Figure 1.

Auxin biosynthesis, homeostasis, and signaling. The main precursor for IAA (indole-3-acetic acid) biosynthesis, L-tryptophan (L-Trp), is synthesized in chloroplasts. The dominant IAA biosynthesis pathway in Arabidopsis is via indole-3-pyuvic acid (IPyA). Free IAA is either oxidized or conjugated to, for example, amino acids and sugars (for review, see Zhang and Peer 2017 and Casanova-Sáez et al. 2021). IAA can either enter cells through the plasma membrane (PM)-localized H⁺/auxin symporter AUX1/LAX or diffuse through the PM in its protonated form (IAAH). Inside the cell, IAA is predominantly in an anionic form, necessitating export, which is mediated mainly by PIN proteins at the PM (for review, see Hammes et al. 2021). PIN proteins undergo constant endocytic cycling and are degraded in the vacuole (for review, see Adamowski and Friml 2015). Auxin influences these processes by an unclear mechanism involving myosin phosphorylation (Han et al. 2021). So-called short PINs and PILS mediate auxin in- and efflux in the endoplasmic reticulum (ER) (for review, see Abdollahi Sisi and Růžička 2020). WAT1 is an auxin transporter located in the tonoplast (Ranocha et al. 2013). In the nucleus, auxin binds to the canonical TIR1/AFB-Aux/IAA receptor complex and activates transcription via ubiquitination and degradation of Aux/IAA transcriptional repressors, which releases repressive ARF-Aux/IAA-TPL (TOPLESS) complexes (for review, see Morffy and Strader 2021). This pathway also regulates transcription of CAMEL. The CAMEL/CANAR complex at the PM interacts with and phosphorylates PINs (Hajný et al. 2020). Furthermore, auxin in the nucleus also releases the repressive complex between ETTIN/ARF3 (ETT) and other transcription factors such as INDEHISCENT (IND), causing transcriptional reprogramming required for various developmental processes. Transmembrane kinase (TMK) proteins are components of cell surface auxin signaling. Auxin can trigger the cleavage of the carboxy-terminal kinase domain of TMK1, which then translocates to the nucleus, where it regulates transcription by binding to the noncanonical AUX/IAAs (for review, see McLaughlin et al. 2021). TMK1 also mediates the auxin effect on AHA phosphorylation leading to apoplast acidification (Li et al. 2021b; Lin et al. 2021). It is unclear how auxin triggers the TMK pathway. The possible function of ABP1 as an auxin receptor in the apoplast and its role in the ER remains controversial (for review, see Napier 2021). TIR1/AFB auxin signaling, by an unknown mechanism, also mediates apoplast alkalinization and PM depolarization (Li et al. 2021b; Serre et al. 2021) and Ca²⁺ influx (Dindas et al. 2018; for review, see Dubey et al. 2021). Green-filled circles depict auxin molecules. Grey dashed arrows indicate hypothetical regulations. Blue arrows indicate IAA biosynthesis and orange arrows indicate metabolic pathways. Figure based on data in Skalický et al. (2018) and Gallei et al. (2020).