Nutrient-driven TOR signalling controls a chromatin-associated complex for orchestrating plant growth and stress tolerance.
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ABSTRACT:
ORGANISM(S): Arabidopsis thaliana
PROVIDER: GSE276448 | GEO | 2025/08/11
REPOSITORIES: GEO
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Project description:Nutrient-driven TOR signalling controls a chromatin-associated complex for orchestrating plant growth and stress tolerance.
| PRJNA1157385 | ENA
Project description:Nutrients and energy have emerged as central modulators of developmental programmes in plants and animals1-3. The evolutionarily conserved target of rapamycin (TOR) kinase is a master integrator of nutrient and energy signalling that controls growth. Despite its key regulatory roles in translation, proliferation, metabolism and autophagy2-5, little is known about how TOR shapes developmental transitions and differentiation. Here we show that glucose-activated TOR kinase controls genome-wide histone H3 trimethylation at K27 (H3K27me3) in Arabidopsis thaliana, which regulates cell fate and development6-10. We identify FERTILIZATION-INDEPENDENT ENDOSPERM (FIE), an indispensable component of Polycomb repressive complex 2 (PRC2), which catalyses H3K27me3 (refs. 6-8,10-12), as a TOR target. Direct phosphorylation by TOR promotes the dynamic translocation of FIE from the cytoplasm to the nucleus. Mutation of the phosphorylation site on FIE abrogates the global H3K27me3 landscape, reprogrammes the transcriptome and disrupts organogenesis in plants. Moreover, glucose-TOR-FIE-PRC2 signalling modulates vernalization-induced floral transition. We propose that this signalling axis serves as a nutritional checkpoint leading to epigenetic silencing of key transcription factor genes that specify stem cell destiny in shoot and root meristems and control leaf, flower and silique patterning, branching and vegetative-to-reproduction transition. Our findings reveal a fundamental mechanism of nutrient signalling in direct epigenome reprogramming, with broad relevance for the developmental control of multicellular organisms.
| S-EPMC9530021 | biostudies-literature
Project description:The target of rapamycin (TOR) kinase is a central signaling hub that plays a crucial role in precisely orchestrating plant growth, development, and stress responses. This suggests that TOR is intricately involved in maintaining the balance between plant growth and stress responses. Nevertheless, despite the observed effects, the specific mechanisms through which TOR operates in these processes remain obscure. In this study, we investigated how the tomato (Solanum lycopersicum) TOR (SlTOR) affects plant growth and cold responses. We demonstrated that SlTOR inhibition transcriptionally primes cold stress responses, consequently enhancing tomato cold tolerance. A widely targeted metabolomics analysis revealed the disruption of amino acid metabolism homeostasis under cold stress upon SlTOR inhibition, which led to the accumulation of two important cryoprotective metabolites: salicylic acid (SA) and putrescine (Put). Next, we discovered SlPGH1 (2-PHOSPHO-D-GLYCERATE HYDRO-LYASE 1) as a direct substrate of SlTOR. Inhibiting SlTOR led to increased SlCBF1 (C-REPEAT-BINDING FACTOR 1) expression via SlPGH1, potentially triggering the activation of cold-responsive genes and subsequent metabolic alterations. Our study provides a mechanistic framework that elucidates how SlTOR modulates amino acid-related metabolism to enhance tomato cold tolerance, which sheds light on the complex interplay between growth and stress responses orchestrated by TOR.
| S-EPMC11630258 | biostudies-literature
Project description:The target of rapamycin (TOR) kinase is a central signaling hub that plays a crucial role in precisely orchestrating plant growth and development. It is increasingly evident that TOR also has a significant impact on plant stress responses. This suggests that TOR is intricately involved in maintaining the balance between plant growth and stress responses. Nevertheless, despite the observed effects, the specific mechanisms through which TOR operates in these processes remain obscure. In this study, we investigated how the tomato (Solanum lycopersicum) TOR (SlTOR) affects plant growth and cold responses. We demonstrated that the inhibition of SlTOR transcriptionally primes cold stress responses, consequently enhancing tomato cold tolerance. Furthermore, a widely targeted metabolomics analysis revealed the disruption of amino acid metabolism homeostasis under cold stress upon SlTOR inhibition. This disruption led to the accumulation of two important defense metabolites: salicylic acid (SA) and putrescine (Put). Subsequent gain- and loss-of-function analyses validated the crucial roles of salicylic acid and putrescine in enhancing tomato cold tolerance. Our study provides a mechanistic framework that elucidates how SlTOR modulates amino acid-related metabolism to enhance tomato cold tolerance, which sheds light on the complex interplay between growth and stress responses orchestrated by TOR.
2024-12-19 | GSE266850 | GEO
Project description:As is well known, nutrition is essential for plant growth and development. Extensive research has demonstrated that the target of rapamycin (TOR) is a crucial growth regulator, receiving nutritional inputs in eukaryotic cells. Nevertheless, the precise mechanisms by which TOR coordinates nutrient conditions and growth remain elusive in plants. In this study, we identified a novel transcriptional repression complex, TRCG, downstream of the TOR signaling pathway. This complex is responsible for regulating plant growth and the nutritional response. In the presence of favorable nutritional conditions, TOR is activated, leading to the translation of the 5’-terminal oligopyrimidine (5’-TOP) mRNA of TRCG. TRCG directly binds numerous nutrition-responsive genes, particularly those belonging to the ERF family of transcription factors, to repress their transcription. This repression is achieved by influencing the initiation and elongation of RNA polymerase II (Pol II), thereby maintaining growth and development. In the absence of nutritional conditions, TOR activity is inhibited, resulting in the repression of TRCG translation. This, in turn, relieves the repression of nutrient response genes, causing a stagnation of growth and poor nutrient resistance, thus contributing to the survival of the plant. Moreover, we observed a higher histone H3 and H4K5 acetylation level in the TRCG targets. Acetylated chromatin has long been associated with transcriptional activation, suggesting that TRCG could bind to acetylated chromatin to repress transcriptional activation. Our findings elucidate a previously unidentified precise mechanism by which TOR-mediated transcriptional repression occurs through the stimulation of translation, thereby regulating plant growth and the nutritional response.
2025-08-11 | GSE276446 | GEO
Project description:As is well known, nutrition is essential for plant growth and development. Extensive research has demonstrated that the target of rapamycin (TOR) is a crucial growth regulator, receiving nutritional inputs in eukaryotic cells. Nevertheless, the precise mechanisms by which TOR coordinates nutrient conditions and growth remain elusive in plants. In this study, we identified a novel transcriptional repression complex, TRCG, downstream of the TOR signaling pathway. This complex is responsible for regulating plant growth and the nutritional response. In the presence of favorable nutritional conditions, TOR is activated, leading to the translation of the 5’-terminal oligopyrimidine (5’-TOP) mRNA of TRCG. TRCG directly binds numerous nutrition-responsive genes, particularly those belonging to the ERF family of transcription factors, to repress their transcription. This repression is achieved by influencing the initiation and elongation of RNA polymerase II (Pol II), thereby maintaining growth and development. In the absence of nutritional conditions, TOR activity is inhibited, resulting in the repression of TRCG translation. This, in turn, relieves the repression of nutrient response genes, causing a stagnation of growth and poor nutrient resistance, thus contributing to the survival of the plant. Moreover, we observed a higher histone H3 and H4K5 acetylation level in the TRCG targets. Acetylated chromatin has long been associated with transcriptional activation, suggesting that TRCG could bind to acetylated chromatin to repress transcriptional activation. Our findings elucidate a previously unidentified precise mechanism by which TOR-mediated transcriptional repression occurs through the stimulation of translation, thereby regulating plant growth and the nutritional response.
2025-08-11 | GSE276444 | GEO
Project description:The nutrient/target-of-rapamycin (TOR) pathway has emerged as a key regulator of tissue and organismal growth in metazoans. The signalling components of the nutrient/TOR pathway are well defined; however, the downstream effectors are less understood. Here, we show that the control of RNA polymerase (Pol) III-dependent transcription is an essential target of TOR in Drosophila. We find that TOR activity controls Pol III in growing larvae via inhibition of the repressor Maf1 and, in part, via the transcription factor Drosophila Myc (dMyc). Moreover, we show that loss of the Pol III factor, Brf, leads to reduced tissue and organismal growth and prevents TOR-induced cellular growth. TOR activity in the larval fat body, a tissue equivalent to vertebrate fat or liver, couples nutrition to insulin release from the brain. Accordingly, we find that fat-specific loss of Brf phenocopies nutrient limitation and TOR inhibition, leading to decreased systemic insulin signalling and reduced organismal growth. Thus, stimulation of Pol III is a key downstream effector of TOR in the control of cellular and systemic growth.
| S-EPMC3343326 | biostudies-literature
Project description:The multidomain target of rapamycin (TOR) is an atypical serine/threonine protein kinase resembling phosphatidylinositol lipid kinases, but retains high sequence identity and serves a remarkably conserved role as a master signalling integrator in yeasts, plants, and humans. TOR dynamically orchestrates cell metabolism, biogenesis, organ growth, and development transitions in response to nutrient, energy, hormone, and environmental cues. Here we review recent findings on the versatile and complex roles of TOR in transcriptome reprogramming, seedling, root, and shoot growth, and root hair production activated by sugar and energy signalling. We explore how co-ordination of TOR-mediated light and hormone signalling is involved in root and shoot apical meristem activation, proliferation of leaf primordia, cotyledon/leaf greening, and hypocotyl elongation. We also discuss the emerging TOR functions in response to sulfur assimilation and metabolism and consider potential molecular links and positive feedback loops between TOR, sugar, energy, and other essential macronutrients.
| S-EPMC6463029 | biostudies-literature
Project description:TOR balances plant growth and cold tolerance by orchestrating amino acid-derived metabolism in tomato
| PRJNA1108424 | ENA
Project description:Autophagy is a bulk proteolytic process that is indispensable for cell survival during starvation. Autophagy is induced by nutrient deprivation via inactivation of the rapamycin-sensitive Tor complex1 (TORC1), a protein kinase complex regulating cell growth in response to nutrient conditions. However, the mechanism by which TORC1 controls autophagy and the direct target of TORC1 activity remain unclear. Atg13 is an essential regulatory component of autophagy upstream of the Atg1 kinase complex, and here we show that yeast TORC1 directly phosphorylates Atg13 at multiple Ser residues. Additionally, expression of an unphosphorylatable Atg13 mutant bypasses the TORC1 pathway to induce autophagy through activation of Atg1 in cells growing under nutrient-rich conditions. Our findings suggest that the direct control of the Atg1 complex by TORC1 induces autophagy.
| S-EPMC2815578 | biostudies-literature