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Publikationen - Molekulare Signalverarbeitung

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Clarke, S.M.; Cristescu, S.M.; Miersch, O.; Harren, F.J.M.; Wasternack, C.; Mur, L.A.J. Jasmonates act with salicylic acid to confer basal thermotolerance in <i>Arabidopsis thaliana</i> New Phytol 182, 175-187, (2009) DOI: 10.1111/j.1469-8137.2008.02735.x

The cpr5-1 Arabidopsis thaliana mutant exhibits constitutive activation of salicylic acid (SA), jasmonic acid (JA) and ethylene (ET) signalling pathways and displays enhanced tolerance of heat stress (HS). cpr5-1 crossed with jar1-1 (a JA-amino acid synthetase) was compromised in basal thermotolerance, as were the mutants opr3 (mutated in OPDA reductase3) and coi1-1 (affected in an E3 ubiquitin ligase F-box; a key JA-signalling component). In addition, heating wild-type Arabidopsis led to the accumulation of a range of jasmonates: JA, 12-oxophytodienoic acid (OPDA) and a JA-isoleucine (JA-Ile) conjugate. Exogenous application of methyl jasmonate protected wild-type Arabidopsis from HS. Ethylene was rapidly produced during HS, with levels being modulated by both JA and SA. By contrast, the ethylene mutant ein2-1 conferred greater thermotolerance. These data suggest that JA acts with SA, conferring basal thermotolerance while ET may act to promote cell death.

Acosta, I. F.; Gasperini, D.; Chételat, A.; Stolz, S.; Santuari, L.; Farmer, E. E. Role of NINJA in root jasmonate signaling Proc Natl Acad Sci USA 110, 15473-15478, (2013) DOI: 10.1073/pnas.1307910110

Wound responses in plants have to be coordinated between organs so that locally reduced growth in a wounded tissue is balanced by appropriate growth elsewhere in the body. We used a JASMONATE ZIM DOMAIN 10 (JAZ10) reporter to screen for mutants affected in the organ-specific activation of jasmonate (JA) signaling in Arabidopsis thaliana seedlings. Wounding one cotyledon activated the reporter in both aerial and root tissues, and this was either disrupted or restricted to certain organs in mutant alleles of core components of the JA pathway including COI1, OPR3, and JAR1. In contrast, three other mutants showed constitutive activation of the reporter in the roots and hypocotyls of unwounded seedlings. All three lines harbored mutations in Novel Interactor of JAZ (NINJA), which encodes part of a repressor complex that negatively regulates JA signaling. These ninja mutants displayed shorter roots mimicking JA-mediated growth inhibition, and this was due to reduced cell elongation. Remarkably, this phenotype and the constitutive JAZ10 expression were still observed in backgrounds lacking the ability to synthesize JA or the key transcriptional activator MYC2. Therefore, JA-like responses can be recapitulated in specific tissues without changing a plant’s ability to make or perceive JA, and MYC2 either has no role or is not the only derepressed transcription factor in ninja mutants. Our results show that the role of NINJA in the root is to repress JA signaling and allow normal cell elongation. Furthermore, the regulation of the JA pathway differs between roots and aerial tissues at all levels, from JA biosynthesis to transcriptional activation.

Farmer, E. E.; Gasperini, D.; Acosta, I. F. The squeeze cell hypothesis for the activation of jasmonate synthesis in response to wounding New Phytol 204, 282-288, (2014) DOI: 10.1111/nph.12897

Jasmonates are lipid mediators that control defence gene expression in response to wounding and other environmental stresses. These small molecules can accumulate at distances up to several cm from sites of damage and this is likely to involve cell‐to‐cell jasmonate transport. Also, and independently of jasmonate synthesis, transport and perception, different long‐distance wound signals that stimulate distal jasmonate synthesis are propagated at apparent speeds of several cm min–1 to tissues distal to wounds in a mechanism that involves clade 3 GLUTAMATE RECEPTOR‐LIKE (GLR) genes. A search for jasmonate synthesis enzymes that might decode these signals revealed LOX6, a lipoxygenase that is necessary for much of the rapid accumulation of jasmonic acid at sites distal to wounds. Intriguingly, the LOX6 promoter is expressed in a distinct niche of cells that are adjacent to mature xylem vessels, a location that would make these contact cells sensitive to the release of xylem water column tension upon wounding. We propose a model in which rapid axial changes in xylem hydrostatic pressure caused by wounding travel through the vasculature and lead to slower, radially dispersed pressure changes that act in a clade 3 GLR‐dependent mechanism to promote distal jasmonate synthesis.
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