Auxin and abiotic stress responses

Abstract

Plants are exposed to a variety of abiotic stresses; these stresses have profound effects on plant growth, survival, and productivity. Tolerance and adaptation to stress require sophisticated stress sensing, signaling, and various regulatory mechanisms. The plant hormone auxin is a key regulator of plant growth and development, playing pivotal roles in the integration of abiotic stress signals and control of downstream stress responses. In this review, we summarize and discuss recent advances in understanding the intersection of auxin and abiotic stress in plants, with a focus on temperature, salt, and drought stresses. We also explore the roles of auxin in stress tolerance and opportunities arising for agricultural applications.

Keywords: Abiotic stress; auxin; drought; phytohormone; salt; temperature.

Fig. 1.

The central pathways for auxin biosynthesis, inactivation, and transport in plants. (A) The primary routes for auxin biosynthesis and inactivation. Indole-3-acetic acid (IAA), as a naturally occurring active auxin, is synthesized from the main precursor l-tryptophan (l-Trp). The Trp-dependent pathways comprise the indole-3-acetaldoxime (IAOx), the indole-3-acetamide (IAM), and the indole-3-pyruvic acid (IPyA) pathways. Amongst these pathways, the IPyA route is considered to be the main contributor to IAA synthesis. In addition to auxin biosynthesis, auxin levels are also regulated by its inactivation through conjugation and degradation. There are three reversible auxin conjugates: ester-linked IAA, amide-linked IAA, and methyl IAA. Irreversible auxin degradation is through the oxidation of IAA to 2-oxindole-3-acetic acid (oxIAA) by the dioxygenase for auxin oxidation (DAO). (B) The intercellular auxin distribution is established by the influx and efflux carriers. AUXIN RESISTANT1/LIKE AUX1 (AUX1/ LAX) transporters facilitate the influx of IAA. PIN-FORMED (PIN) and ATP-BINDING CASSETTE SUBFAMILY B (ABCB) protein families facilitate the efflux of IAA. The long canonical PIN proteins, PIN1, PIN2, PIN3, PIN4, and PIN7, are polarly localized to the plasma membrane (PM). The short non-canonical PIN proteins, PIN5, PIN6, and PIN8, localize to the endoplasmic reticulum (ER) membrane. PIN-LIKES (PILS) proteins are ER localized and contribute to intracellular auxin transport. In addition, the transporters of auxin precursor indole 3-butyric acid (IBA), that is converted to IAA by a β-oxidation in peroxisome, mediates auxin metabolism.

Fig. 2.

The central pathways for auxin signal transduction. Nuclear auxin signal transduction is mediated by the TRANSPORT INHIBITOR RESPONSE1/AUXIN SIGNALING F-BOX PROTEINS (TIR1/AFBs) pathway, which includes the AUXIN RESPONSE FACTOR (ARF) transcription factors and Auxin/INDOLE-3-ACETIC ACID (Aux/IAA) repressor proteins. The E3 ubiquitin ligase TIR1/AFBs are complexed with the S PHASE KINASE-ASSOCIATED PROTEIN1 (SKP1) (or ASK1 in plants), CULLIN1 (CUL1), and RING BOX1 (RBX1), forming an SCF^TIR1/AFB complex. Aux/IAAs interact with ARFs to prevent auxin signaling under low levels of auxin. As the auxin levels increase, auxin induces Aux/IAA binding to the SCF^TIR1/AFB complex, causing the ubiquitination and degradation of Aux/IAA proteins through the 26S proteasome. The degradation of Aux/IAA proteins relieves ARF repression to allow ARF-mediated transcription to proceed. In parallel, the E3 ubiquitin ligase AUXIN RESPONSE FACTOR F-BOX1 (AFF1) facilitates the ubiquitylation of ARF7 and ARF19 for degradation through the 26S proteasome, regulating the auxin signaling transduction. Additionally, the transmembrane kinase (TMK) proteins localized in the plasma membrane mediate cell surface auxin signal transduction by binding to the non-canonical IAA32 and IAA34. The auxin-binding protein 1 (ABP1) also medicates auxin signaling through the TMK1-based cell surface pathway.