Nutrient-driven TOR signaling mediates transcriptional repression by promoting translation to regulate plant growth [RNA-seq]
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ABSTRACT:
PROVIDER: PRJNA1157390 | ENA |
REPOSITORIES: ENA
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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:Nutrient-driven TOR signaling mediates transcriptional repression by promoting translation to regulate plant growth
| PRJNA1157385 | ENA
Project description:Nutrient-driven TOR signaling mediates transcriptional repression by promoting translation to regulate plant growth [ChIP-seq]
| PRJNA1157391 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below.
2025-08-11 | GSE276448 | GEO
Project description:Upon illumination, etiolated seedlings experience a transition from heterotrophic to photoautotrophic growth. During this process, the tetrapyrrole biosynthesis pathway provides chlorophyll for photosynthesis. This pathway has to be tightly controlled to prevent the accumulation of photoreactive metabolites and to provide stoichiometric amounts of chlorophyll for its incorporation into photosynthetic protein complexes. Therefore, plants have evolved regulatory mechanisms to synchronize the biosynthesis of chlorophyll and chlorophyll-binding proteins. Two phytochrome-interacting factors (PIF1 and PIF3) and the DELLA proteins, which are controlled by the gibberellin pathway, are key regulators of this process. Here, we show that impairment of TARGET OF RAPAMYCIN (TOR) activity in Arabidopsis (Arabidopsis thaliana), either by mutation of the TOR complex component RAPTOR1B or by treatment with TOR inhibitors, leads to a significantly reduced accumulation of the photoreactive chlorophyll precursor protochlorophyllide in darkness but an increased greening rate of etiolated seedlings after exposure to light. Detailed profiling of metabolic, transcriptomic, and physiological parameters revealed that the TOR-repressed lines not only grow slower, they grow in a nutrient-saving mode, which allows them to resist longer periods of low nutrient availability. Our results also indicated that RAPTOR1B acts upstream of the gibberellin-DELLA pathway and its mutation complements the repressed greening phenotype of pif1 and pif3 after etiolation.
2018-07-17 | GSE114639 | GEO
Project description:TARGET OF RAPAMYCIN (TOR) is a deeply conserved protein kinase that coordinates eukaryotic metabolism with nutrient availability. In mammals, TOR specifically promotes translation of ribosomal protein mRNAs when amino acids are available to support protein synthesis. The mechanisms controlling translation downstream from TOR remain contested, however, and are largely unexplored in plants. Here, we took parallel global profiling approaches to define the in planta TOR-regulated proteome, and phosphoproteome. We found that TOR regulates ribosome biogenesis in plants at multiple levels. To investigate this further, we focused on a putative TOR substrate identified in our phosphoproteome: LARP1, a eukaryotic RNA-binding protein that is proposed to mediate TOR translational control of 5′TOP mRNAs in humans.
2021-01-05 | PXD019942 | Pride
Project description:TARGET OF RAPAMYCIN (TOR) is a deeply conserved protein kinase that coordinates eukaryotic metabolism with nutrient availability. In mammals, TOR specifically promotes translation of ribosomal protein mRNAs when amino acids are available to support protein synthesis. The mechanisms controlling translation downstream from TOR remain contested, however, and are largely unexplored in plants. Here, we took parallel global profiling approaches to define the in planta TOR-regulated proteome, and phosphoproteome. We found that TOR regulates ribosome biogenesis in plants at multiple levels. To investigate this further, we focused on a putative TOR substrate identified in our phosphoproteome: LARP1, a eukaryotic RNA-binding protein that is proposed to mediate TOR translational control of 5′TOP mRNAs in humans.
2021-01-05 | PXD019904 | Pride
Project description:Rapamycin-sensitive transgenic Arabidopsis lines (BP12) expressing yeast FK506 Binding Protein12 (FKBP12) were developed. Inhibition of TOR in BP12 plants by rapamycin resulted in slower overall root, leaf and shoot growth and development leading to poor nutrient uptake and light energy utilization. Genetic and physiological studies together with RNA-Seq and metabolite analysis of TOR-suppressed lines revealed that TOR regulates development and lifespan in Arabidopsis by restructuring cell growth, carbon and nitrogen metabolism, gene expression, ribosomal RNA and protein synthesis.
2012-12-18 | GSE42968 | GEO