Plant Signaling

Plants produce and respond to chemical, electrical, and mechanical signals continuously. They coordinate their own development, defend against herbivores and pathogens, attract pollinators, and exchange information with neighboring plants and soil organisms. None of this requires a nervous system. Plant signaling operates through hormone transport, volatile organic compounds, electrical impulses, and peptide signals, using receptor proteins and kinase cascades that are structurally and functionally distinct from animal signaling systems but no less sophisticated.

Internal hormone signaling

Plants use at least nine major classes of hormones to coordinate growth, development, and stress responses:

Auxin (primarily indole-3-acetic acid, IAA) controls cell elongation, root initiation, apical dominance, and tropisms (directional growth responses to light and gravity). It is synthesized mainly in young leaves and shoot tips, transported directionally through PIN-FORMED efflux carriers, and perceived by the TIR1/AFB receptor complex, which triggers degradation of Aux/IAA transcriptional repressors.

Jasmonic acid (JA) and its bioactive form jasmonoyl-isoleucine (JA-Ile) mediate defense against herbivorous insects and necrotrophic pathogens. When a caterpillar chews a leaf, damaged cells release linolenic acid from membrane lipids, which is converted to JA through the octadecanoid pathway. JA-Ile is perceived by the COI1 receptor, which triggers degradation of JAZ repressor proteins and activates transcription of defense genes — including those encoding proteinase inhibitors, polyphenol oxidases, and enzymes for toxic secondary metabolite synthesis.

Salicylic acid (SA) mediates defense against biotrophic pathogens (those that feed on living tissue). SA accumulates in response to pathogen detection by pattern recognition receptors (PRRs) and resistance (R) proteins, and it activates systemic acquired resistance (SAR) — a whole-plant immune response described below.

Abscisic acid (ABA) regulates drought response, seed dormancy, and stomatal closure. Under water stress, ABA is synthesized rapidly in roots and leaves and triggers guard cell ion efflux through the PYR/PYL/RCAR-SnRK2-SLAC1 signaling cascade.

Ethylene (C2H4), a gaseous hormone, promotes fruit ripening, leaf abscission, and responses to flooding (in rice, ethylene triggers internode elongation that allows submerged plants to grow above the waterline). It is perceived by the ethylene receptor family (ETR1/ERS1), which are unusual in that the receptor is active in the absence of ligand and is inactivated when ethylene binds.

Strigolactones, discovered as plant hormones only in 2008, suppress axillary bud outgrowth (controlling branching architecture) and serve as root-exuded signals that recruit mycorrhizal fungi. Strigolactone biosynthesis increases under phosphorus deficiency, linking plant architecture and symbiotic recruitment to soil nutrient status.

Volatile signaling between plants

When plants are attacked by herbivores, they release volatile organic compounds (VOCs) into the air. These volatiles include green leaf volatiles (GLVs) such as (Z)-3-hexenal and (E)-2-hexenal (released within seconds of tissue damage), methyl jasmonate, methyl salicylate, and diverse terpenes.

These volatiles serve multiple functions simultaneously:

• Indirect defense. Many herbivore-induced VOCs attract predators and parasitoids of the attacking herbivore. Maize plants damaged by caterpillars release specific terpene blends that attract parasitic wasps.
• Plant-plant signaling. Neighboring plants exposed to herbivore-induced VOCs upregulate their own defense gene expression and accumulate defense compounds, even before being attacked themselves. This was first demonstrated by Baldwin and Schultz (1983) in poplar and sugar maple and has since been confirmed in dozens of species.
• Within-plant signaling. Volatiles can travel through the air from a damaged leaf to undamaged leaves on the same plant faster than internal vascular signals can move, providing a rapid self-signaling mechanism.

Field studies (reviewed by Heil and Karban, 2010) have confirmed that VOC-mediated defense priming operates under natural conditions, not just in sealed laboratory chambers — but the effective range is typically limited to plants within roughly 50-100 cm of the emitter, because VOC concentration drops rapidly with distance.

Electrical signaling

Plants generate and propagate electrical signals in response to wounding, temperature changes, and other stimuli. Two main types have been characterized:

Action potentials propagate at roughly 1-10 cm per second through the phloem and involve transient depolarization of the plasma membrane, mediated by calcium and chloride channel activation followed by potassium efflux repolarization. They resemble animal action potentials in waveform but travel much more slowly.

Variation potentials (also called slow wave potentials) propagate more slowly (0.1-1 cm/s) and involve sustained depolarizations driven by hydraulic pressure waves in the xylem.

A breakthrough came from the Mousavi et al. 2013 study in Science, which demonstrated that glutamate receptor-like (GLR) channels in Arabidopsis mediate long-distance wound signaling. When a leaf is wounded, glutamate released from damaged cells activates GLR channels, which trigger calcium waves that propagate through the vasculature to distant leaves within minutes. These calcium waves activate jasmonic acid biosynthesis in the receiving leaves, causing systemic defense induction. Toyota et al. (2018, Science) directly visualized this process using genetically encoded calcium sensors in live Arabidopsis plants, showing that calcium waves propagate through the vasculature at roughly 1 mm per second after wounding, coupled with reactive oxygen species (ROS) waves mediated by the NADPH oxidase RBOHD. These two studies together established a molecular mechanism for how a wound on one leaf triggers defensive chemical production in undamaged leaves elsewhere on the plant.

Systemic acquired resistance (SAR)

When a pathogen infects a local tissue, the plant can activate immune defenses throughout its entire body — a response called systemic acquired resistance. SAR is triggered by local salicylic acid accumulation and propagated by mobile signals that travel through the phloem to distal tissues. Multiple mobile signals have been identified:

• Methyl salicylate — a volatile and phloem-mobile derivative of SA
• Azelaic acid — a C9 dicarboxylic acid that primes SA accumulation in receiving tissues
• Glycerol-3-phosphate (G3P) — acts synergistically with azelaic acid
• Pipecolic acid and N-hydroxy-pipecolic acid (NHP) — NHP, identified in 2018, appears to be the most critical SAR mobile signal. It is synthesized from lysine by the enzymes ALD1 and FMO1, and NHP-deficient Arabidopsis mutants are almost completely SAR-deficient.

In receiving tissues, SAR primes defense genes for faster and stronger activation upon subsequent pathogen challenge. This priming involves epigenetic modifications — particularly histone H3 lysine 4 trimethylation (H3K4me3) and H3 lysine 9 acetylation (H3K9ac) at WRKY transcription factor promoters (Jaskiewicz et al., 2011) — and the accumulation of inactive MAP kinases (MPK3/MPK6) that can be rapidly activated upon pathogen detection. Priming persists for weeks and, in some cases, can be transmitted to the next generation through DNA methylation and small RNA pathways (transgenerational priming; Luna et al., 2012; Rasmann et al., 2012).

A major advance in understanding the initial pathogen detection step came from the structural resolution of the ZAR1 resistosome (Wang et al., 2019, Science). ZAR1 is a plant immune receptor (NLR protein) that, upon recognizing a pathogen effector, oligomerizes into a wheel-shaped pentameric complex that inserts into the plasma membrane and functions as a calcium-permeable channel. This calcium influx triggers immune cell death. The ZAR1 structure was the first demonstration that plant NLR immune receptors directly form membrane pores, providing a mechanistic link between pathogen recognition and the hypersensitive response.

Root signaling and kin recognition

Plant roots distinguish their own root system from those of neighbors and competitors. Susan Dudley and Amanda File (2007) showed that Cakile edentula (American sea rocket) allocates more biomass to roots when sharing soil with strangers than with siblings, a response consistent with kin recognition. Murphy and Dudley (2009) confirmed kin-mediated root allocation differences in Impatiens pallida. This kin recognition appears to operate through root exudate chemistry — plants secrete species- and genotype-specific mixtures of organic acids, amino acids, flavonoids, and other compounds into the rhizosphere, and root tips detect and respond to these chemical profiles.

Root tips also detect and avoid their own roots (self-inhibition), distinguish between living and dead neighboring roots, and preferentially proliferate in nutrient-rich patches while suppressing growth in nutrient-poor zones — behaviors that involve local auxin redistribution, nitrate and phosphate transporter regulation, and peptide signaling through the CLE (CLAVATA3/ESR-related) peptide family.

Related

• Stomata — guard cells as signal-integrating regulators
• Phloem — the internal transport system carrying signaling molecules
• Root — site of belowground signaling and exudate-mediated communication
• Niche Construction — how signaling organisms modify their shared environment
• Symbiosis — signaling molecules that recruit and regulate symbiotic partners