Dokument: Environmental influences and genetic regulation on systemic acquired resistance

Titel:	Environmental influences and genetic regulation on systemic acquired resistance
URL für Lesezeichen:	https://docserv.uni-duesseldorf.de/servlets/DocumentServlet?id=50046
URN (NBN):	urn:nbn:de:hbz:061-20200716-095230-6
Kollektion:	Dissertationen
Sprache:	Englisch
Dokumententyp:	Wissenschaftliche Abschlussarbeiten » Dissertation
Medientyp:	Text
Autor:	Ajamirashidi, Ziba [Autor]
Dateien:	[Dateien anzeigen] Adobe PDF [Details] 8,21 MB in einer Datei [ZIP-Datei erzeugen] Dateien vom 28.06.2019 / geändert 28.06.2019
Beitragende:	Prof. Dr. Zeier, Jürgen [Gutachter] Prof. Dr. Rose, Laura [Gutachter]
Dewey Dezimal-Klassifikation:	500 Naturwissenschaften und Mathematik » 570 Biowissenschaften; Biologie
Beschreibung:	Systemic acquired resistance (SAR) is induced by a localized leaf inoculation with pathogenic microbes and constitutes a state of elevated, broad spectrum disease resistance to microbial pathogen within the entire plant foliage. Activation of SAR enables the plant to respond more quickly and vigorously to subsequent microbial attack (SAR priming). For SAR to happen, a signal must be generated and translocated to the leaves distal to the site of pathogen infection. In the last decade, a number of potential SAR signals such as non-protein amino acid pipecolic acid (Pip), methyl salicylate (MeSA), glycerol-3-phosphate (G3P), dihydroabetinal (DA), DIR1 and azelaic acid (AzA), have been proposed. Pip is considered as an endogenous regulator of SAR and plants defective in production of Pip (ald1) are compromised in SAR. SAR establishment and the associated priming of defense responses are regulated by Pip. Exogenous Pip application strongly increases pathogen resistance in wild-type and in ald1 plants and promotes the plants into a primed SAR-like state (Pip-priming). Moreover, Pip positively regulates biosynthesis of another immune regulator salicylic acid (SA) and primes the plants for accumulation of phytoalexin camalexin and expression of defense genes such as PR1. SA, itself is not a mobile signal, however its accumulation in systemic leaves is required for SAR establishment. Pip orchestrates SAR via salicylic acid (SA)-dependent and -independent pathways. Our research group has recently discovered that Pip is further N-hydroxylated to a SAR-activating metabolite N-hydroxypipecolic acid (NHP) by flavin-dependent monooxygenase1 (FMO1). NHP is the main regulatory metabolite which mediates SAR against bacterial and oomycete pathogens and NHP induces expression of defense genes and it primes the plants for effective defense activation towards pathogens. In this thesis, we investigated whether and to which extend the putative SAR signals (G3P, MeSA, AzA, and DIR1) interact with Pip in resistance induction and contribute to SAR establishment in an Arabidopsis-Pseudomonas syringae interaction. To address these questions, we first examined the SAR establishment in a series of Arabidopsis mutants impaired in the production of G3P (gli1-1 and gly1-1), MeSA (bsmt1-1), DIR1 (dir1-1), and also plants defective in azelaic acid signaling pathway (azi1-2). We observed that irrespective to the time of pathogen attack, SAR is established in the putative SAR signaling mutants, indicating that in contrast to previous reports from other publications, G3P, AzA, MeSA, and DIR1 are not central SAR regulators under our laboratory conditions. In addition, irrespective to the time of infiltration, virulent and avirulent Pseudomonas syringae strains induce SAR in all SAR signaling mutant lines. gli1-1 mutant lines showed a weaker SAR than wild-type, suggesting that GLI1 is required for full SAR establishment upon morning and evening infiltration of Psm. Furthermore, irrespective to the time of Psm infiltration (morning or evening), all SAR signaling mutants accumulate Pip and SA (as two main SAR regulators) in their local (infiltrated) and systemic (non-infiltrated) leaves. gly1-1 mutant lines accumulate local and systemic Pip to significantly lower level than wild-type. Therefore, a connection between G3P and Pip biosynthesis is likely to exist. To further understand if there is a connection between putative signals and Pip signaling, we tested how SAR signaling mutants (gli1-1, gly1-1, azi1-2, dir1-1, and bsmt1-1) respond to exogenous Pip (Pip-induced resistance (Pip-IR)). We observed that these was no contribution of MeSA, AzA, DIR1, and G3P to Pip-IR and Pip-IR developed similarly in all SAR signaling mutants and wild-type plants. Next, we examined whether there is an interplay between SA and each individual SAR signals. All SAR signaling mutants also positively respond to exogenous SA, indicating that SA acts downstream of MeSA, AzA, DIR1, and G3P for induction of resistance towards Psm. In second and third chapters of this study, we investigated the role of environmental factors (light and nitrogen supply) on Pip biosynthesis, defense priming, and SAR. We confirmed that SAR is a light-dependent process. Pip biosynthesis and its regulatory role in defense priming are positively influenced by light. In addition, SA biosynthesis and SA-induced PR1 expression depend on a light-related factor. Although the length of Light applied to Arabidopsis plants after Psm infiltration negatively correlates with the basal bacterial growth, the production of defense metabolites (Pip and SA) are positively and directly regulated by light. Similar to light effect, adequate nitrogen (N) supply in plants, stimulates the pathogen-induced Pip accumulation and is a prerequisite for effective SAR induction. It is more likely that nitrogen supply positively affects the systemic accumulation of Psm-induced SA. In contrast, a higher concentration of nitrate causes a reduced level of SA at the site of pathogen attack. Our study provides the framework for future studies on how plants adapt SAR and defense priming responses to changing environmental conditions.
Lizenz:	Urheberrechtsschutz
Fachbereich / Einrichtung:	Mathematisch- Naturwissenschaftliche Fakultät
Dokument erstellt am:	16.07.2020
Dateien geändert am:	16.07.2020
Promotionsantrag am:	11.12.2018
Datum der Promotion:	12.02.2019