Acknowledgements
I thank Prof. Anna Amtmann and Amanda Rasmussen for valuable comments.
I’m also grateful to Prof. Monika Hilker and Nina Fatouros for providing
image material.
Figure 1 : Cellular responses that are part of both the
pathogen-induced hypersensitive (HR) response (solid black arrows) and
the oviposition-induced HR-like response (dashed grey arrows).
Pathogen-associated molecular patterns (PAMPs) bind to membrane
receptors (e.g. flg22 binding to the FLS2-BAK1 complex) and trigger ROS
production, callose deposition, SA synthesis, and activation of
pathogenesis-related genes (PR1, PR5). All of these metabolic
adaptations are also elicited by the deposition of herbivore eggs, but
details about the perception pathway are missing so far (Monika Hilker
& Fatouros, 2015, 2016; Reymond, 2013; Smith et al., 2014).
Figure 2 : Arabidopsis infestation by Pieris brassicae .
Left: A female butterfly that was not treated with antibiotics has large
accessory reproductive glands (ARGs), and produces ample secretion
during egg deposition. The secretion elicits the plant’s defence
response, which leads to poor larvae growth and development. Right: The
ARGs of an antibiotics-treated butterfly are smaller, and less secretion
is released for egg attachment. The plant does not up-regulate defence
mechanisms, and the larvae can successfully infest the leaf (after
Monika Hilker and Fatouros (2015)).