Date of Award


Document Type

Open Access Dissertation


Biological Sciences

First Advisor

Johannes W Stratmann


Methanol is a byproduct of cell wall modification. It is released through the action of pectin methylesterases (PMEs), which demethylate cell wall pectins. Plant PMEs play not only a role in developmental processes but also in responses to herbivory and infection by fungal or microbial pathogens, resulting in increased methanol release. To break down the cell wall barrier, pathogens employ their own PMEs. Interestingly, the infection process also regulates the expression of certain plant PMEs. Methanol is toxic to a number of herbivores and reduces their fitness. At high concentrations, it upregulates signaling and defense genes. However, molecular mechanisms that explain how methanol affects plant defenses are poorly understood. Here we show that methanol alone has weak effects on defense signaling, however it profoundly alters signaling responses to danger- and microbe-associated molecular patterns (DAMPs, MAMPs) such as the alarm hormone systemin, the bacterial flagellum-derived flg22 peptide, and the fungal cell wall-derived oligosaccharide chitosan. Methanol application shifts DAMP/MAMP-induced MAP kinase (MAPK) activity in tobacco and tomato cell cultures, as well as Arabidopsis seedlings. It also shifts a flg22-induced ROS burst in tomato leaf tissue. We propose that the cell wall breakdown product methanol is perceived by plant cells as a DAMP-like alarm signal that alters defense responses to other DAMPs and MAMPs.