Identification of genetic modifiers of ACCELERATED CELL DEATH 6 (ACD6) in natural Arabidopsis thaliana accessions

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Aufrufstatistik

URI: http://hdl.handle.net/10900/72881
http://nbn-resolving.de/urn:nbn:de:bsz:21-dspace-728819
http://dx.doi.org/10.15496/publikation-14291
Dokumentart: Dissertation
Date: 2016-10-31
Language: English
Faculty: 7 Mathematisch-Naturwissenschaftliche Fakultät
7 Mathematisch-Naturwissenschaftliche Fakultät
Department: Mathematisch-Naturwissenschaftliche Fakultät
Advisor: Weigel, Detlef (Prof. Dr.)
Day of Oral Examination: 2016-07-29
DDC Classifikation: 500 - Natural sciences and mathematics
570 - Life sciences; biology
580 - Plants (Botany)
Keywords: Schmalwand <Arabidopsis> , Ackerschmalwand , Autoimmunität
Other Keywords:
ACD6
plant immunity
genetic modifiers
population genetics
evolution
Cress <Arabidopsis> Genetics
General Botany
QTL
genetic map
plants
autoimmunity
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Abstract:

Plants defend themselves against pathogens by activating responses that can also cause unintended collateral damage to the plant itself. Improved understanding of the evolutionary constraints and molecular mechanisms affecting these responses can provide means to minimize the tradeoff between disease-related losses and hyperimmunity-related yield drag in crops. As a model to investigate this problem, I have exploited natural variation at the ACCELERATED CELL DEATH 6 (ACD6) gene, which controls a major trade-off between growth and disease resistance among natural accessions of Arabidopsis thaliana. The hyperactive allele ACD6-Est-1 is known to confer broad-spectrum immunity, but at the same time to also negatively affect growth in many A. thaliana accessions. Here, I first surveyed a large collection of A. thaliana genomes for the presence of Est-like ACD6 alleles. I confirmed that not all accessions with this allele express overt hyperimmunity. I then demonstrated that Est-like ACD6 alleles from accessions that do not show the typical autoimmune phenotype normally associated with this allele could confer hyperimmunity when transformed into a different genetic background, indicating that the attenuation of the Est-like ACD6 phenotype was likely due to extragenic modifiers. I then investigated pathogen responses of several of these accessions more closely. My experiments revealed that reduced growth and immune responses were partially uncoupled in some of these accessions. These findings dovetailed with genetic results suggesting that different accessions contain genetically distinct modifiers of the typical Est-like ACD6 phenotype. Finally, I demonstrated by quantitative trait loci (QTL) mapping that these modifiers are located in different regions of the genome, with one of the modifiers potentially being a gene in cluster of genes encoding nucleotide-binding domain and leucine-rich repeat (NLR) immune receptors. This is an important finding, as ACD6 had previously been linked only to PAMP-triggered immunity (PTI), but not to effector-triggered immunity (ETI), which predominantly relies on NLR immune receptors. My study thus provides new insights into the complex genetic interactions that affect disease resistance and growth.

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