Callose Deposition: A Multifaceted Plant Defense Response

TLDR

Callose deposition in Arabidopsis is a widely used model for plant immunity, yet recent reports have contradicted each other regarding its regulation by pathogens. The study aimed to resolve conflicting reports by testing callose deposition robustness across growth conditions and two PAMPs, Flg22 and chitosan. We examined callose deposition under varied growth conditions and in response to Flg22 and chitosan using a hydroponic culture system. Callose deposition varies strongly with growth conditions, correlating with H₂O₂ levels and modulated by ABA, and while Flg22- and chitosan-induced callose share environmental sensitivity, they differ in timing, tissue specificity, H₂O₂ colocalization, and dependence on RBOHD, VTC1, PEN2, and PMR4, demonstrating that callose is a multifaceted defense regulated by distinct signaling pathways.

Abstract

Callose deposition in Arabidopsis has emerged as a popular model system to quantify activity of plant immunity. However, there has been a noticeable rise in contradicting reports about the regulation of pathogen-induced callose. To address this controversy, we have examined the robustness of callose deposition under different growth conditions and in response to two different pathogen-associated molecular patterns, the flagellin epitope Flg22 and the polysaccharide chitosan. Based on a commonly used hydroponic culture system, we found that variations in growth conditions have a major impact on the plant's overall capacity to deposit callose. This environmental variability correlated with levels of hydrogen peroxide (H₂O₂) production. Depending on the growth conditions, pretreatment with abscissic acid stimulated or repressed callose deposition. Despite a similar effect of growth conditions on Flg22- and chitosan-induced callose, both responses showed differences in timing, tissue responsiveness, and colocalization with H₂O₂. Furthermore, mutant analysis revealed that Flg22- and chitosan-induced callose differ in the requirement for the NADPH oxidase RBOHD, the glucosinolate regulatory enzymes VTC1 and PEN2, and the callose synthase PMR4. Our study demonstrates that callose is a multifaceted defense response that is controlled by distinct signaling pathways, depending on the environmental conditions and the challenging pathogen-associated molecular pattern.