Gene expression study of candidate Arabidopsis defence genes in response to the bacterial wilt pathogen, Ralstonia solanacearum

Abstract

Arabidopsis thaliana is a model plant widely used to gain insights in the so called plant-pathogen interactions. This is so because plants are sessile organisms living in an environment rich in disease causing microbes. In contrast, plants cannot relocate to avoid pathogen attacks like animals. As a result, plants rely on their immune responses to rapidly detect invading pathogens so as to fight and defend themselves against pathogens. Over the years, Ralstonia solanacearum has been recognised as an economically important causal agent of bacterial wilt in a vast distribution of plants ranging from important solanaceous crops, leguminous plants, a few monocotyledonous plants (Genin & Boucher, 2002) to major forest trees such as Eucalyptus (Coutinho et al., 2000). It has been documented that R. solanacearum affects over 200 plant species representing 50 botanical families (Hayward, 1991). Thus it is of utmost importance to gain as much insight into this devastating phytopathogen in order to accomplish better control methods. Chemical control is not an option for bacterial diseases, in contrast to fungal diseases. Integrated Pest Management (IPM) of bacterial wilt is considered to be a sustainable approach (Smith, 2000). Hence there is a need to generate disease resistant plants as part of IPM of bacterial wilt across the world. The first step in understanding resistance is to study compatible host plant responses to infection with R. solanacearum. A fascinating discovery was that A. thaliana is a compatible host to bacterial wilt. This has built a strong foundation, a step forward to gaining knowledge as to what happens in a host plant upon R. solanacearum infection. The study of the A. thaliana - R. solanacearum pathosystem has revealed that different ecotypes of Arabidopsis have different responses to the bacterium. Resistant and tolerant ecotypes of Arabidopsis are due to the possession of the recessive gene, AtRRS1-R on chromosome five. The RRS1-R protein physically interacts with an effector protein from the Type III Secretion System (T3SS) of R. solanacearum called PopP2 to elicit Effector Triggered Immunity (ETI) (Coutinho et al., 2000; Deslandes et al., 1998; Deslandes et al., 2002; Deslandes et al., 2003). The interaction thereof is strongly suggested to localise in the nucleus of the host plant involving at least two more A. thaliana proteins, RPS4 (Narusaka et al., 2009) and RD9 (Rivas, 2012). This further suggests that Arabidopsis responses to bacterial wilt involve an extensive cascade of distinct genes.