(a) GABA synthesis (based on Fait et al., 2008 and Gilliham and Tyerman, 2016). GABA is synthesised via two main routes. In the context of the GABA shunt, it is synthesised in the cytoplasm from glutamate by glutamate decarboxylase (GAD) and is then imported to the mitochondria, where it is converted to succinic semialdehyde. In the plastids and the peroxisomes, it is synthesised from the diamine putrescine. The ability of the GABA shunt to control the C/N ratio makes GABA a pivotal metabolite under various stress conditions. Similarly, the importance of polyamines in stress mechanisms also connects GABA to the maintenance of cell physiology. In addition, since the GAD reaction consumes a proton, GABA might act as a pH regulator. (b) GABA in signalling. Suggested GABA signalling events depend on the ALMT protein family. In the roots, GABA inhibits the transport of malate through ALMT1 upon Al3+ stress. In the leaves, GABA might regulate stomatal closure during drought by inhibiting Cl− transport through the tonoplast localised ALMT9 (which does not count as an intercellular signalling event by our criteria). GABA can also regulate stomatal closure through ALMT12. However, the precise physiological relevance of this process is still not clear. GABA inhibition of ALMT1 malate transport might be achieved through an interaction with a peptide moiety at the cytoplasmic side. It is not known whether this is achieved primarily by GABA imported to the cell via ALMT1 itself or by endogenous cytoplasmic GABA. The possible involvement of GABA in pollen tube growth is not shown since the underlying mechanism is not yet deciphered. Similarly, the putative interactions between GABA and GORK is not shown. GAD, glutamate decarboxylase; SSR, semialdehyde reductase; GABA-T, GABA transaminase; SSADH, succinic semialdehyde dehydrogenase; GABP, mitochondrial GABA transporter; GAT, GABA transporters; CuAO, copper-containing amine oxidase; ALDH, aldehyde dehydrogenase.