Signalling pathways associated with acyl-CoA-binding proteins (ACBPs) following abiotic stresses in Arabidopsis thaliana. In transgenic Arabidopsis Class II AtACBP1-overexpressors (OEs), PLDα1 was induced upon cold stress, causing a decrease in the ratio of PC to PA leading to membrane instability and freezing sensitivity [88]. In contrast, transgenic Arabidopsis Class I AtACBP6-OEs were conferred freezing tolerance via the PLDδ-mediated pathway in rosettes and the ABA-mediated pathway in flowers, resulting in changes in lipids, sugars and stress-related genes [87,123]. During drought, transgenic Arabidopsis Class II AtACBP2-OEs exhibited elevated AtAREB1 and AtRBOHF expression which led to ROS production, subsequent stomatal closure and reduced water loss [90]. Proper stem cuticle development conferred by Class I AtACBP6, Class III AtACBP3 or Class IV AtACBP4 protects wild-type Arabidopsis from water loss [25]. Under high salinity, AtACBP1 and AtAREB1 expression were upregulated in wild-type seeds [80]. The overexpression of AtACBP1 in transgenic Arabidopsis triggers nuclear translocation of AtAREB1, leading to the induction of stress marker genes (RD22 and RD29B) and AtAREB1 target genes (PKS5 and RAB18), thereby promoting stronger ABA responses during seed germination and seedling establishment [80]. When wild-type Arabidopsis undergoes hypoxia, the RAP2.12 transcription factor bound to AtACBP1 or AtACBP2, translocates to the nucleus and activates hypoxia-responsive gene transcription, conferring hypoxic protection [77,128,134,139]. Another hypoxic tolerance pathway involves the interaction of unsaturated VLC ceramide and the CTR1 protein with subsequent nuclear translocation of EIN2, resulting in the activation of CTR1-mediated ethylene signalling [137]. AtACBP1 is involved in phytoremediation and its overexpression in transgenic Arabidopsis confers Pb(II) tolerance [135]. AtACBP2 can interact with AtFP6 or LYSOPL2, mediating heavy metal transport and phospholipid repair respectively, and hence transgenic Arabidopsis AtACBP2-OEs were resistant to Cd(II) and Cd(II)-induced oxidative stress [75,76,82]. On wounding, the up-regulation of AtACBP3 and AtACBP6 expression in the wild type suggested their involvement in JA-mediated local and systemic wound responses [125,126]. Orange and yellow boxes indicate transgenic Arabidopsis AtACBP-OEs and wild-type Arabidopsis AtACBPs respectively, used in studies on abiotic stress. Blue boxes represent the signalling pathways. White boxes indicate the molecular events that occur along the signalling pathway. Red and blue arrows indicate increase and a decrease, respectively. Black arrows denote the flow of events. ABA, abscisic acid; ACBP, acyl-CoA-binding protein; AREB1, ABA-RESPONSIVE ELEMENT BINDING PROTEIN1; FP6, FARNESYLATED PROTEIN6; COR, COLD-RESPONSIVE; CTR1, CONSTITUTIVE TRIPLE RESPONSE1; EIN2, ETHYLENE-INSENSITIVE2; JA, jasmonic acid; LYSOPL2, LYSOPHOSPHOLIPASE2; MGDG, monogalactosyldiacylglycerol; PA, phosphatidic acid; PC, phosphatidylcholine; PKS5, PROTEIN KINASE SOS2-LIKE5; PLD, PHOSPHOLIPASE D; RAB18, RESPONSIVE TO ABA18; RAP2.12, RELATED TO APETALA2.12; RBOHF, RESPIRATORY BURST OXIDASE HOMOLOG F; RD, RESPONSIVE TO DESSICATION; ROS, reactive oxygen species; VLC, very-long-chain.