Modulation of plant immunity by atmospheric CO2

Abstract

The continuously increasing CO2 levels in the atmosphere is considered to be core among climate changes and is expected to affect plant diseases in the future, posing a new challenge for future strategies in plant protection. In this thesis we explore signaling mechanisms underlying atmospheric CO2-modulated defense responses in Arabidopsis plants. We demonstrate that the disease resistance against the hemi-biotroph Pseudomonas syringae pv. tomato DC3000 (Pst) decreases and the disease resistance against the necrotroph Botrytis cinerea increases as the level of atmopheric CO2 increases. By employing genetic, physiological and biochemical analysis, we further demonstrated that ABA signaling plays a central role in CO2-regulated defense against Pst. The CO2-controlled stomatal reopening is dependent on ABA signaling in the plant, whereby the low ABA concentration under a low CO2 regime leads to prolonged closure of the stomata after infection with Pst. This ABA-dependent effect on the opening of the stomata is correlated with an increased resistance against this pathogen that invades the plant through the stomata. Together, our findings highlight the importance of ABA signaling for fine tuning atmospheric CO2-regulated defense responses. In a search for potential components involved in CO2-modulated defense responses, we reveal that two carbonic anhydrases (CAs), CA1 and CA4, are important regulators in pathogen associated molecular patterns (PAMPs)-triggered immunity (PTI). We demonstrate that these CAs have an antagonizing effect on the SA signaling pathway. We further propose a model for the function of CAs in mediating PTI. Upon recognition of PAMPs, CA1 and CA4 are down-regulated in plants, resulting in enhanced ROS production and increased defense-related gene expression. This ultimately leads to enhanced SA-dependent defenses and inhibition of pathogen growth. Moreover, we show that these two CA genes play a role in atmospheric CO2-regulated defense against Pst. These results together suggest that CAs might serve as an important node connecting CO2 and plant defense signaling. Finally, our results reveal that changes in atmospheric CO2 do not significantly influence soil-borne diseases caused by Rhizoctonia solani and Fusarium oxysporum f.sp. raphani in Arabidopsis. Possibly, this is caused by the fact that CO2 levels in the soil are ready much higher than in the atmosphere. In conclusion, our research demonstrates that hormonal signaling pathways and CAs are important regulators in CO2-modulated defense responses. This knowledge provides a new perspective on future investigations into the functioning of the plant immune system under changed atmospheric CO2 conditions and ultimately can be utilized to improve crop protection and crop breeding in the face of changing climate change.