Abstract
Plants are frequently attacked by a multitude of invaders, i.e. herbivorous insects or microbial pathogens. In order to cope with these unfavorable conditions Arabidopsis thaliana possesses a variety of induced defenses, which are initiated upon recognition of the attacker. Three plant signaling molecules, salicylic acid (SA), jasmonic acid (JA), and
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ethylene (ET) have been shown to be involved in these responses. Their levels accumulating in invaded tissue and can trigger defense reactions that mount resistance at the site of interaction (local) or throughout the whole plant (systemic).
In this thesis we addressed several questions. At first, the interaction between Arabidopsis thaliana and a variety of attackers with distinct feeding strategies, such as leaf pathogenic bacteria Pseudomonas syringae pv. tomato, the fungal pathogen Alternaria brassicicola, tissue-chewing larvae of Pieris rapae, cell-piercing thrips (Franklinella occidentalis), and phloem-sucking Myzus persicae, was investigated. We monitored the levels of SA, JA, and ET during the time course of each Arabidopsis-attacker combination. The data shows that each Arabidopsis-attacker combinations lead to the accumulation of a specific blend of these signaling molecules, the so-called signal signature. Although JA accumulated in four out of the five interactions studied, the signal signature of each interactions varied in composition, amplitude, and timing. Moreover, plant gene expression upon attack by each single invader was studied using microarray technology from Affymetrix (ATH1). Comparing the transcriptome changes in Arabidopsis upon attack showed only limited overlap between each interaction.
Next we investigated whether prior attack by one invader would influence the resistance against a subsequent attacker. To this end, we developed a bio-assay in which plants were infested by JA-inducing larvae of P. rapae and subsequently attacked by various microbial pathogens. We hypothesized that prior infestation by P. rapae would lead to increase levels of JA and thus would mount resistance against microbial pathogens that are restricted by JA-dependent defense responses (e.g. A. brassicicola) while microbial pathogens arrested through SA-dependent defenses (e.g. turnip crinkle virus) are not affected. Both hypotheses appeared to be false, indicating that it is extremely hard to predict if a particular infection will influence resistance against subsequent attackers.
Chapter 4 focuses on P. rapae-mediated suppression of host defenses in order to investigate the underlying molecular mechanisms. In addition to feeding larvae, application of regurgitant to mechanically damaged leaves also suppressed plant defenses Recently, a MYC-family transcription factor, AtMYC2, was shown to be involved in the regulation of the JA-dependent defenses. This prompted us to investigate whether AtMYC2 was up-regulated by P. rapae feeding. Indeed, AtMYC2 expression was induced upon feeding by P. rapae larvae. In contrast to Col-0 wild-type, AtMYC2 impaired jin1-2 mutant was not able to suppress plant host defenses, indicating that AtMYC2 plays a crucial role in P. rapae-mediated host gene suppression. It is tempting to speculate that P. rapae actively interferes with the host defense responses and thereby make it more suitable for infestation.
In conclusion, we demonstrate that plants are highly flexible in recognizing different attacker and respond by inducing a attacker specific signal signature and transcript profile. Furthermore, we have shown that specialized attackers might use signal pathway cross-talk for their own benefit and thereby make the host plant more susceptible for infection by pathogenic micro-organisms or infestation by herbivorous insects. This leaves us with intriguing questions that relate to the continuing arms raise between host and specialized attackers.
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