A multi-layered immune system protects plants against pathogens. Adapted pathogens overcome or evade this immune system by
secreting small proteins, called effectors. Often susceptibility genes encode host targets for these effectors, and loss-of-function
mutations in such target genes can confer insensitivity to the pathogen. Fusarium oxysporum f.sp. lycopersici (Fol), a soil-born
fungus, invades tomato roots and colonizes xylem vessels thereby causing wilt disease. Fourteen effector candidates, called
Six1-Six14, have been identified in this fungus. Fol effector knockout strains were less pathogenic than the wildtype fungus
and inoculation with four of five SIX knockout strains specifically altered the xylem sap proteome composition. Each SIX knockout
strain induced, besides a common, also a unique change in the proteome composition. Hence, a reduced pathogenicity correlates
with a unique Six protein-specific fingerprint.
A Fol knockout of Six6 reduced the ability of Fol to cause disease, which
qualified Six6 as genuine effector. Notably, Six6 suppressed cell death induced upon I-2-activation. Six8, in contrary, which
is encoded by a multi-copy gene family, was found to enhance host cell death upon immune activation. The co-repressor TOPLESS
was identified as a potential Six8 target. TPL functions as a negative regulator in various developmental, hormonal and stress
processes in plants. Hijacking TPL by Six8 might manipulate specific host processes aiding susceptibility. Genetic evidence
in A. thaliana indicates that SNC1 recognizes the TPL-Six8 complex resulting in the induction of a constitutive defense response.
Hence, SNC1 seems to guard TPL as perturbation of TPL by Six8 triggers immune responses.