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)).