The site of a plant pathogen infection is where a range of immediate defense responses take place. We propose that among these responses are specific changes in activity of various TE families. We hypothesize that TE products as well as epigenetic changes and TE insertions or excisions have been co-opted by the host into the systems that steer infected cells toward a resistance response. We propose that it is the actual ability of TEs to respond to pathogen stress which increases the fitness of the host, and which is therefore selected for. Conversely, we propose that pathogens recruit TE activity analogously in their infection process. In consequence, only few new TE insertions would be passed on to offspring, and pathogen-triggered TE response can only be detected in somatic cells.
To test this hypothesis we will take advantage of natural and induced TE diversity of selected wheat lines. We will develop an experimental system confronting wheat lines to pathogens which differ in their disease pattern as well as in their TE silencing mechanisms. This will allow us to address the central question about the contribution of TEs to the infection processes and the responses to it.