Ustilago hordei is the causative
agent of covered smut on barley and oat. This basidiomycetous
fungus establishes a biotrophic interaction with its host
plant and therefore relies on a great variety of secreted
effector proteins in order to cope with plant defense
responses. This particularly implies the avoidance of host
cell death reactions. Deletion mutants of the secreted
effector Pep1 are blocked in epidermal penetration and elicit
various plant defense responses, eventually leading to death
of the invaded cell. The virulence factor Pep1 is
functionally conserved in the corn smut pathogen Ustilago
maydis and was recently shown to directly interact with
apoplastic peroxidases, thus inhibiting the PAMP-triggered
oxidative burst. Barley infections with the incompatible
non-host pathogen U. maydis also result in epidermal cell
death, which is similar to the hypersensitive response (HR).
This study concentrates on molecular and cellular processes
determining compatibility and incompatibility in different
Ustilago/barley-interactions. Based on transcriptional
analyses of U. hordei genes involved in compatible and
incompatible plant interactions, 18 candidate genes were
selected and further analyzed for a potential role during
host colonization. So far, preliminary results point towards
a virulenz function of five candidates. In the second part of
this study cellular responses of barley were investigated,
comparing the compatible U. hordei-interaction with responses
during incompatibility caused by the non-host pathogen U.
maydis as well as U. hordei and U. maydis pep1 mutants.
Although incompatibility leads to programmed cell death
respectively, a combination of live cell imaging techniques,
an enzymatic activity assay and infections of transgenic
plants overexpressing Bax Inhibitor-1 (BI-1) enabled the
differentiation of two distinct pathways. While cell death
responses towards pep1 mutants involve autophagy, non-host
reactions after U. maydis infection trigger BI-1-dependent
apoptosis-like cell death. These data sets were supported by
transmission electron microscopy. Additionally, by evaluating
H2O2 contents in apoplastic fluid and the transcriptional
regulation of typical HR-associated marker genes, it became
apparent ...