Publikationen - Molekulare Signalverarbeitung

Jasmonic acid (JA) signaling can be switched off by metabolism of JA. The master regulator MYC2, interacting with MED25, has been shown to be deactivated by the bHLH transcription factors MTB1, MTB2, and MTB3. An autoregulatory negative feedback loop has been proposed for this termination in JA signaling.

Electric signaling and Ca2+ waves were discussed to occur in systemic wound responses. Two new overlapping scenarios were identified: (i) membrane depolarization in two special cell types followed by an increase in systemic cytoplasmic Ca2+ concentration ([Ca2+]cyt), and (ii) glutamate sensed by GLUTAMATE RECEPTOR LIKE proteins and followed by Ca2+-based defense in distal leaves.

For the first time in 25 years, a new pathway for biosynthesis of jasmonic acid (JA) has been identified. JA production takes place via 12-oxo-phytodienoic acid (OPDA) including reduction by OPDA reductases (OPRs). A loss-of-function allele, opr3-3, revealed an OPR3-independent pathway converting OPDA to JA.

Auxin coordinates plant development largely via hierarchical control of gene expression. During the past decades, the study of early auxin genes paired with the power of Arabidopsis genetics have unraveled key nuclear components and molecular interactions that perceive the hormone and activate primary response genes. Recent research in the realm of structural biology allowed unprecedented insight into: (i) the recognition of auxin-responsive DNA elements by auxin transcription factors; (ii) the inactivation of those auxin response factors by early auxin-inducible repressors; and (iii) the activation of target genes by auxin-triggered repressor degradation. The biophysical studies reviewed here provide an impetus for elucidating the molecular determinants of the intricate interactions between core components of the nuclear auxin response module.

Viroids, due to their small size and lack of protein-coding capacity, must rely essentially on their hosts for replication. Intriguingly, viroids have evolved the ability to replicate in two cellular organella, the nucleus (family Pospiviroidae) and the chloroplast (family Avsunviroidae). Viroid replication proceeds through an RNA-based rolling-circle mechanism with three steps that, with some variations, operate in both polarity strands: i) synthesis of longer-than-unit strands catalyzed by either the nuclear RNA polymerase II or a nuclear-encoded chloroplastic RNA polymerase, in both instances redirected to transcribe RNA templates, ii) cleavage to unit-length, which in the family Avsunviroidae is mediated by hammerhead ribozymes embedded in both polarity strands, while in the family Pospiviroidae the oligomeric RNAs provide the proper conformation but not the catalytic activity, and iii) circularization. The host RNA polymerases, most likely assisted by additional host proteins, start transcription from specific sites, thus implying the existence of viroid promoters. Cleavage and ligation in the family Pospiviroidae is probably catalyzed by an RNase III-like enzyme and an RNA ligase able to circularize the resulting 5’ and 3’ termini. Whether a chloroplastic RNA ligase mediates circularization in the family Avsunviroidae, or this reaction is autocatalytic, remains an open issue.

Viroids are small single-stranded circular RNAs able to infect plants. Chrysanthemum chlorotic mottle was one of the first viroid diseases reported, but identification and characterization of the causing RNA was delayed by its low accumulation in vivo. Chrysanthemum chlorotic mottle viroid (CChMVd) (398-401 nt) adopts a branched conformation instead of the rod-like secondary structure characteristic of most viroids. The natural sequence variability and the effects of artificial mutants support that the branched conformation is physiologically relevant and additionally stabilized by a kissing-loop interaction critical for RNA in vitro folding and in vivo viability. CChMVd shares structural similarities with peach latent mosaic viroid, with which forms the genus Pelamoviroid within the family Avsunviroidae. CChMVd adopts hammerhead structures that catalyze self-cleavage of the oligomeric strands of both polarities resulting from replication through a symmetric rolling-circle mechanism. The two CChMVd hammerheads display peculiarities: the plus has an extra A close to the central conserved core, and the minus an unsually long helix II. There are non-symptomatic strains (CChMVd-NS) that protect against challenge inoculation with severe strains (CChMVd-S). Introduction by site-directed mutagenesis of one of the CChMVd-NS specific mutations (UUUC?GAAA) is sufficient to change the symptomatic phenotype into non-symptomatic without altering the viroid titer. This pathogenicity determinant maps at a tetraloop of the CChMVd branched conformation. Co-inoculations with typical CChMVd-S and -NS variants showed that the infected plants remain symptomless only when the latter was in more than a 100-fold excess, indicating the higher fitness of the S variant. RNA silencing could mediate the observed cross-protection.

Oilseed germination is characterized by the mobilization of storage lipids as a carbon source for the germinating seedling. In spite of the importance of lipid mobilization, its mechanism is only partially understood. Recent data suggest that a novel degradation mechanism is initiated by a 13-lipoxygenase during germination, using esterified fatty acids specifically as substrates. This 13-lipoxygenase reaction leads to a transient accumulation of ester lipid hydroperoxides in the storage lipids, and the corresponding oxygenated fatty acid moieties are preferentially removed by specific lipases. The free hydroperoxy fatty acids are subsequently reduced to their hydroxy derivatives, which might in turn undergo β-oxidation.

Jasmonic acid is distributed throughout higher plants, synthesized from linolenic acid via the octadecanoic pathway. An important and probably essential role seems to be its operation as a ‘master switch’, responsible for the activation of signal transduction pathways in response to predation and pathogen attack. Proteins encoded by jasmonate-induced genes include enzymes of alkaloid and phytoalexin synthesis, storage proteins, cell wall constituents and stress protectants. The wound-induced formation of proteinase inhibitors is a well-studied example, in which jasmonic acid combines with abscisic acid and ethylene to protect the plant from predation.