Simon Saucet
Post Graduate Student
Contact details
Email: simon.saucet@sainsbury-laboratory.ac.uk
Research interests
Plants have a two-layered immune system to prevent pathogen infection (Jones and Dangl, 2006). Pattern recognition receptors (PRR) recognize pathogen associated molecular patterns (PAMPs) which initiates PAMP triggered immunity (PTI). Some plant pathogenic bacteria have evolved a type three secretion system (TTSS) to translocate effector proteins into the plant cell and suppress PTI responses. In turn, plants make resistance (R) proteins able to detect these effectors and trigger an effector-triggered immunity (ETI). The plant pathogen Pseudomonas syringae carries a TTSS that enable the injection of type three secreted effectors (TTSEs) into its plant hosts. The P. syringae pv pisi TTSE AvrRps4 triggers resistance in Arabidopsis accessions carrying the corresponding functional R gene RPS4 (Hinsch and Staskawicz,1996), a member of the TIR-NB-LRR family (Gassmann et al., 1999). The mapping of RPS4 was carried out by crossing the AvrRps4-resistant accession Ws-0 with the susceptible accession RLD. However, little is known about the mechanism of AvrRps4 recognition. A study has identified another R gene, RRS1, as involved in AvrRps4-triggered resistance in Arabidospsis. It has been demonstrated that RPS4 and RRS1 act in tandem for the recognition of AvrRps4 but also PopP2, a Ralstonia solanacearum effector, in Arabidopsis accession Ws-0 (Narusaka et al., 2009). This can be described as a genes-for-genes concept. Interestingly, bacterial growth analysis and hypersensitive reaction (HR) tests in the single mutant rps4-21 and the double mutant rps4-21/rrs1-1 suggest the presence of an additional R gene in Ws-0 recognizing AvrRps4. We aim to identify this new R gene using a segregating population resulting from the cross between RLD (susceptible) and Ws-0 rps4-21 (resistant).
