LOXs) produce JA precursors in Arabidopsis (Arabidopsis thaliana) leaves, but the 13-LOXs responsible for growth restriction have not yet been identified. Through loss-of-function genetic analyses, we identified LOX3 and LOX4 as the principal 13-LOXs responsible for vegetative growth restriction after repetitive wounding. Additional genetic studies were carried out in the gain-offunction fatty acid oxygenation 2 (fou2) mutant that, even when undamaged, shows JA-dependent leaf growth restriction. The fou2 lox3 lox4 triple mutant suppressed the fou2 JA-dependent growth phenotype, confirming that LOX3 and LOX4 function in leaf growth restriction. The fou2 mutation affects the TWO PORE CHANNEL1 (TPC1) ion channel. Additional genetic approaches based on this gene were used to further investigate LOX3 function in relation to leaf growth. To activate LOX3-dependent JA production in unwounded plants, we employed hyperactive TPC1 variants. Expression of the TPC1DCa i variant in phloem companion cells caused strongly reduced rosette growth in the absence of wounding. Summarizing, in parallel to their established roles in male reproductive development in Arabidopsis, LOX3 and LOX4 control leaf growth rates after wounding. The process of wound-response growth restriction can be recapitulated in unwounded plants when the LOX3 pathway is activated genetically using a hyperactive vacuolar cation channel.

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“…The slow part in slow wave potential reflects a delayed repolarization, and slow wave potentials are dampened in amplitude in more distal parts of the plant. On the other hand, action potentials are characterized by their all-or-none depolarization traveling without attenuation (Favre and Agosti, 2007;Cuin et al, 2018). Systems potentials are mainly different to the aforementioned signals in that they are hyperpolarized instead of depolarized (Zimmermann et al, 2009).…”

Section: Systemic Wound Tides: Hydraulic Waves Electric Torrents Anmentioning

confidence: 99%

Breaking Bad News: Dynamic Molecular Mechanisms of Wound Response in Plants

et al. 2020

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Recognition and repair of damaged tissue are an integral part of life. The failure of cells and tissues to appropriately respond to damage can lead to severe dysfunction and disease. Therefore, it is essential that we understand the molecular pathways of wound recognition and response. In this review, we aim to provide a broad overview of the molecular mechanisms underlying the fate of damaged cells and damage recognition in plants. Damaged cells release the so-called damage associated molecular patterns to warn the surrounding tissue. Local signaling through calcium (Ca2+), reactive oxygen species (ROS), and hormones, such as jasmonic acid, activates defense gene expression and local reinforcement of cell walls to seal off the wound and prevent evaporation and pathogen colonization. Depending on the severity of damage, Ca2+, ROS, and electrical signals can also spread throughout the plant to elicit a systemic defense response. Special emphasis is placed on the spatiotemporal dimension in order to obtain a mechanistic understanding of wound signaling in plants.

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A light-dependent molecular link between competition cues and defence responses in plants

Cited by 113 publications

References 63 publications

Far‐red light promotes Botrytis cinerea disease development in tomato leaves via jasmonate‐dependent modulation of soluble sugars

Far‐red light promotes Botrytis cinerea disease development in tomato leaves via jasmonate‐dependent modulation of soluble sugars

Jasmonate Precursor Biosynthetic Enzymes LOX3 and LOX4 Control Wound-Response Growth Restriction

Breaking Bad News: Dynamic Molecular Mechanisms of Wound Response in Plants

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