Plant Responses to Herbivory, Wounding, and Infection

Abstract

Plants have various self-defense mechanisms against biotic attacks, involving both physical and chemical barriers. Physical barriers include spines, trichomes, and cuticle layers, whereas chemical barriers include secondary metabolites (SMs) and volatile organic compounds (VOCs). Complex interactions between plants and herbivores occur. Plant responses to insect herbivory begin with the perception of physical stimuli, chemical compounds (orally secreted by insects and herbivore-induced VOCs) during feeding. Plant cell membranes then generate ion fluxes that create differences in plasma membrane potential (Vm), which provokes the initiation of signal transduction, the activation of various hormones (e.g., jasmonic acid, salicylic acid, and ethylene), and the release of VOCs and SMs. This review of recent studies of plant-herbivore-infection interactions focuses on early and late plant responses, including physical barriers, signal transduction, SM production as well as epigenetic regulation, and phytohormone responses.

Keywords: airborne signaling; epigenetic regulation; intracellular signaling; physical barrier; plant–herbivore interaction; secondary metabolite; signal transduction.

Figure 1

Schematic diagram of plant physical barriers against herbivory attack, including wax cuticle layers, trichomes, thorns, and hairs.

Figure 2

Schematic diagram of the calcium signaling pathway following biotic attack. After an attack, resistance elicitors are released in herbivore oral secretions (OS), precipitated, and bound to receptors, causing a rapid increase in calcium cytosolic ([Ca²⁺] _cyt) content. Calcium channels and ATP-dependent Ca²⁺ pumps in the cell membrane and cell organelles (e.g., mitochondria, vacuoles, and endoplasmic reticulum) organize Ca²⁺ ions inside and outside the cell/organelles. Greater increases in Ca²⁺ ions trigger potassium (K⁺) channel activation, causing plasma membrane potential (Vm) depolarization. Different calcium receptors (e.g., CBL–CIPK, calcineurin B-like protein- CBL interacting protein kinase, CML42/CML43, calmodulin-like proteins 42/43, and CPK3/CPK13, calcium-dependent protein kinases3/13) increase to activate transcription factors, such as HSFB2A. Finally, transcriptional regulation in the nucleus induces plant herbivore defense (Modified from [5]).

Figure 3

Schematic diagram of the interactions among reactive oxygen species (ROS), Ca²⁺, and phytohormones (JA, jasmonic acid, SA, salicylic acid, and ethylene) within the cell upon biotic attack. Ca²⁺ influxes activate ethylene and calmodulins (CaMs) of JAV1, dismantling the JAV1–JAZ8–WRKY51 (JJW) complex to activate JA biosynthesis and thereby producing jasmonoyl-L-isoleucine (JA-Ile). High JA concentrations cause ROS accumulation, which in turn induces SA and vice versa. Distal transfer of Ca²⁺ (through glutamate receptor-like (GLR) channels), JA, and JA-Ile occurs between cells.

Figure 4

The main plant secondary metabolites (SMs) involved in plant defenses against herbivores, broadly classified as phenolics, terpenes, and sulfur (S)- and nitrogen (N)-containing compounds.