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.
