The Genetic basis of resistance and susceptibility in the Albugo laibachii-Arabidopsis thaliana pathosystem

Albugo is a genus of biotrophic plant pathogens that can infect an extensive range of hosts including many Brassicaceae crop species. Little is known about the molecular mechanisms by which Albugo species can suppress host immunity and the mechanisms by which plants can resist Albugo infection. Albugo laibachii (Al) is a specialized pathogen of Arabidopsis thaliana (At). It can colonize ~90% of At accessions and suppress effector-triggered-immunity to other pathogens. It is postulated that Al secretes effector proteins. Analysis of the A. laibachii genome by Kemen et al, (2011, PLoS Biology) revealed a potential class of effectors with a ‘CHXC’ motif in their N-terminus that can mediate translocation into host cells. However, there are only ~35 CHXC effectors in A. laibachii, suggesting that they might not represent its entire effector complement. I took a traditional method to identify Al effectors: clone “avirulence (Avr) genes”. These typically encode effectors that are recognized and trigger a strong response by the immune system of some host accessions. I identified and sequenced four Al isolates from field samples. Using differential phenotype information to guide a genome-­‐ ide analysis, and my expectations of the allelic diversity of Avr genes, I identified two novel recognized effectors. These effectors, short secreted proteins named “SSP16” and “SSP18”, are recognized by the Arabidopsis accessions HR-5 and Ksk-1 respectively. I used classical and Illumina-­‐based genetic mapping to identify the locus conferring SSP16 recognition in HR-5, Resistance to A. laibachii 4 (RAL4). This locus contains three putative CC-NB-LRR class Resistance protein-encoding genes with similarity to Resistance to Peronospora parasitica 7 (RPP7). I demonstrated the utility of combined genomics approaches to identify recognized effectors without known motifs. The identification of the first Avr-Resistance gene pair will pave the way for further dissection of the molecular interactions in this pathosystem.

Name dc:type.qualificationname

phd

Level dc:type.qualificationlevel

doctoral

Grantor dc:publisher.institution

University of East Anglia

Year dc:date.issued

2014

Author dc:creator

• Furzer, Oliver

Language dc:language

en