Strategies for Enhancing Plant Immunity and Resilience Using Nanomaterials for Sustainable Agriculture

Abstract

Research on plant-nanomaterial interactions has greatly advanced over the past decade. One particularly fascinating discovery encompasses the immunomodulatory effects in plants. Due to the low doses needed and the comparatively low toxicity of many nanomaterials, nanoenabled immunomodulation is environmentally and economically promising for agriculture. It may reduce environmental costs associated with excessive use of chemical pesticides and fertilizers, which can lead to soil and water pollution. Furthermore, nanoenabled strategies can enhance plant resilience against various biotic and abiotic stresses, contributing to the sustainability of agricultural ecosystems and the reduction of crop losses due to environmental factors. While nanoparticle immunomodulatory effects are relatively well-known in animals, they are still to be understood in plants. Here, we provide our perspective on the general components of the plant's immune system, including the signaling pathways, networks, and molecules of relevance for plant nanomodulation. We discuss the recent scientific progress in nanoenabled immunomodulation and nanopriming and lay out key avenues to use plant immunomodulation for agriculture. Reactive oxygen species (ROS), the mitogen-activated protein kinase (MAPK) cascade, and the calcium-dependent protein kinase (CDPK or CPK) pathway are of particular interest due to their interconnected function and significance in the response to biotic and abiotic stress. Additionally, we underscore that understanding the plant hormone salicylic acid is vital for nanoenabled applications to induce systemic acquired resistance. It is suggested that a multidisciplinary approach, incorporating environmental impact assessments and focusing on scalability, can expedite the realization of enhanced crop yields through nanotechnology while fostering a healthier environment.

Keywords: Crop protection agents; biostimulants; nanotechnology; plant defense; plant immunity; plant resilience; plant science; safe-by-design.

Figure 1

Publication activity for nano related immunomodulatory effects for plants. Publication search results using descriptors “nano* ” and “immunomodulatory effects* ” in the ISI Web of Knowledge database from 2010 to 2021. Green data represents articles on plants.

Figure 2

Key pathogen recognition mechanisms and signaling pathways can be modulated by nanoparticle exposure. a: Pathogen recognition mechanisms. Figure reproduced from Meng and Zhang 2013. Pathogens can be recognized via the binding to pattern recognition receptors (PRRs) of a) pathogen-specific molecules - pathogen/microbe-associated molecular patterns (PAMP/MAMP), b) molecules on the surface of the pathogen directly, or c) plant-derived molecules associated with cell damage - damage-associated molecular patterns (DAMP). The ensuing immunity is called PAMP-triggered immunity (PTI). Furthermore, molecules called effectors produced by the pathogen to suppress plant immunity can be recognized by plant-specific resistance proteins (R proteins), which trigger effector-triggered immunity (ETI). After the recognition, different signaling pathways lead to different plant defense responses. For example, mitogen-activated protein kinase (MAPK) cascades (orange) lead to the phosphorylation of target proteins. These, in turn, trigger the signaling by defense hormones such as salicylic acid (SA) and ethylene, the activation of defense genes, the synthesis of antimicrobial metabolites, and reactive oxygen species, including NO. Nanoparticles can most notably interfere with plant immunity before the stage of the MAPK, perhaps by the induction of DAMPs and by the direct generation of reactive oxygen species (ROS). The signaling components which determine the specific response are an active research field. b: Signaling network of three signal transduction pathways of the plant hormones salicylic acid (SA), jasmonic acid (JA), and ethylene (ET). Figure reproduced from Kunkel and Brooks 2002. Note the mutual antagonistic and synergistic interactions of the SA, JA, and ET pathways.