Impact of environmental factors on PAMP-induced callose in hydroponically grown Arabidopsis

Abstract: Plants respond to pathogenic microbes by depositing callose-rich papillae, whichprevents further colonization by the pathogen at an early stage of infection. Recently, it wasdiscovered that induced callose deposition is regulated by glucosinolate metabolites (Nishimuraet al., 2003). To further study the impact of environmental factors on this defence reaction, westudied callose deposition in hydroponically grown Arabidopsis seedlings upon challenge withtwo pathogen-associated molecular patterns (PAMPs), flagellin and chitosan. Seedlings exposedto high light intensity (~150μM/m2/s) showed significantly enhanced amounts of callosedeposition compared to those exposed to relatively low light intensity (~75μM/m2/s), suggestingthat light potentiates callose deposition. Conversely, increasing concentrations of sucrose in themedium suppressed basal and PAMP-induced callose depositions, possibly due to a suppressionof photosynthesis activity (Clay et al., 2009). Interestingly, addition of antioxidant vitamins to thegrowth medium suppressed basal and PAMP-induced callose deposition, suggesting that reactiveoxygen species (ROS) enhance PAMP-induced callose deposition. Since the plant hormone ABAis involved in priming of pathogen-induced callose (Gomez-Gomez & Boller, 2000), sugarsignalling (Iriti & Faoro, 2008) and ROS production (Kohler et al., 2002), we investigated theeffects of this hormone in our model system. Addition of ABA to the growth medium augmentedboth basal and PAMP-induced callose. This outcome suggests a positive influence of ABA oncallose deposition, consistent with a stimulatory role of ROS in callose deposition. However, thisresult is not consistent with findings by other labs, who reported suppressive effects by ABA oninduced callose deposition (Nishimura et al., 2003). Based on our finding that variousenvironmental factors can influence callose deposition, we propose that the variable effects byABA are caused by interactions between ABA signalling and other abiotic stress pathways.