Fig. 1. The core energy management machinery, comprising SnRKs, TORC, and the T6P pathway, and its interactions with multiple signals through complex feedback regulation to regulate growth and resilience trade-offs.

The cover depicts a whiteboard illustration of the original concept behind the workshop ‘Plant Energy Management: Molecular Mechanisms and Signalling,’ held at UPSC, Sweden, in August 2024. The aim was to expand upon the original TOR meeting by focusing on the inputs and outputs of the core energy management machinery in a species-agnostic manner. (Credit: Benoît Menand, Johannes Hanson, and Vanessa Wahl.) Link: https://academic.oup.com/jxb/issue/77/5

Summary of the special issue on #PlantTOR, #SnRK1 and #T6P that was edited by Wahl, Hanson and Menand (2026). 🌱⚡
"The plant energy management machinery: an essential hub for stress resilience and developmental dynamics with great potential for crop improvement"
🔗 academic.oup.com/jxb/article/...

Great preprint by Liu, Blanford et al. (2025) on how trehalose 6-phosphate #T6P stimulates plant cell growth via #PlantTOR and is required for sucrose-induced TOR activation in #Arabidopsis by suppressing #SnRK1 in a dose-dependent manner, thereby mediating the antagonistic TOR–SnRK1 relationship.

Fig. 8 Hypothetical model showing the reciprocal regulation of target of rapamycin (TOR) and abscisic acid (ABA) signaling during the transition from the cell division to the cell expansion phase of legume seed development. The activators of TOR observed in this paper are shown, but further molecular and hormonal influences on the developmental transition are omitted for simplicity. The bottom panel extends a basic model by Weber et al. (2005) to show the approximate timing of relative changes in three established signaling metabolites: Glc, glucose; Suc, sucrose; and Gln, glutamine. Sucrose levels are known to be correlated with the signaling metabolite T6P.

Fig. 5. Glutamine (Gln) activates target of rapamycin (TOR) in developing pea cotyledons. (a) The in vivo RPS6-Ser240 phosphorylation status in pea embryos throughout development. Replicate immunoblots are shown in Supporting Information Fig. S5. (b) The relative RPS6-Ser240 phosphorylation signal is plotted, and the fresh weight of the embryos is plotted against days after pollination (DAP). Error bars represent the standard error of the mean. (c–e) RPS6-Ser240 phosphorylation was assessed in 90–130 mg pea embryos incubated for 2 or 4 h with or without Gln (62.5 mM) and sucrose (142 mM) (c), Gln (62.5 mM) and glucose (100 mM) (d) or individual amino acids (62.5 mM) and NH4NO3 (20 mM) (e). Two biological replicates are shown. Replicate immunoblots are shown in Fig. S6.

Great work by O’Leary et al. (2025) on how Gln-driven #PlantTOR signaling occurs during the early development of pea embryos (i.e. cell division phase), but is unexpectedly inactive during #legume seed storage protein biosynthesis. #Pisum #glutamine

🔗 nph.onlinelibrary.wiley.com/doi/10.1111/...

Great preprint by Upadhyaya et al. (2025) on using a #multiomics approach to study #PlantTOR signaling in the unicellular green alga #Chromochloris zofingiensis, particularly showing the upregulation of #AminoAcid biosynthesis pathways during TOR inhibition with AZD8055.
#Algae #Phosphoproteomics 🔗⬇️

Fig. 6 | Working model for the role of the nutrient–TOR–CACG axis in balancing plant growth and stress tolerance. In the presence of adequate nutrients, TOR is active and promotes the translation of CACG mRNAs. The pyrimidine-rich motifs present in the 5′ UTRs of CACG mRNAs facilitate target selection by TOR. The CACG complex directly binds to numerous stress-responsive genes marked by histone acetylation, thereby repressing their transcription, which contributes to plant growth and development. Conversely, under nutrient-deficient conditions, TOR becomes inactive, leading to decreased translation of CACG mRNAs. This results in the alleviation of the repression of stress-response genes, causing reduced growth but increased stress tolerance. The nutrient–TOR–CACG axis is crucial for balancing plant growth with stress tolerance, promoting survival and reproductive success in variable environmental conditions. conditions. Image partially created in BioRender. He, X.

Fig. 1 | Identification of a multi-subunit protein complex involved in nutrient-responsive growth. a) Protein–protein interaction networks were generated from mass spectrometry data using Cytoscape. The edges show the interactions identified by AP–MS. CACG subunits are shown in pink, while COMPASS subunits and the INO80 complex (INO80-C) are shown in blue. b) Interactions among CACG subunits as determined by Y2H and pull-down assays. Interactions revealed by Y2H assays are shown in yellow, those shown by pull-down assays in red and those confirmed by both methods in orange. Protein names in bold denote those analysed through pull-down assays. c) Detection of a high-molecular-weight complex by gel filtration. Proteins extracted from Flag-tagged GTE1, DP1, EMB1967 and CP2 transgenic plants were separated in a Superose 6 column (10/300 GL; GE Healthcare Life Sciences) and were detected by immunoblotting. d) Immunoblot analysis of protein levels in the indicated Flag-tagged transgenic plants under different nutrient conditions. Twelve-day-old plants grown in solid MS medium were transferred to liquid MS, H2O or reduced concentrations of MS for 4 days. The actin protein level is shown as a loading control. e) Fresh weight of wild-type plants irrigated with water or liquid MS medium (n = 24). The values are means ± s.d. f) Immunoblot analysis of protein levels in the indicated Flag-tagged transgenic plants irrigated with water or liquid MS medium. The actin protein level is shown as a loading control. g) Morphological phenotypes of 20-day-old wild-type and mutant plants (top) and 12-day-old wild-type and mutant plants (bottom). Scale bars, 1 cm. The experiments in c, d and f were repeated independently twice and showed similar results.

Modified Fig. 4 | The CACG complex suppresses the expression of stress-responsive genes to coordinate plant growth and stress tolerance. g) Morphological phenotypes of wild-type plants and CACG mutants under control, drought stress and rehydration conditions. Twelve-day-old plants grown in solid MS medium were transferred to soil and subsequently subjected to drought treatment until the Col-0 plants began to show mortality. The phenotypes are shown before and three days after rehydration with MS. Plants watered with MS serve as the control. h) The survival rate of wild-type plants and CACG mutants under drought stress conditions (n = 24). Each bar shows the mean ± s.d. from three independent biological replicates. P values were determined using two-tailed Student’s t-tests. i) Immunoblot analysis of the protein levels of CACG components under the indicated conditions. TOR activity was monitored by the phosphorylation state of S6K. The actin protein level is shown as a loading control. The experiments were independently repeated twice and showed similar results. j) Statistical analysis of pS6K protein levels. Actin was used as a loading control. Each black dot represents an independent biological replicate.

Great work by Wang et al. (2025) on how #PlantTOR dynamically regulates the translation of a chromatin-associated complex for growth (CACG) in #Arabidopsis, which represses the expression of stress-responsive genes to coordinate plant growth and stress tolerance 🌱⚖️🏜️.
🔗 www.nature.com/articles/s41...

Figure 1. Target of rapamycin complex (TORC) activity is rapidly repressed by salt stress. A) Dose dependance of salt-mediated TOR repression. 35S:S6K1-HA seedlings were treated with different NaCl concentrations for 4 h. Band intensity in the immunoblots indicates the level of total protein (anti-HA in lower panel) or T449-phosphorylated form of S6K1 (anti-p-T449 in upper panel). B) Quantification of relative p-T449 intensity in A). The data represent the ratio of intensity of p-T449 over S6K1-HA, and the value for the sample “0 mM NaCl” was set as 1. C) Time course of salt-mediated TOR repression. 35S:S6K1-HA seedlings were treated with 200 mM NaCl for indicated times. D) Quantification of relative p-T449 intensity in C). The value at 0 min was set as 1. E) TORC activity was restored following salt recovery treatment. 35S:S6K1-HA seedlings were treated with 200 mM NaCl for 15 min, and then transferred to the recovery medium for indicated times. Rec, recovery. F) Quantification of relative p-T449 intensity in E). In B), D), and F), the data represent the ratio of intensity of p-T449 over S6K1-HA, data are means±SEM, n=3 (biologically independent experiments). Different letters in B) and D) represent significant difference between samples by one-way ANOVA (P<0.05, Supplementary Data Set 1). In F), *P<0.05 (one-way ANOVA, Supplementary Data Set 1)

Figure 6.The salt-tolerant phenotype shown in raptor1b mutant is abolished in the absence of SOS2/Calcineurin B-Like (CBL)-Interacting Protein Kinase 24 (CIPK24). A) Representative images of Col-0, cipk24, raptor1-2, and raptor1-2cipk24 mutant under normal or salt conditions in post-germination assays. Scale bar: 1 cm. B) Chlorophyll content per 4 seedlings measured at the end of the assay shown in A). Quantitative data are mean±SD of three biological repeats. Statistical analyses were performed by one-way ANOVA. (***P<0.001, ****P<0.0001, n.s., not significant). C) Working model for target of rapamycin complex (TORC), abscisic acid (ABA), and CBL–CIPK signaling pathways to orchestrate growth and salt stress response under changing salinity status. In response to salt stress, ABA pathway and CBL–CIPK pathway dominate, suppressing TORC by phosphorylating RAPTOR1B and slowing down the growth to facilitate stress adaptation. Upon the removal of salt stress, TORC rapidly activates to suppress the ABA- and CBL–CIPK-mediated salt stress response network and promotes plant growth.

Great work by Li et al. (2025) on identifying the regulatory loop between #PlantTOR complex (TORC) via its RAPTOR1B subunit (Ser897) and the CBL4/CBL10–CIPK24 module in #Arabidopsis, which regulates the balance between plant growth and #SaltStress response ⚖️.
#PlantScience

🔗 doi.org/10.1093/plce...

Great #preprint by Chen et al. (2025) on revealing the role of #SalicylicAcid (SA) in controlling central metabolic regulators #SnRK1 and #PlantTOR to coordinate plant immunity and growth by differential phosphorylation of #Arabidopsis NPR1, a key SA receptor (Ser-557 and Ser-55/59, respectively)🤯.

Great work by Mallén-Ponce et al. (2025) on how they identified #dihydroxyacetone phosphate (DHAP) as a key metabolite regulating the activation of #PlantTOR in the green alga #Chlamydomonas reinhardtii in response to #CO2 availability and light signals 🌅.
@ibvf-sevilla.bsky.social #PlantScience ⬇️

Target of Rapamycin (TOR): A Master Regulator in Plant Growth, Development, and Stress Responses | Annual Reviews The target of rapamycin (TOR) is a central regulator of growth, development, and stress adaptation in plants. This review delves into the molecular intricacies of TOR signaling, highlighting its conse...

📜 Target of Rapamycin (TOR): A Master Regulator in Plant Growth, Development, and Stress Responses

🧑‍🔬 Yanlin Liu, Jun Hu, Yan Xiong, et al.

📔 @annualreviews.bsky.social

🔗 www.annualreviews.org/content/jour...

#️⃣ #PlantScience #PlantDevelopment #PlantStress #PlantTOR

Figure 2. Representative TOR-specific chemical inhibitors in the green plant lineage. The structures of ATP and TOR-specific chemical inhibitors docking to plant TOR complexes were predicted by using AlphaFold 3. For more detail, please refer to Supplemental Table 2. Abbreviations: Ath, Arabidopsis thaliana; FKBP12, FK506-binding protein 12; FRB, FKBP-rapamycin binding; LST8, lethal with SEC13 protein 8; TOR, target of rapamycin.

Figure 3. Upstream signals and regulators of plant TOR signaling. The plant TORC integrates a variety of upstream signals to gate its own activity and function. Activation of TORC only occurs when glucose/energy, mineral nutrients, growth-related hormones, and favorable environmental conditions are all readily available. Conversely, low energy, nutrient scarcity, and stresses lead to TORC inhibition. Transporters depicted include AKT, Arabidopsis potassium (KC) transporter (65); AMT, ammonium (NH4 C) transporter (74); IRT, iron (Fe2C) transporter (24); NRT, nitrate (NO3 -) transporter (74); PHT, phosphate (PO4 3-) transporter (23); and SULTR, sulfate (SO4 2-) transporter (141). Positive regulators of TORC are depicted in orange; negative regulators are in light gray blue.

Figure 4. Downstream targets and molecular functions of plant TOR signaling. Plant TORC orchestrates a myriad of cellular, molecular, and metabolic changes to balance anabolic and catabolic programs by directly or indirectly regulating key components. (a–e, left) Summary of plant TORC downstream substrates, regulators, and their related molecular functions. (Right) Illustration of the central dogma in the plant cell. ( f ) Summary of plant TORC-regulated hormone signaling pathways. Positive regulators are depicted in light green; negative regulators are in light gray-blue. Phosphorylation regulation is depicted by the phosphate group shown in pink, and the biological processes are shown in light cyan. Solid lines with triangle arrows (positive) and with vertical bars (negative) represent confirmed signaling regulation. The dashed line indicates that this regulation needs further experimental validation.

Figure 5. Physiological roles of TOR signaling in plant growth, development, and stress adaptation. (a, i–vii) By integrating upstream signals and regulating multiple cellular processes, plant TOR signaling ultimately regulates every stage of an individual life cycle, from embryo development to senescence, and (b) participates in diverse stress adaptation and growth–defense trade-offs. The key upstream signals and regulators are shown. External and internal signals involved in TOR regulating plant growth, development, and stress adaptation processes are labeled in brown (activation signals) and blue (inhibition signals). Positive and negative regulators are labeled in orange and black, respectively. Black lines with triangle arrows (positive) and with vertical bars (negative) represent signaling regulation.

Very interesting review by Liu, Hu et al. (2025) on the signaling landscape of #PlantTOR pathway (i.e. upstream signals and downstream effectors) and the physiological roles of #PlantTOR signaling in plant growth, development, and stress responses 🌱. www.annualreviews.org/content/jour...

Figure 1. Combining different treatments and baits determines different components of the TORC interactome. A) Scheme illustrating PUP-IT in the context of TOR signaling. PafA fused to the baits LST8-1, RAPTOR1, and ScFKBP labels individual and TOR complex associated protein interactors, while a GFP fusion acts as a control for unspecific interactions. B–E) Volcano plots showing proteins significantly enriched in LST8-1 B,D) and RAPTOR1 C,E) baits using constitutive B,C) or inducible D,E) FLAG::PUP(E) expression. F–G) Treatment-dependency of identified interactors using LST8-1 G) or RAPTOR1 H) baits and inducible FLAG::PUP(E) expression. Treatment-specific interactors are those only identified in one of the two treatments. H) Rapamycin response of WT and ScFKBP-producing seedlings (n = 10 seedlings). Bar height indicates group median. I) Volcano plot showing proteins significantly enriched in the ScFKBP bait using constitutive FLAG::PUP(E) expression. In all volcano plots, fold changes are calculated from n = 3 replicates using MsqRob2, p-values are corrected for multiple comparisons using the Benjamini–Hochberg FDR method. Different letters in panel (H) indicate statistically significant differences between groups based on a one-way ANOVA followed by a Tukey-HSD test (𝛼 = 0.05).

Figure 2. Identification of phosphorylated direct interactors of the TOR complex and in silico corroboration using AlphaFold2. A,B) Phosphorylated proteins enriched in LST8-1 and RAPTOR1 against the GFP control after 4 h A) and 24 h B) of sucrose treatment and FLAG::PUP(E) induction. Phosphorylation sites previously associated with TOR are indicated in blue, new sites in proteins previously reported to be phosphorylated by TOR in turquoise. Fold changes are calculated from n = 3 replicates using MsqRob2, p-values are corrected for multiple comparisons using the Benjamini–Hochberg FDR method. C,D) The two significantly enriched motifs among the identified phosphorylation sites. The “SP” motif C) mirrors previous reports from TOR substrates, while the “RxxS” motif D) has previously been associated with TOR downstream interactor S6K1. E) Interactions of 20 proteins from the four shown groups with the TORC components TOR, LST8-1, and RAPTOR1 were predicted using AlphaFold2 multimer. Vertical lines indicate the median of the local interaction score (LIS) distribution by group. F) Predicted structures of the top-scoring interactions for each group: newly identified TORC interactor PANK2, TORC subunit RAPTOR1, senescence regulator S40-7, and KIN10 paralog KIN11. Models are colored by predicted local distance difference test (pLDDT), with values above 70 indicating high confidence predictions.

Great work by Zheng et al. (2025) on how employing pupylation-based proximity labeling (PUP-IT) unravels a comprehensive #interactome of #Arabidopsis TOR complex.
Newly identified #PlantTOR interactors, like PANK2, were also supported by #AlphaFold2.
advanced.onlinelibrary.wiley.com/doi/10.1002/...

Great work by Komiya, Pancha et al. (2025) on how #PlantTOR signaling regulates (floridean) starch degradation in extremophilic red microalga #Cyanidioschyzon merolae (rapamycin-sensitive SF12 strain), by modulating the phosphorylation status of α-glucan, water dikinase (CmGWD) at Ser264 residue.

Fig. 5. RAPTOR1B functions upstream of GIGANTEA (GI) to contribute to CONSTANS (CO) stability at dusk and thus promote the floral transition in Arabidopsis. (F) Proposed model for the role of RAPTOR during floral transition in long days (LD). The length of the light period is primarily sensed in leaves by the combined action of light signaling (mediated by PHYA and CRYs) and the circadian clock (driving gene expression of effector proteins, such GI and FKF1). This accounts for protein accumulation of CONSTANS at dusk, which in turn, upregulates the florigen, FT. FT protein travels from the leaves into the shoot apex via the vasculature to induce the expression of floral integrator genes (such SOC1) and flower promoting genes (such SPL3/4/5). GI, similar to CO, accumulates over the day and is degraded at night. Independent, or together with FKF1 in response to blue light-mediated by CRYs, GI helps to stabilize CONSTANS at dusk in LD. RAPTOR, which is part of the TORC, contributes to CO stability at dusk by promoting GI levels posttranscriptionally. TORC is known to be activated by light and sugars, suggesting that RAPTOR conveys nutrient status, in this case carbon availability, to regulate GI accumulation and thus fine-tune flowering via the photoperiod pathway. Remarkably, TOR is essential for sugar-mediated regulation of the circadian period, while GI integrates signals from the circadian clock, thus strengthening the potential crosstalk between these proteins.

Great work by Urrea-Castellanos et al. (2025) on how RAPTOR1B, a subunit of #PlantTOR complex (TORC), post-transcriptionally regulates CONSTANS (CO), a component of the #photoperiod pathway to promote flowering, via #circadian clock-associated protein GIGANTEA (GI) 🌻.
🔗 www.pnas.org/doi/10.1073/...

Figure 8. The interplay of glucose, auxin and TOR-E2Fa in mediating root growth repression by the defense hormone, salicylic acid (SA). A testable model for glucose and SA crosstalk. Glucose promotes root growth by stimulating auxin biosynthesis, signaling and transport. Both glucose and auxin activate TOR kinase, which, in turn, activate RPS6 and E2Fa, key players in cell cycle regulation. E2Fa binds to S-phase cell cycle gene promoters, upregulating their expression and promoting cell growth and proliferation. Conversely, SA appears to inhibit root growth by antagonizing auxin signaling and transport. Additionally, SA reduces the phosphorylation levels of both RPS6 and E2Fa, negatively impacting cell growth and proliferation processes, ultimately leading to root growth inhibition.

Great #preprint by Rawat and Laxmi (2025) on how salicylic acid (SA)-induced primary root growth inhibition in #Arabidopsis seedlings is regulated by the glucose-auxin-TOR-E2Fa module. #PlantTOR
🔗 www.biorxiv.org/content/10.1...

Figure 6. Cytochrome c (CYTc) deficiency affects TOR pathway activity, downstream of SnRK1. (A) Western blot analysis of RPS6 phosphorylation in WT plants, cytc-1a and akin10-2 single mutants, and cytc-1a akin10-2 double mutants using anti-P-RPS6 antibodies. Extracts were prepared from seedlings grown for 3.5 days in 0.59 MS medium, followed by an extended night (16 h) for nutrient depletion and treatment with 20 mM glucose for 3 h to activate TOR (Xiong et al., 2013). Anti-RPS6 antibodies were used as a control of total RPS6 levels. Anti-Actin antibodies were used for the control of loading. The original uncropped image is shown in Figure S8. On the right, a quantification of P-RPS6 and total RPS6 band intensities relative to WT plants after normalisation with actin is shown. Different letters indicate significant differences (three independent experiments; P < 0.05; ANOVA). (B) Hypocotyl growth in WT plants, cytc-1a and akin10-2 single mutants, and cytc-1a akin10-2 double mutants grown as in (A) and supplemented with different concentrations of selective TOR inhibitor AZD-8055. Hypocotyl length was measured using ImageJ software. Asterisks indicate significant differences with WT (n = 20; P < 0.05; ANOVA). (C) Representative images of the experiment shown in (B). Bar: 0.5 cm.

Figure 6D. Model of the connection between cytochrome c (CYTc) levels and plant growth and stress responses. Under normal conditions (left), CYTc, probably acting as an OXPHOS component, exerts repression on SnRK1 activity, thus allowing TOR activation and plant growth. A decrease in CYTc levels (right) derepresses SnRK1, leading to growth inhibition and the activation of autophagy and stress responses. Since stress conditions affect mitochondrial function, it can be envisaged that CYTc dependent processes are part of a signal that influences the balance between growth and stress responses through SnRK1.

Great work by Coronel et al. (2024) on how altering cytochrome c (CYTc) levels affected #SnRK1 activity in #Arabidopsis 🌱, indicating a molecular link between #mitochondrial function and #PlantTOR -mediated growth under normal and mannitol stress conditions.
🔗 onlinelibrary.wiley.com/doi/10.1111/...

Figure 7. Target of Rapamycin (TOR) kinase is a positive regulator of plant fatty acid and lipid synthesis. Plant TOR is activated by light and sugars. Once activated, TOR positively regulates fatty acid (FA) and lipid synthesis by upregulating genes involved in de novo fatty acid synthesis and downregulating genes associated with lipid turnover. Additionally, TOR promotes the biosynthesis of proteins, cell walls, DNA, RNA, and the other essential cellular components. TOR complex shown in the figure is comprising of LST8-1 (Lethal with SEC13 protein 8-1, in green), TOR (in purple) and RAPTOR1B (Regulatory-associated protein of TOR 1B, in yellow) and its 3D structure model is predicated by AlphaFold 3.

Figure 1. Transient expression of TOR in Nicotiana benthamiana (N. benth) leaves increases the levels of total fatty acids (TFAs). A) Representative fluorescence confocal image of N. benth leaf samples taken 4 days after agroinfiltration with TOR-GFP. Bar = 50 µm. B) Immunoblotting with anti-GFP antibody shows TOR-GFP is detected in protein samples extracted from N. benth leaves 4 days after infiltration with agrobacterium containing plasmid TOR/pCHF3-hGFP (TOR-GFP), but not pCHF3-hGFP (Empty vector, EV). Ponceau S staining of PVDF membrane after protein transfer is shown as a protein loading control. M, protein markers. Multiple lanes for the same construct represent biological replicates. C) Transient expression of TOR for 4 days after agroinfiltration significantly elevates total fatty acids content in N. benth leaves after. Bar values represent mean ± SD (n = 6), with each data point represented by a dot. Asterisks denote a statistically difference from the EV (Student's t-test, **, P < 0.01).

Figure 5. Suppression of TOR activity by Torin 2 in a Brassica napus suspension cell culture results in significant reduction in the accumulation of both total fatty acid (TFA) and triacylglycerol (TAG). A) TFA content in Brassica napus microspore-derived suspension cells cultured in medium supplemented without (−) or with (+) 1 μM Torin 2 for the indicated time periods. B) TAG content in the Brassica napus suspension cells in (A). In this figure, bar values represent mean ± SD (n = 4), with each data point represented by a dot. Asterisks denote statistically significant differences from the non-Torin 2 treatment controls (Student’s t-test, *, P < 0.05; ***, P < 0.001).

Great work by Liu et al. (2024) on how #PlantTOR kinase positively regulates plant #FattyAcid and lipid synthesis in #Nicotiana benthamiana leaves 🍃, #Arabidopsis seedlings 🌱 and #Brassica napus suspension cells.
PS. Relatively short periods were used for the assays.
academic.oup.com/plphys/advan...