Figures (3)  Tables (1)

    • Figure 1. 

      Integrated network of ABA biosynthesis, transport, signaling, and downstream physiological responses. (1) Abiotic stress perception induces ABA biosynthesis through the plastidial carotenoid pathway involving NCED3/NCED9, ABA2, and AAO3. (2) ABA homeostasis is regulated by CYP707A-mediated catabolism, ABA-GE hydrolysis by β-glucosidases, and ABA transport via ABCG25/ABCG40 transporters. (3) Perception of ABA by PYR/PYL/RCAR receptors inhibits PP2C phosphatases, enabling RAF–SnRK2 kinase activation and downstream phosphorylation events. (4) Activated SnRK2 coordinates physiological adaptation through regulation of AREB/ABF, SLAC1, GORK, RBOHF, and RAPTOR, integrating ABA signaling with stomatal closure, osmotic adjustment, ROS signaling, autophagy activation, and growth inhibition.

    • Figure 2. 

      Proposed ABA–TOR bistable molecular switch controlling the transition between stress survival and growth. Under abiotic stress, ABA signaling activates the PYR/PYL–PP2C–RAF–SnRK2 cascade, resulting in phosphorylation of RAPTOR, suppression of TORC1 activity, activation of autophagy, and induction of stress-adaptive responses. Under favorable conditions, TOR signaling promotes anabolic metabolism, ribosome biogenesis, protein synthesis, cell cycle progression, and organ growth while repressing ABA-mediated stress responses. The reciprocal antagonism between ABA and TOR represents a proposed bistable regulatory switch coordinating plant adaptation to changing environmental conditions.

    • Figure 3. 

      Integrated microbiome–ABA interaction network in the rhizosphere. The rhizosphere microbiome functions as an integrated regulatory system that modulates the ABA-dominant abiotic stress tolerance state. PGPR, AMF, endophytes, and actinomycetes regulate ABA biosynthesis (NCED3), PYR/PYL–PP2C–RAF–SnRK2 signaling, ROS homeostasis, nutrient acquisition, and phytohormone balance. These complementary microbial activities promote osmoprotection, autophagy, stress-responsive gene expression, and epigenetic stress memory, thereby enhancing plants' adaptation and resilience under abiotic stress.

    • FeatureSA-dominant stateJA/ET-dominant stateABA-dominant stateTOR-dominant (growth) state
      Major triggersBiotrophic pathogens, PAMPs, effectorsNecrotrophic pathogens, herbivory, woundingDrought, salinity, heat, osmotic stress, low water potentialNutrient repletion, high sucrose/glucose, favorable temperature and light
      Key hormonal signals↑SA; ↓AUX, GA, CK↑JA, ↑ET; ↓GA (DELLA stabilised)↑ABA; ↓CK, AUX, GA; partial suppression of SA↑AUX, GA, BR, CK; ↓ABA, SA, JA
      Core signaling componentsNPR1, ICS1, TGA factors, PR1COI1, JAZ, MYC2, ERF1, PDF1.2NCED3, PYR/PYL, PP2C, SnRK2.6/OST1, AREB/ABF, RAF kinasesTOR–RAPTOR–LST8 (TORC1), S6K1/2, eIF4E, BZR1, ARF
      TOR/SnRK1 status↓TOR; ↑SnRK1 (moderate)Moderate ↓TOR; partial SnRK1 activation↓TOR (SnRK2-mediated RAPTOR phosphorylation; SnRK1 co-activation); ↑SnRK1; ↑autophagy↑TOR; ↓SnRK1; ↑T6P; high ATP/AMP; ↓autophagy
      Physiological outputsPR gene expression, SAR, growth restrictionPhytoalexins, protease inhibitors, ISR, moderate growth inhibitionStomatal closure, osmoprotectant accumulation (proline, trehalose, LEA proteins), ROS/NO signaling; autophagic recycling; epigenetic stress memoryRibosome biogenesis, cell cycle progression, anabolic metabolism, organ expansion
      Representative marker genesNPR1, ICS1, PR1, TGA2MYC2, ERF1, PDF1.2, COI1NCED3, RD29A/B, RAB18, SnRK2.6 (OST1), SLAC1TOR, S6K1/2, CYCD, BZR1, ARF

      Table 1. 

      Comparison of the four proposed regulatory attractor states in the SA–JA/ET–ABA–TOR network.