Karrikin signalling: impacts on plant development and abiotic stress tolerance

Abstract

Plants rely upon a diverse range of metabolites to control growth and development, and to overcome stress that results from suboptimal conditions. Karrikins (KARs) are a class of butenolide compounds found in smoke that stimulate seed germination and regulate various developmental processes in plants. KARs are perceived via a plant α/β-hydrolase called KARRIKIN INSENSITIVE2 (KAI2), which also functions as a receptor for a postulated phytohormone, provisionally termed KAI2 ligand (KL). Considered natural analogues of KL, KARs have been extensively studied for their effects on plant growth and their crosstalk with plant hormones. The perception and response pathway for KAR-KL signalling is closely related to that of strigolactones, another class of butenolides with numerous functions in regulating plant growth. KAR-KL signalling influences seed germination, seedling photomorphogenesis, root system architecture, abiotic stress responses, and arbuscular mycorrhizal symbiosis. Here, we summarize current knowledge of KAR-KL signalling, focusing on its role in plant development, its effects on stress tolerance, and its interaction with other signalling mechanisms.

Keywords: Abiotic stress; butenolide; development; hormone; karrikin; photomorphogenesis; root architecture; signalling.

Fig. 1.

Signalling pathways for KAR–KL and SL feature shared and homologous components. The α/β-hydrolase KAI2 is the receptor for karrikins (or karrikin metabolites; KAR), and an assumed butenolide ligand (KL) of unknown structure (?). Its homologue, D14, is the receptor for strigolactones (SLs). Ligand binding induces a conformational change in the receptor, probably facilitating an interaction with MAX2, the F-box subunit of the SCF class of the E3 ubiquitin–protein ligase complex. The receptor and/or MAX2 interact with one or more specific members of the SMXL family of repressor proteins, which are then degraded. In part through changes in transcription of varied target genes, this degradation process activates downstream responses such as seed germination, modifications to root architecture, and stimulation of arbuscular mycorrhizal symbiosis.

Fig. 2.

Schematic model of KAR–KL signalling in response to drought stress. Under water-limited conditions, KL production is tentatively elevated, and levels of activated KAI2 increase. This triggers the formation of the SCF^MAX2–KAI2–SMAX1 (or SMXL2) complex. SMAX1 is then polyubiquitinated and degraded, activating KAR–KL downstream responses that include a reduction in stomatal aperture. This effect may come about through a transcriptionally mediated increase in ABA biosynthesis (Li et al. 2017). This short-term mechanism regulates drought responses by controlling water loss through transpiration. In addition to this immediate response, longer term KAR–KL mediated adaptations to drought conditions include an increase in cuticular deposition.