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Abstract Background When subject to stress conditions such as nutrient limitation microalgae accumulate triacylglycerol (TAG). Fatty acid, a substrate for TAG synthesis is derived from de novo synthesis or by membrane remodeling. The model industrial alga Chlorella sorokiniana accumulates TAG and other storage compounds under nitrogen (N)-limited growth. Molecular mechanisms underlying these processes are still to be elucidated. Result Previously we used transcriptomics to explore the regulation of TAG synthesis in C. sorokiniana. Surprisingly, our analysis showed that the expression of several key genes encoding enzymes involved in plastidic fatty acid synthesis are significantly repressed. Metabolic labeling with radiolabeled acetate showed that de novo fatty acid synthesis is indeed downregulated under N-limitation. Likewise, inhibition of the Target of Rapamycin kinase (TOR), a key regulator of metabolism and growth, decreased fatty acid synthesis. We compared the changes in proteins and phosphoprotein abundance using a proteomics and phosphoproteomics approach in C. sorokiniana cells under N-limitation or TOR inhibition and found extensive overlap between the N-limited and TOR-inhibited conditions. We also identified changes in the phosphorylation status of TOR complex proteins, TOR-kinase, and RAPTOR, under N-limitation. This indicates that TOR signaling is altered in a nitrogen-dependent manner. We find that TOR-mediated metabolic remodeling of fatty acid synthesis under N-limitation is conserved in the chlorophyte algae Chlorella sorokiniana and Chlamydomonas reinhardtii. Conclusion Our results indicate that under N-limitation there is significant metabolic remodeling, including fatty acid synthesis, mediated by TOR signaling. This process is conserved across chlorophyte algae. Using proteomic and phosphoproteomic analysis, we show that N-limitation affects TOR signaling and this in-turn affects the metabolic status of the cells. This study presents a link between N-limitation, TOR signaling and fatty acid synthesis in green-lineage.

SUMMARY: The target of rapamycin (TOR) kinase serves as a central regulator that integrates nutrient and energy signals to orchestrate cellular and organismal physiology in both animals and plants. Despite significant advancements having been made in understanding the molecular and cellular functions of plant TOR kinases, the upstream regulators that modulate TOR activity are not yet fully elucidated. In animals, the translationally controlled tumor protein (TCTP) is recognized as a key player in TOR signaling. This study reveals that two TCTP isoforms from Cucumis sativus, when introduced into Arabidopsis, are instrumental in balancing growth and defense mechanisms against the fungal pathogen Golovinomyces cichoracearum. We hypothesize that plant TCTPs act as upstream regulators of TOR in response to powdery mildew caused by Podosphaera xanthii in Cucumis. Our research further uncovers a stable interaction between CsTCTP and a small GTPase, CsRab11A. Transient transformation assays indicate that CsRab11A is involved in the defense against P. xanthii and promotes the activation of TOR signaling through CsTCTP. Moreover, our findings demonstrate that the critical role of TOR in plant disease resistance is contingent upon its regulated activity; pretreatment with a TOR inhibitor (AZD‐8055) enhances cucumber plant resistance to P. xanthii, while pretreatment with a TOR activator (MHY‐1485) increases susceptibility. These results suggest a sophisticated adaptive response mechanism in which upstream regulators, CsTCTP and CsRab11A, coordinate to modulate TOR function in response to P. xanthii, highlighting a novel aspect of plant–pathogen interactions. Significance Statement: Target of rapamycin (TOR) signaling pathway serves as a central integrator of diverse nutrient, energy, hormone, and environmental signals, playing a pivotal role in the precise regulation of cellular and organismal physiology. In this study, we reveal a novel mechanism involving the TCTP‐Rab11A module, which significantly contributes to plant stress responses by positively regulating the TOR signaling pathway. This discovery not only enhances our understanding of the complex regulatory networks in plants but also provides potential targets for improving plant resistance to biotic and abiotic stresses. [ABSTRACT FROM AUTHOR]

mTORC1 senses nutrients and growth factors and phosphorylates downstream targets, including the transcription factor TFEB, to coordinate metabolic supply and demand. These functions position mTORC1 as a central controller of cellular homeostasis, but the behavior of this system in individual cells has not been well characterized. Here, we provide measurements necessary to refine quantitative models for mTORC1 as a metabolic controller. We developed a series of fluorescent protein-TFEB fusions and a multiplexed immunofluorescence approach to investigate how combinations of stimuli jointly regulate mTORC1 signaling at the single-cell level. Live imaging of individual MCF10A cells confirmed that mTORC1-TFEB signaling responds continuously to individual, sequential, or simultaneous treatment with amino acids and the growth factor insulin. Under physiologically relevant concentrations of amino acids, we observe correlated fluctuations in TFEB, AMPK, and AKT signaling that indicate continuous activity adjustments to nutrient availability. Using partial least squares regression modeling, we show that these continuous gradations are connected to protein synthesis rate via a distributed network of mTORC1 effectors, providing quantitative support for the qualitative model of mTORC1 as a homeostatic controller and clarifying its functional behavior within individual cells.

Summary: Mitochondrial function is essential for plant growth, but the mechanisms involved in adjusting growth and metabolism to changes in mitochondrial energy production are not fully understood.We studied plants with reduced expression of CYTC‐1, one of two genes encoding the respiratory chain component cytochrome c (CYTc) in Arabidopsis, to understand how mitochondria communicate their status to coordinate metabolism and growth.Plants with CYTc deficiency show decreased mitochondrial membrane potential and lower ATP content, even when carbon sources are present. They also exhibit higher free amino acid content, induced autophagy, and increased resistance to nutritional stress caused by prolonged darkness, similar to plants with triggered starvation signals. CYTc deficiency affects target of rapamycin (TOR)‐pathway activation, reducing S6 kinase (S6K) and RPS6A phosphorylation, as well as total S6K protein levels due to increased protein degradation via proteasome and autophagy. TOR overexpression restores growth and other parameters affected in cytc‐1 mutants, even if mitochondrial membrane potential and ATP levels remain low.We propose that CYTc‐deficient plants coordinate their metabolism and energy availability by reducing TOR‐pathway activation as a preventive signal to adjust growth in anticipation of energy exhaustion, thus providing a mechanism by which changes in mitochondrial activity are transduced to the rest of the cell. [ABSTRACT FROM AUTHOR]

Certain proteins assemble into diverse complex states, each having a distinct and unique function in the cell. Target of rapamycin (Tor) complex 1 (TORC1) plays a central role in signalling pathways that allow cells to respond to the environment, including nutritional status signalling. TORC1 is widely recognised for its association with various diseases. The budding yeast Saccharomyces cerevisiae has two types of TORC1, Tor1-containing TORC1 and Tor2-containing TORC1, which comprise different constituent proteins but are considered to have the same function. Here, we computationally modelled the relevant complex structures and then, based on the structures, rationally engineered a Tor2 mutant that could form Tor complex 2 (TORC2) but not TORC1, resulting in a redesign of the complex states. Functional analysis of the Tor2 mutant revealed that the two types of TORC1 induce different phenotypes, with changes observed in rapamycin, caffeine and pH dependencies of cell growth, as well as in replicative and chronological lifespan. These findings uncovered by a general approach with huge potential - model structure-based engineering - are expected to provide further insights into various fields such as molecular evolution and lifespan. [ABSTRACT FROM AUTHOR]

Rice production accounts for approximately half of the freshwater resources utilized in agriculture, resulting in greenhouse gas emissions such as methane (CH 4) from flooded paddy fields. To address this challenge, environmentally friendly and cost-effective water-saving techniques have become widely adopted in rice cultivation. However, the implementation of water-saving treatments (WSTs) in paddy-field rice has been associated with a substantial yield loss of up to 50% as well as a reduction in nitrogen use efficiency (NUE). In this study, we discovered that the target of rapamycin (TOR) signaling pathway is compromised in rice under WST. Polysome profiling-coupled transcriptome sequencing (polysome-seq) analysis unveiled a substantial reduction in global translation in response to WST associated with the downregulation of TOR activity. Molecular, biochemical, and genetic analyses revealed new insights into the impact of the positive TOR-S6K-RPS6 and negative TOR-MAF1 modules on translation repression under WST. Intriguingly, ammonium exhibited a greater ability to alleviate growth constraints under WST by enhancing TOR signaling, which simultaneously promoted uptake and utilization of ammonium and nitrogen allocation. We further demonstrated that TOR modulates the ammonium transporter AMT1;1 as well as the amino acid permease APP1 and dipeptide transporter NPF7.3 at the translational level through the 5′ untranslated region. Collectively, these findings reveal that enhancing TOR signaling could mitigate rice yield penalty due to WST by regulating the processes involved in protein synthesis and NUE. Our study will contribute to the breeding of new rice varieties with increased water and fertilizer utilization efficiency. Water-saving techniques can reduce freshwater consumption and greenhouse gas emissions but lead to yield penalty. This study discovered that water-saving treatment inhibits TOR activity and affects protein translation and the expression ofgenes responsible for NH 4 + absorption and nitrogen allocation efficiency. Interestingly, overexpression of TOR in rice could mitigate these impacts through translational regulatory mechanisms under limited water conditions. [ABSTRACT FROM AUTHOR]

The TOR (Target of Rapamycin) signaling pathway, which takes TOR kinase as the core, regulates the absorption, distribution, and recycling of nutrients by integrating metabolic network and other signaling pathways, thus participating in the plant growth-defense trade-off. While terpenoids play an important role in plant growth, development, stress response, and signal transduction. The effect of the TOR signaling pathway on terpenoid biosynthesis in plants has yet to be studied in detail. In this study, the tissue culture seedlings of Salvia miltiorrhiza were treated with the TOR inhibitor AZD8055. The results show that the roots of the control group had begun to grow on the 8th day, while the seedlings treated with AZD8055 had no rooting signs. Combined with the expression changes of genes related to the TOR signaling pathway in the first 8 days, samples on the 3rd, 6th, and 8th days were selected for RNA-Seq analysis. Through RNA-Seq analysis, a total of 50,689 unigenes were obtained from the samples of these three periods, of which 4088 unigenes showed differential expression. The function enrichment and time-series analysis of differentially expressed genes (DEGs) showed that the main influence of the TOR signal pathway on plant growth-related processes was gradually transmitted with treatment time after TOR was inhibited. Pathway enrichment analysis of DEGs showed that the genes in the biosynthesis of terpenoids, such as diterpenoid and carotenoid biosynthetic pathways, could be regulated. Compared with other stages, DEGs related to terpenoid biosynthesis were mainly regulated in the S2 stage. In addition, the genes involved in terpenoid skeleton biosynthesis was also considerably enriched in the S2 stage, according to the results of gene set enrichment analysis (GSEA) of unigenes. Inhibition of the TOR signaling pathway may affect the biosynthesis of terpenoid signaling molecules, inhibit gibberellin’s biosynthesis, and promote abscisic acid’s biosynthesis. This study has discussed the effect of interfering with the TOR pathway on terpenoid biosynthesis in S. miltiorrhiza from the perspective of omics and provides new insight into the interaction between the terpenoid biosynthesis pathway and the growth-defense trade-off of medicinal plants.

To ensure survival and promote growth, sessile plants have developed intricate internal signaling networks tailored in diverse cells and organs with both shared and specialized functions that respond to various internal and external cues. A fascinating question arises: how can a plant cell or organ diagnose the spatial and temporal information it is experiencing to know "where I am," and then is able to make the accurate specific responses to decide "where to go" and "how to go," despite the absence of neuronal systems found in mammals. Drawing inspiration from recent comprehensive investigations into diverse nutrient signaling pathways in plants, this review focuses on the interactive nutrient signaling networks mediated by various nutrient sensors and transducers. We assess and illustrate examples of how cells and organs exhibit specific responses to changing spatial and temporal information within these interactive plant nutrient networks. In addition, we elucidate the underlying mechanisms by which plants employ posttranslational modification codes to integrate different upstream nutrient signals, thereby conferring response specificities to the signaling hub proteins. Furthermore, we discuss recent breakthrough studies that demonstrate the potential of modulating nutrient sensing and signaling as promising strategies to enhance crop yield, even with reduced fertilizer application. Plants have intricate signaling networks that respond to internal and external cues. This review focuses on nutrient signaling pathways mediated by sensors and transducers, and analyze recent studies about how cells and organs respond to spatial and temporal information within these networks. Furthermore, the authors discuss the integration of nutrient signals through posttranslational modifications and the potential of modulating nutrient sensing to enhance crop yield. [ABSTRACT FROM AUTHOR]

The molecular mechanisms that drive circadian (24 h) rhythmicity have been investigated for many decades, but we still do not have a complete picture of eukaryotic circadian systems. Although the transcription/translation feedback loop (TTFL) model has been the primary focus of research, there are many examples of circadian rhythms that persist when TTFLs are not functioning, and we lack any good candidates for the non-TTFL oscillators driving these rhythms. In this hypothesis-driven review, the author brings together several lines of evidence pointing towards the Target of Rapamycin (TOR) signalling pathway as a good candidate for a non-TTFL oscillator. TOR is a ubiquitous regulator of metabolism in eukaryotes and recent focus in circadian research on connections between metabolism and rhythms makes TOR an attractive candidate oscillator. In this paper, the evidence for a role for TOR in regulating rhythmicity is reviewed, and the advantages of TOR as a potential oscillator are discussed. Evidence for extensive feedback regulation of TOR provides potential mechanisms for a TOR-driven oscillator. Comparison with ultradian yeast metabolic cycles provides an example of a potential TOR-driven self-sustained oscillation. Unanswered questions and problems to be addressed by future research are discussed. [ABSTRACT FROM AUTHOR]

TOR proteins, also known as targets of rapamycin, are serine/threonine kinases involved in various signaling pathways that regulate cell growth. The protozoan parasite Giardia lamblia is the causative agent of giardiasis, a neglected infectious disease in humans. In this study, we used a bioinformatics approach to examine the structural features of GTOR, a G. lamblia TOR-like protein, and predict functional associations. Our findings confirmed that it shares significant similarities with functional TOR kinases, including a binding domain for the FKBP-rapamycin complex and a kinase domain resembling that of phosphatidylinositol 3-kinase-related kinases. In addition, it can form multiprotein complexes such as TORC1 and TORC2. These results provide valuable insights into the structure–function relationship of GTOR, highlighting its potential as a molecular target for controlling G. lamblia cell proliferation. Furthermore, our study represents a step toward rational drug design for specific anti-giardiasis therapeutic agents. [ABSTRACT FROM AUTHOR]

Target of rapamycin complex 1 (TORC1), a serine/threonine-protein kinase complex highly conserved among eukaryotes, coordinates cellular growth and metabolism with environmental cues, including nutrients and growth factors. Aberrant TORC1 signaling is associated with cancers and various human diseases, and TORC1 also plays a key role in ageing and lifespan, urging current active research on the mechanisms of TORC1 regulation in a variety of model organisms. Identification and characterization of the RAG small GTPases as well as their regulators, many of which are highly conserved from yeast to humans, led to a series of breakthroughs in understanding the molecular bases of TORC1 regulation. Recruitment of mammalian TORC1 (mTORC1) by RAGs to lysosomal membranes is a key step for mTORC1 activation. Interestingly, the RAG GTPases in fission yeast are primarily responsible for attenuation of TORC1 activity on vacuoles, the yeast equivalent of lysosomes. In this review, we summarize our current knowledge about the functions of TORC1 regulators on yeast vacuoles, and illustrate the conserved and divergent mechanisms of TORC1 regulation between yeasts and mammals.

The coordinated redistribution of sugars from mature "source" leaves to developing "sink" leaves requires tight regulation of sugar transport between cells via plasmodesmata (PD). Although fundamental to plant physiology, the mechanisms that control PD transport and thereby support development of new leaves have remained elusive. From a forward genetic screen for altered PD transport, we discovered that the conserved eukaryotic glucose-TOR (TARGET OF RAPAMYCIN) metabolic signaling network restricts PD transport in leaves. Genetic approaches and chemical or physiological treatments to either promote or disrupt TOR activity demonstrate that glucose-activated TOR decreases PD transport in leaves. We further found that TOR is significantly more active in mature leaves photosynthesizing excess sugars than in young, growing leaves, and that this increase in TOR activity correlates with decreased rates of PD transport. We conclude that leaf cells regulate PD trafficking in response to changing carbohydrate availability monitored by the TOR pathway.

Tomato fruit ripening is a unique process of nutritional and energy metabolism. Target of rapamycin (TOR), a conserved serine/threonine protein kinase in eukaryotes, controls cell growth and metabolism by integrating nutrient, energy, and hormone signals. However, it remains unclear whether TOR participates in the modulation of tomato fruit ripening. Here, we showed that the manipulation of SlTOR by chemical or genetic methods greatly alters the process of tomato fruit maturation. Expression pattern analysis revealed that the transcripts of SlTOR declined as fruit ripening progressed. Moreover, suppression of SlTOR by TOR inhibitor AZD8055 or knock down of its transcripts by inducible RNA interference, accelerated fruit ripening, and led to overall effects on fruit maturity, including changes in colour and metabolism, fruit softening, and expression of ripening-related genes. Genome-wide transcription analysis indicated that silencing SlTOR reprogrammed the transcript profile associated with ripening, including cell wall and phytohormone pathways, elevated the expression of ethylene biosynthetic genes, and further promoted ethylene production. In contrast, the ethylene action inhibitor 1-MCP efficiently blocked fruit maturation, even following SlTOR inhibition. These results suggest that accelerated fruit ripening caused by SlTOR inhibition depends on ethylene, and that SlTOR may function as a regulator in ethylene metabolism. [ABSTRACT FROM AUTHOR]

Target of rapamycin (TOR) functions as a central sensory hub linking a wide range of external stimuli to gene expression. The mechanisms underlying stimulus-specific transcriptional reprogramming by TOR remain elusive. Here, we describe an in silico analysis in Arabidopsis demonstrating that TOR-repressed genes are associated with either bistable or silent chromatin states. Both states regulated by the TOR signaling pathway are associated with a high level of histone H3K27 trimethylation (H3K27me3) deposited by CURLY LEAF in a specific context with LIKE HETEROCHROMATIN PROTEIN1. The combination of the two epigenetic histone modifications H3K4me3 and H3K27me3 implicates a bistable feature that alternates between an 'on' and an 'off' state, allowing rapid transcriptional changes upon external stimuli. The chromatin remodeler SWI2/SNF2 ATPase BRAHMA activates TOR-repressed genes only at bistable chromatin domains to rapidly induce biotic stress responses. Here, we demonstrate both in silico and in vivo that TOR represses transcriptional stress responses through global maintenance of H3K27me3. [ABSTRACT FROM AUTHOR]

Diaphorina citri is an important vector of Citrus Huanglongbing (HLB) disease. After feeding on young host plant shoots, the population of D. citri can increase significantly. Females also only lay eggs on young shoots. However, there are few studies on the mechanism of this phenomenon. Exogenous nutrient signals can affect the insulin signaling system of D. citri after feeding on young shoots. In this study, the expression of upstream factors DcILP1, DcILP2, and DcIR in the insulin signaling system of D. citri was upregulated after feeding on young shoots. After being silenced by RNA interference technology, the results showed that the number of oviposited eggs of D. citri was significantly decreased and the ovarian development was inhibited with severe vacuolation. In addition, detection using quantitative reverse transcription–polymerase chain reaction showed that the upstream regulatory gene DcRheb of the target of rapamycin (TOR) pathway and the downstream reproduction‐related DcVg gene were also significantly downregulated. These results suggest that feeding upon young shoots may upregulate the expression levels of upstream factors DcILP1, DcILP2, and DcIR in the insulin signaling system. The signal will be through upregulating the expression of DcRheb, an upstream gene of the TOR signaling pathway. This in turn influences yolk metabolism, which eventually causes the ovaries of female D. citri to mature and therefore initiate oviposition behavior. [ABSTRACT FROM AUTHOR]

Introduction: Biofungicides with low toxicity and high efficiency are a global priority for sustainable agricultural development. Phytohormone salicylic acid (SA) is an ancient medicine against various diseases in humans and activates the immune system in plants, but little is known of its function as a biofungicide. Objectives: Here, Fusarium oxysporum, the causal agent of devastating Fusarium wilt and immunodepressed patients, was used as a model system to explore whether SA can enter the pathogen cells and suppress key targets of the pathogen. Methods: Oxford Nanopore MinION sequencing and high-throughput chromosome conformation capture (Hi-C) sequencing were used to analyzed the genome of F. oxysporum. In addition, RNA-seq, qRT-PCR, and western blotting were conducted to detect gene and protein expression levels. Results: We isolated and sequenced the genome of F. oxysporum from potato dry rot, and the F. oxysporum included 12 chromosomes and 52.3 Mb genomic length. Pharmacological assays showed that exogenous application of SA can efficiently arrest hyphal growth, spore production, and pathogenicity of F. oxysporum, whereas endogenous salicylate hydroxylases significantly detoxify SA. The synergistic growth inhibition of F. oxysporum was observed when SA was combined with rapamycin. Kinase assays showed that SA inhibits FoTOR complex 1 (FoTORC1) by activating FoSNF1 in vivo. Transgenic potato plants with the interference of FoTOR1 and FoSAH1 genes inhibited the invasive growth of hyphae and significantly prevented the occurrence of Fusarium wilt. Conclusion: This study revealed the underlying mechanisms of SA against F. oxysporum and provided insights into SA in controlling various fungal diseases by targeting the SNF1-TORC1 pathway of pathogens.

The target of rapamycin (TOR) protein phosphorylates its downstream effector p70kDa ribosomal protein S6 kinases (S6K1) for ribosome biogenesis and translation initiation in eukaryotes. However, the molecular mechanism of TOR-S6K1-ribosomal protein (RP) signaling is not well understood in plants. In the present study, we report the transcriptional upregulation of ribosomal protein large and small subunit (RPL and RPS) genes in the previously established TOR overexpressing transgenic lines of rice (in Oryza sativa ssp. indica, variety BPT-5204, TR-2.24 and TR-15.1) and of Arabidopsis thaliana (in Col 0 ecotype, ATR-1.4.27 and ATR-3.7.32). The mRNA levels of RP genes from this study were compared with those previously available in transcriptomic datasets on the expression of RPs in relation to TOR inhibitor and in the TOR-RNAi lines of Arabidopsis thaliana. We further analyzed TOR activity, i.e., S6K1 phosphorylation in SALK lines of Arabidopsis with mutation in rpl6, rpl18, rpl23, rpl24 and rps28C, where the rpl18 mutant showed inactivation of S6K1 phosphorylation. We also predicted similar putative Ser/Thr phosphorylation sites for ribosomal S6 kinases (RSKs) in the RPs of Oryza sativa ssp. indica and Arabidopsis thaliana. The findings of this study indicate that the TOR pathway is possibly interlinked in a cyclic manner via the phosphorylation of S6K1 as a modulatory step for the regulation of RP function to switch 'on'/'off' the translational regulation for balanced plant growth. [ABSTRACT FROM AUTHOR]

Summary: The target of rapamycin (TOR) protein kinase is a master regulator of cell growth in all eukaryotes, from unicellular yeast and algae to multicellular animals and plants. Target of rapamycin balances the synthesis and degradation of proteins, lipids, carbohydrates and nucleic acids in response to nutrients, growth factors and cellular energy to promote cell growth. Among nutrients, amino acids (AAs) and glucose are central regulators of TOR activity in evolutionary distant eukaryotes such as mammals, plants and algae. However, these organisms obtain the nutrients through totally different metabolic processes. Although photosynthetic eukaryotes can use atmospheric CO2 as the sole carbon (C) source for all reactions in the cell, heterotrophic organisms get nutrients from other sources of organic C including glucose. Here, we discuss the impact of autotrophic and heterotrophic metabolism on the nutrient regulation of TOR, focusing on the role of AAs and C sources upstream of this signaling pathway. [ABSTRACT FROM AUTHOR]

To survive and sustain growth, sessile plants have developed sophisticated internal signalling networks that respond to various external and internal cues. Despite the central roles of nutrient and hormone signaling in plant growth and development, how hormone-driven processes coordinate with metabolic status remains largely enigmatic. Target of rapamycin (TOR) kinase is an evolutionarily conserved master regulator that integrates energy, nutrients, growth factors, hormones, and stress signals to promote growth in all eukaryotes. Inspired by recent comprehensive systems, chemical, genetic, and genomic studies on TOR in plants, this review discusses a potential role of TOR as a 'global positioning system' that directs plant growth and developmental programs both temporally and spatially by integrating dynamic information in the complex nutrient and hormonal signaling networks. We further evaluate and depict the possible functional and mechanistic models for how a single protein kinase, TOR, is able to recognize, integrate, and even distinguish a plethora of positive and negative input signals to execute appropriate and distinct downstream biological processes via multiple partners and effectors. [ABSTRACT FROM AUTHOR]

mRNA translation is the growth rate-limiting step in genome expression. Target of rapamycin (TOR) evolved a central regulatory role in eukaryotes as a signaling hub that monitors nutrient availability to maintain homeostasis and promote growth, largely by increasing the rate of translation initiation and protein synthesis. The dynamic pathways engaged by TOR to regulate translation remain debated even in well-studied yeast and mammalian models, however, despite decades of intense investigation. Recent studies have firmly established that TOR also regulates mRNA translation in plants through conserved mechanisms, such as the TOR–LARP1–5ʹTOP signaling axis, and through pathways specific to plants. Here, we review recent advances in our understanding of the regulation of mRNA translation in plants by TOR. [ABSTRACT FROM AUTHOR]

The TOR (target of rapamycin) signalling network plays a pivotal role in sugar metabolism and plant growth. In this study, we used grape (Vitis vinifera L.) calli to explore the function of the kinase and FATC domains (C-terminal of FAT (FRAP-ATM-TTRAP) of VvTOR (Vitis vinifera target of rapamycin). We found that the activity of VvTOR affected sugar-related gene expression. VvTOR-VvS6K pathway potentially participated in regulating sugar gene expression. We obtained the over-expression of kinase and FATC domains in transgenic calli by Agrobacterium -mediated transformation. Even though the kinase and FATC domains all belong to VvTOR protein, their functions were different in the regulating sugar accumulation and sugar-related gene expression. We speculated that the kinase domain positively regulated sugar accumulation and FATC domain may negatively influenced sugar accumulation. FATC and kinase domains of VvTOR co-regulated sugar accumulation in grape. These observations will provide framework for future investigations to address other functions of TOR signalling in plant development and signalling pathways. The activity of VvTOR (Vitis vinifera target of rapamycin) could affect sugar-related gene expression. The kinase and FATC (C -terminal of FAT (FRAP-ATM-TTRAP)) domains of VvTOR could affect sugar accumulation and sugar-related gene expression in grape (Vitis vinifera L.). Even though the kinase and FATC domains all belong to VvTOR protein, their functions were different in the regulating sugar accumulation and sugar-related gene expression. These observations will provide framework for future investigations to address other functions of TOR signalling in plant developmental and signalling pathways. [ABSTRACT FROM AUTHOR]

Low temperature (LT) is an important environmental factor affecting the growth and yield of plants. Melatonin (MT) can effectively enhance the LT tolerance of cucumber. This study found that LT stress induced the expression of Comt1 (caffeic acid O-methyltransferase 1), with the highest expression being about 2-times that of the control. Meanwhile, the content of MT was found to be roughly 63.16% of that in the control samples. Compared with LT treatment alone, exogenous MT pretreatment upregulated the expression levels of TOR (Target of rapamycin), PIN1 (Pin-formed 1), and YUC4 (YUCCA 4) , with maximum upregulations reaching approximately 66.67%, 79.32%, and 42.86%, respectively. These results suggest that MT may modulate the tolerance of cucumber seedlings to LT stress by regulating the expression of TOR , PIN1 , and YUC4. In addition, co-treatment with AZD-8055 (a TOR inhibitor) or NPA (N-1-naphthylphthalamic acid, an auxin polar transport inhibitor) and MT attenuated MT-induced resistance to LT stress, leading to higher levels of reactive oxygen species (ROS), reduced antioxidant defense capacity, and increased damage to the membrane system in cucumber seedlings. Concurrently, the content of osmoregulatory substances and the photosynthesis decreased. These results demonstrate that both TOR and auxin were required for MT to alleviate LT-induced damage in cucumber. In summary, the present study demonstrates that TOR and auxin signaling synergistically contribute to alleviating LT damage in cucumber seedlings by exogenous MT. These findings help us understand the function of MT and provide insights into the regulatory network of MT that regulates the LT tolerance of plants. • Melatonin (MT) responds positively to low temperature (LT) stress and enhances LT tolerance in cucumber seedlings. • Under LT stress, MT induces the expression of target of rapamycin (TOR) and auxin signaling related genes. • MT pretreatment enhances LT stress tolerance through interaction with TOR and auxin signaling. [ABSTRACT FROM AUTHOR]

The molecular mechanisms that drive circadian (24 h) rhythmicity have been investigated for many decades, but we still do not have a complete picture of eukaryotic circadian systems. Although the transcription/translation feedback loop (TTFL) model has been the primary focus of research, there are many examples of circadian rhythms that persist when TTFLs are not functioning, and we lack any good candidates for the non-TTFL oscillators driving these rhythms. In this hypothesis-driven review, the author brings together several lines of evidence pointing towards the Target of Rapamycin (TOR) signalling pathway as a good candidate for a non-TTFL oscillator. TOR is a ubiquitous regulator of metabolism in eukaryotes and recent focus in circadian research on connections between metabolism and rhythms makes TOR an attractive candidate oscillator. In this paper, the evidence for a role for TOR in regulating rhythmicity is reviewed, and the advantages of TOR as a potential oscillator are discussed. Evidence for extensive feedback regulation of TOR provides potential mechanisms for a TOR-driven oscillator. Comparison with ultradian yeast metabolic cycles provides an example of a potential TOR-driven self-sustained oscillation. Unanswered questions and problems to be addressed by future research are discussed.

Insulin resistance, the failure to activate insulin signaling in the presence of ligand, leads to metabolic diseases, including type 2 diabetes. Physical activity and mechanical stress have been shown to protect against insulin resistance, but the molecular mechanisms remain unclear. Here, we address this relationship in the Drosophila larval fat body, an insulin-sensitive organ analogous to vertebrate adipose tissue and livers. We found that insulin signaling in Drosophila fat body cells is abolished in the absence of physical activity and mechanical stress even when excess insulin is present. Physical movement is required for insulin sensitivity in both intact larvae and fat bodies cultured ex vivo. Interestingly, the insulin receptor and other downstream components are recruited to the plasma membrane in response to mechanical stress, and this membrane localization is rapidly lost upon disruption of larval or tissue movement. Sensing of mechanical stimuli is mediated in part by integrins, whose activation is necessary and sufficient for mechanical stress-dependent insulin signaling. Insulin resistance develops naturally during the transition from the active larval stage to the immotile pupal stage, suggesting that regulation of insulin sensitivity by mechanical stress may help coordinate developmental programming with metabolism.

Plant defense to microbial pathogens is often accompanied by significant growth inhibition. How plants merge immune system function with normal growth and development is still poorly understood. Here, we investigated the role of target of rapamycin (TOR), an evolutionary conserved serine/threonine kinase, in the plant defense response. We used rice as a model system and applied a combination of chemical, genetic, genomic and cell-based analyses. We demonstrate that ectopic expression of TOR and Raptor (regulatory-associated protein of mTOR), a protein previously demonstrated to interact with TOR in Arabidopsis, positively regulates growth and development in rice. Transcriptome analysis of rice cells treated with the TOR-specific inhibitor rapamycin revealed that TOR not only dictates transcriptional reprogramming of extensive gene sets involved in central and secondary metabolism, cell cycle and transcription, but also suppresses many defense-related genes. TOR overexpression lines displayed increased susceptibility to both bacterial and fungal pathogens, whereas plants with reduced TOR signaling displayed enhanced resistance. Finally, we found that TOR antagonizes the action of the classic defense hormones salicylic acid and jasmonic acid. Together, these results indicate that TOR acts as a molecular switch for the activation of cell proliferation and plant growth at the expense of cellular immunity.

An eight weeks feeding trial was conducted to evaluate the potential of cottonseed oil (CSO) as a substitute for fish oil (FO) on juvenile black seabream (Acanthopagrus schlegelii) (2.29 ± 0.01 g). Five diets were formulated with pure FO (FO) or partial CSO replacement of FO: 20% CSO (CSO20), 40% CSO (CSO40), 60% CSO (CSO60) and 80% CSO (CSO80), respectively. Results showed that fish fed CSO60 diet significantly increased growth performance compared to control group. Hepatic expression of genes related to long-chain polyunsaturated fatty acid biosynthesis were significantly up-regulated by dietary CSO60 compared to FO group. Hepatic paraffin section and serum biochemical indices showed that fish fed dietary CSO80 could increase vacuolar fat drops and cause liver damage. The expression levels of peroxisome proliferators-activated receptor alpha and its downstream lipolysis related genes were markedly up-regulated with the increasing of replacement levels of CSO, opposite results were recorded in sterol regulatory element-binding protein-1c and lipogenesis related genes. The malondialdehyde content in liver was decreased with the increasing replacement levels of CSO, whereas the antioxidant parameters were significantly higher in CSO60 group compared to FO group. Phosphatidylinositol-3 kinase and protein kinase B expression levels were significantly up-regulated by dietary CSO80, triggering inflammation by activating nuclear factor kappa b. Dietary CSO60 dramatically promote target of rapamycin expression level. With the increasing replacement levels of FO by CSO, the expression level of ribosomal protein S6 kinase 1 was significantly increased, whereas opposite result was found for the eukaryotic translation initiation factor 4E binding protein 2. Collectively, based on weight gain, double broken line model analysis showed that a maximum growth occurred at 59.13% replacement of dietary FO by CSO. These findings demonstrate that dietary CSO60 can improve growth and antioxidant capacity. However, dietary CSO80 can result in lipid deposition, liver injury and inflammation, hence, suppress growth performance.

Initiation of vitellogenesis by blood feeding is essential for egg maturation in ticks. Nutrients derived from the blood meal are utilized by female ticks to synthesize the yolk protein precursor vitellogenin (Vg). Engorged Ornithodoros moubata ticks can synthesize Vg whether mated or virgin, thus O. moubata is an excellent model for studying the relative roles of blood feeding and mating in tick vitellogenesis. Injection of rapamycin into engorged O. moubata resulted in a reduction of ovarian growth and yolk accumulation in the oocytes of mated females. OmVg expression in the midgut and fat body and protein concentrations in the hemolymph significantly decreased in mated ticks after injection with rapamycin, indicating that inhibition of the nutrient‐sensing target of rapamycin (TOR) pathway disrupts egg maturation at the levels of Vg expression and synthesis. These results suggest that the TOR‐signaling pathway induces vitellogenesis in response to nutritional stimulation after a blood meal in O. moubata and is functionally independent of the mating‐induced pathway. [ABSTRACT FROM AUTHOR]

Sublethal concentrations of insecticides can affect the population dynamics of insects by inducing changes in their reproductive traits; however, the underlying molecular mechanisms remain unclear. In previous transcriptomic experiments, triazophos was found to promote SfTOR transcription. Therefore, in this study, two representative insecticides, thiamethoxam (inhibiting reproduction) and triazophos (stimulating reproduction), were selected to evaluate the transcription of the key genes involved in the target of rapamycin (TOR) and juvenile hormone (JH) pathways under stress in Sogatella furcifera. The results showed that thiamethoxam could significantly inhibit the transcription of SfRheb, SfTOR, SfS6K, and SfHMGR, whereas triazophos significantly promoted the transcription of SfRheb, SfTOR, SfS6K, SfHMGR, SfMet, and SfKr-h1. Moreover, RNA interference (RNAi) technology was used to target and silence TOR signaling pathway-related genes. The results showed that RNAi-mediated silencing of SfRheb, SfTOR, and SfS6K significantly inhibited ovarian development and fecundity. The transcription of JH signaling pathway-related genes (i.e., SfHMGR, SfFAMeT, SfMet, and SfKr-h1) and SfVg was significantly inhibited. However, the effects of SfRheb and SfTOR silencing on female reproduction were partially mitigated by the JH analog methoprene. These results indicate that the TOR signaling pathway can regulate the JH signaling pathway and SfVg transcription. In addition, insecticide stress can influence the transcription of TOR signaling pathway-related genes and transduction of stress signals via the JH signaling pathway, thereby affecting the transcription of SfVg and ultimately regulating reproduction in females. [ABSTRACT FROM AUTHOR]

TOR proteins, also known as targets of rapamycin, are serine/threonine kinases involved in various signaling pathways that regulate cell growth. The protozoan parasite Giardia lamblia is the causative agent of giardiasis, a neglected infectious disease in humans. In this study, we used a bioinformatics approach to examine the structural features of GTOR, a G. lamblia TOR-like protein, and predict functional associations. Our findings confirmed that it shares significant similarities with functional TOR kinases, including a binding domain for the FKBP-rapamycin complex and a kinase domain resembling that of phosphatidylinositol 3-kinase-related kinases. In addition, it can form multiprotein complexes such as TORC1 and TORC2. These results provide valuable insights into the structure–function relationship of GTOR, highlighting its potential as a molecular target for controlling G. lamblia cell proliferation. Furthermore, our study represents a step toward rational drug design for specific anti-giardiasis therapeutic agents.

The phytohormone abscisic acid (ABA) promotes plant tolerance to major stresses such as drought, partly by modulating growth through poorly understood mechanisms. Here, we show that ABA-triggered repression of cell proliferation in the Arabidopsis thaliana root meristem relies on the swift subcellular relocalization of SNF1-RELATED KINASE 1 (SnRK1). Under favorable conditions, the SnRK1 catalytic subunit, SnRK1α1, is enriched in the nuclei of root cells, and this is accompanied by normal cell proliferation and meristem size. Depletion of two key drivers of ABA signaling, SnRK2.2 and SnRK2.3, causes constitutive cytoplasmic localization of SnRK1α1 and reduced meristem size, suggesting that, under nonstress conditions, SnRK2s promote growth by retaining SnRK1α1 in the nucleus. In response to ABA, SnRK1α1 translocates to the cytoplasm, and this is accompanied by inhibition of target of rapamycin (TOR), decreased cell proliferation, and reduced meristem size. Blocking nuclear export with leptomycin B abrogates ABA-driven SnRK1α1 relocalization to the cytoplasm and ABA-elicited inhibition of TOR. Furthermore, fusing SnRK1α1 to an SV40 nuclear localization signal leads to defective ABA-dependent TOR repression. Altogether, we demonstrate that SnRK2-dependent changes in SnRK1α1 subcellular localization are crucial for inhibiting TOR and root growth in response to ABA. Rapid relocalization of central regulators such as SnRK1 may represent a general strategy of eukaryotic organisms to respond to environmental changes [ABSTRACT FROM AUTHOR]

Target of rapamycin (TOR) is a serine/threonine protein kinase that plays a central regulating role in cell proliferation, growth, and metabolism, but little is known about the TOR signaling pathway in Chlorella sorokiniana. In this study, a Chlorella sorokiniana DP-1 strain was isolated and identified, and its nutritional compositions were analyzed. Based on homologous sequence analysis, the conserved CsTOR protein was found in the genome of Chlorella sorokiniana. In addition, the key components of TOR complex 1 (TORC1) were present, but the components of TORC2 (RICTOR and SIN1) were absent in Chlorella sorokiniana. Pharmacological assays showed that Chlorella sorokiniana DP-1 was insensitive to rapamycin, Torin1 and KU0063794, whereas AZD8055 could significantly inhibit the growth of Chlorella sorokiniana. RNA-seq analysis showed that CsTOR regulated various metabolic processes and signal transduction pathways in AZD8055-treated Chlorella sorokiniana DP-1. Most genes involved in photosynthesis and carbon fixation in Chlorella sorokiniana DP-1 were significantly downregulated under CsTOR inhibition, indicating that CsTOR positively regulated the photosynthesis in Chlorella sorokiniana. Furthermore, CsTOR controlled protein synthesis and degradation by positively regulating ribosome synthesis and negatively regulating autophagy. These observations suggested that CsTOR plays an important role in photosynthesis and cellular metabolism, and provide new insights into the function of CsTOR in Chlorella sorokiniana. [ABSTRACT FROM AUTHOR]

[Display omitted] • Isolating and sequencing the genome of F. oxysporum from potato tubers with dry rot symptoms. • SA efficiently arrests hyphal growth, sporular production and pathogenicity of F. oxysporum. • SA inhibits the activity of FoTORC1 via activating FoSNF1 in F. oxysporum. • Transgenic potato plants with interference of FoTOR1 and FoSAH1 genes prevent the occurrence of Fusarium wilt. • Providing insights SA into controlling various fungal diseases by targeting the SNF1-TORC1 pathway of pathogens. Biofungicides with low toxicity and high efficiency are a global priority for sustainable agricultural development. Phytohormone salicylic acid (SA) is an ancient medicine against various diseases in humans and activates the immune system in plants, but little is known of its function as a biofungicide. Here, Fusarium oxysporum , the causal agent of devastating Fusarium wilt and immunodepressed patients, was used as a model system to explore whether SA can enter the pathogen cells and suppress key targets of the pathogen. Oxford Nanopore MinION sequencing and high-throughput chromosome conformation capture (Hi-C) sequencing were used to analyzed the genome of F. oxysporum. In addition, RNA-seq, qRT-PCR, and western blotting were conducted to detect gene and protein expression levels. We isolated and sequenced the genome of F. oxysporum from potato dry rot, and the F. oxysporum included 12 chromosomes and 52.3 Mb genomic length. Pharmacological assays showed that exogenous application of SA can efficiently arrest hyphal growth, spore production, and pathogenicity of F. oxysporum , whereas endogenous salicylate hydroxylases significantly detoxify SA. The synergistic growth inhibition of F. oxysporum was observed when SA was combined with rapamycin. Kinase assays showed that SA inhibits FoTOR complex 1 (FoTORC1) by activating FoSNF1 in vivo. Transgenic potato plants with the interference of FoTOR1 and FoSAH1 genes inhibited the invasive growth of hyphae and significantly prevented the occurrence of Fusarium wilt. This study revealed the underlying mechanisms of SA against F. oxysporum and provided insights into SA in controlling various fungal diseases by targeting the SNF1-TORC1 pathway of pathogens. [ABSTRACT FROM AUTHOR]

An 8-week feeding trial was conducted to evaluate the effects of sodium butyrate (SB) on growth, digestive enzymes, body composition and nutrient retention-related gene expression of juvenile yellow catfish (Pelteobagrus fulvidraco). Five isonitrogenous and isolipidic diets (420 g/kg protein and 90 g/kg lipid) were formulated to contain 0 (control), 250, 500, 1,000 or 2,000 mg/kg SB. Triplicate groups of 40 fish (BW = 1.26 ± 0.01 g) per tank (300-L cylindrical fiberglass tanks) for each diet were fed to apparent satiation twice daily. Stomach, hepatopancreas and intestine samples were obtained for digestive enzymes activities analyses. A real-time quantitative PCR analysis was performed to determine the relative expression of target of rapamycin (TOR) and lipoprotein lipase (LPL) in the hepatopancreas and intestine. Fish fed the diets supplemented with SB at 500 and 1,000 mg/kg showed significantly higher specific growth rate and significantly lower feed conversion ratio compared to the control (P < 0.05). Dietary SB inclusion did not alter activities of intestinal amylase, creatine kinase and sodium–potassium adenosine triphosphatase (Na+/K+-ATPase), but increased activities of hepatic trypsin, stomachic lipase, intestinal lipase, alkaline phosphatase and γ-glutamyl transpeptidase for fish fed 1,000 mg/kg SB compared to the control (P < 0.05). Intestine length index, intestine somatic index, fold height and muscular thickness of distal intestine were significantly higher in 1,000 mg/kg SB groups compared to the control (P < 0.05). Significantly higher levels of whole-body crude protein, ash, calcium, phosphorus, nutrition retention and relative mRNA of intestinal TOR were observed in 1,000 mg/kg SB group (P < 0.05). Whole-body lipid content and hepatopancreas LPL mRNA expression in 2,000 mg/kg SB group were significantly higher than the control (P < 0.05). Relative mRNA levels of intestinal LPL and hepatopancreas TOR were significantly higher in the 500 mg/kg SB group compared to those in other groups (P < 0.05). The increased growth performance, digestive enzymes and nutrient retention in fish fed the diets supplemented with SB at 500 and 1,000 mg/kg suggests that SB can be a desirable growth promoter as an antibiotic alternative in diets.

TOR complex 1 (TORC1) is an evolutionarily conserved protein kinase complex that promotes cellular macromolecular synthesis and suppresses autophagy. Amino-acid-induced activation of mammalian TORC1 is initiated by its recruitment to the RagA/B-RagC/D GTPase heterodimer, which is anchored to lysosomal membranes through the Ragulator complex. We have identified in the model organism Schizosaccharomyces pombe a Ragulator-like complex that tethers the Gtr1-Gtr2 Rag heterodimer to the membranes of vacuoles, the lysosome equivalent in yeasts. Unexpectedly, the Ragulator-Rag complex is not required for the vacuolar targeting of TORC1, but the complex plays a crucial role in attenuating TORC1 activity independently of the Tsc1-Tsc2 complex, a known negative regulator of TORC1 signaling. The GATOR1 complex, which functions as Gtr1 GAP, is essential for the TORC1 attenuation by the Ragulator-Rag complex, suggesting that Gtr1GDP-Gtr2 on vacuolar membranes moderates TORC1 signaling for optimal cellular response to nutrients.

Target of rapamycin (TOR) is an evolutionarily conserved protein kinase that controls multiple cellular processes upon various intracellular and extracellular stimuli. Since its first discovery, extensive studies have been conducted both in yeast and animal species including humans. Those studies have revealed that TOR forms two structurally and physiologically distinct protein complexes; TOR complex 1 (TORC1) is ubiquitous among eukaryotes including animals, yeast, protozoa, and plants, while TOR complex 2 (TORC2) is conserved in diverse eukaryotic species other than plants. The studies have also identified two crucial regulators of mammalian TORC1 (mTORC1), Ras homolog enriched in brain (RHEB) and RAG GTPases. Of these, RAG regulates TORC1 in yeast as well and is conserved among eukaryotes with the green algae and land plants as apparent exceptions. RHEB is present in various eukaryotes but sporadically missing in multiple taxa. RHEB, in the budding yeast Saccharomyces cerevisiae, appears to be extremely divergent with concomitant loss of its function as a TORC1 regulator. In this review, we summarize the evolutionarily conserved functions of the key regulatory subunits of TORC1 and TORC2, namely RAPTOR, RICTOR, and SIN1. We also delve into the evolutionary conservation of RHEB and RAG and discuss the conserved roles of these GTPases in regulating TORC1.

The target of rapamycin (TOR) protein kinase forms multi-subunit TOR complex 1 (TORC1) and TOR complex 2 (TORC2), which exhibit distinct substrate specificities. Sin1 is one of the TORC2-specific subunit essential for phosphorylation and activation of certain AGC-family kinases. Here, we show that Sin1 is dispensable for the catalytic activity of TORC2, but its conserved region in the middle (Sin1CRIM) forms a discrete domain that specifically binds the TORC2 substrate kinases. Sin1CRIM fused to a different TORC2 subunit can recruit the TORC2 substrate Gad8 for phosphorylation even in the sin1 null mutant of fission yeast. The solution structure of Sin1CRIM shows a ubiquitin-like fold with a characteristic acidic loop, which is essential for interaction with the TORC2 substrates. The specific substrate-recognition function is conserved in human Sin1CRIM, which may represent a potential target for novel anticancer drugs that prevent activation of the mTORC2 substrates such as AKT.

In Dermanyssus gallinae , a hematophagous mite, the initiation of vitellogenesis induced by blood feeding is essential for its reproduction. However, the precise gene structures and physiological functions of Vg in D. gallinae and its upstream gene, Target of Rapamycin (TOR), have not been fully understood. This study revealed the presence of four homologous genes within D. gallinae , named Dg-Vg1, Dg-Vg1-like, Dg-Vg2, and Dg-Vg2-like, especially, Dg-Vg2-like was firstly identified in the mites. The expression levels of all these Vg genes were significantly higher in adult females than other stages. Following blood feeding, the expression levels of these genes increased significantly, followed by a subsequent decrease, aligning with egg production. Silencing Dg-Vgs by RNA interference (RNAi) led to decreased fecundity and egg hatching rates, as well as abnormal embryonic development, suggesting a vital role for Dg-Vgs in both egg formation and embryonic development. Furthermore, the knockdown of Dg-TOR significantly reduced the expression of Dg-Vgs and negatively impacted the reproductive capabilities of PRMs, indicating that TOR influences PRM reproduction by regulating the expression of Dg-Vgs. In summary, these findings demonstrated the crucial roles of Dg-Vgs and Dg-TOR in PRM reproduction, highlighting their potential as targets for pest control. [Display omitted] • Four Vitellogenin (Vg) genes were identified in PRMs with Dg-Vg2-like being discovered for the first time. • Expression levels of Dg-Vg genes in adult females peaked after blood feeding, aligning with egg production dynamics. • All Dg-Vg genes play an important role in the reproduction of adult females. • Dg-TOR affects the reproduction of PRMs by regulating the expression of Dg-Vgs. [ABSTRACT FROM AUTHOR]

An 8‐week feeding trial was conducted to determine dietary isoleucine (Ile) requirement of rainbow trout, Oncorhynchus mykiss fingerlings. Six isonitrogenous (450 g kg−1) and isocaloric (20.90 kJ g−1, gross energy) diets were designed with varied Ile levels (6.0–18.5 g kg−1, dry diet). Twenty fish (1.66 ± 0.02 g/fish; 5.25 ± 0.34 cm/fish) were distributed in triplicate groups in 75‐L troughs attached to flow‐through system (2–2.5 L minute−1) and were fed twice daily (09:00 and 17:00 hours) at 5% BW day−1. Maximum live weight gain (LWG %), specific growth rate (SGR), protein efficiency ratio (PER) and the best‐feed conversion ratio (FCR) were observed at 13.5 g kg−1 Ile fed diet. Quadratic regression analysis of growth data predicts optimum Ile requirement to be at 13.73 (LWG %), 13.41 (FCR), 13.44 (PER) and 13.35 (BPD) g kg−1 respectively. Highest (p < 0.05) protein, lowest moisture and intermediate fat contents were noted at 13.5 g kg−1 Ile fed diet. Haematological variables such as haemoglobin (Hb), haematocrit (Hct) and red blood cell (RBC) count also showed highest values at 13.5 g kg−1 Ile diet. Plasma cholesterol, triglycerides, glucose and urea did not produce any significant (p > 0.05) changes among the groups, while as alanine transaminase (ALT), aspartate transaminase (AST) and uric acid levels showed significant (p ˂ 0.05) variations. Highest total protein content and lowest alkaline phosphatase (ALP) were observed at 13.5 g kg−1 Ile fed diet, while albumin and globulin content did not produce any significant (p > 0.05) difference among the groups. Significant (p ˂ 0.05) differences were also observed in intestinal enzymatic activities and antioxidant status. Highest (p < 0.05) TOR and 4E‐BP mRNA gene expression level were also found at 13.5 g kg−1 Ile fed diet. On the basis of above data, it is recommended that 13.48 g kg−1 Ile, corresponding to 29.95 g kg−1 of dietary protein, would be useful for optimum growth and best nutrient conversion of this species. [ABSTRACT FROM AUTHOR]

The target of rapamycin (TOR) signalling network plays a pivotal role in sugar metabolism and plants growth. In this article, we made use of the grape (Vitis vinifera) calli as experiment materials to explore the function of VvTOR gene and protein. By dual-luciferase reporter system, We found that VvTOR promoter could respond to ABA (Abscisic Acid) signal and VvTOR 1200 bp promoter fragment had stronger activity. By the treatment of AZD8055, an inhibitor of VvTOR, the sugars (glucose, sucrose, fructose) contents of grape calli had different changes and the growth of grape calli could be repressed. We further found that VvTOR could affect grape growth and sugar metabolism genes expression under the different treatments of ABA and AZD8055. These results provide a new evidence to support the viewpoint that VvTOR could respond to ABA signal and affect sugar related genes expression in grapes. [ABSTRACT FROM AUTHOR]

Eukaryotic cells monitor and regulate metabolism through the atypical protein kinase target of rapamycin (TOR) regulatory hub. TOR is activated by amino acids in animals and fungi through molecular signaling pathways that have been extensively defined in the past ten years. Very recently, several studies revealed that TOR is also acutely responsive to amino acid metabolism in plants, but the mechanisms of amino acid sensing are not yet established. In this review, we summarize these discoveries, emphasizing the diversity of amino acid sensors in human cells and highlighting pathways that are indirectly sensitive to amino acids, i.e., how TOR monitors changes in amino acid availability without a bona fide amino acid sensor. We then discuss the relevance of these model discoveries to plant biology. As plants can synthesize all proteinogenic amino acids from inorganic precursors, we focus on the possibility that TOR senses both organic metabolites and inorganic nutrients. We conclude that an evolutionary perspective on nutrient sensing by TOR benefits both agricultural and biomedical science, contributing to ongoing efforts to generate crops for a sustainable agricultural future. [ABSTRACT FROM AUTHOR]

The study aims at discussing abiotic stress-related genes and metabolites in the crosstalking signal transduction pathways with emphasis to those in leaves of wild barley Hordeum spontaneum. Selected pathways involve tryptophan and target of rapamycin (or TOR) complex as core metabolites. In H. spontaneum, route towards tryptophan production seems to be mediated via anthranilate synthase acting as a master switch. Downstream auxin-related factors and proteins can secure plant's ability to maintain proper growth rates and stress tolerance. Detected TOR in H. spontaneum participates in several signal transduction related pathways with a central role in nutrient starvation, ribosome biogenesis and protein synthesis and in standing oxidative and other abiotic stresses. TOR also participates as a master regulator of lifespan, aging and autophagy in H. spontaneum to regulate growth and maintain plant yield and its attributes under stress conditions. In conclusion, the present study emphasizes some mechanisms by which wild plant species, e.g., H. spontaneum, utilize to cope with abiotic stresses. [ABSTRACT FROM AUTHOR]

Target of rapamycin (TOR) is an evolutionarily conserved protein kinase that functions as a central signaling hub to integrate diverse internal and external cues to precisely orchestrate cellular and organismal physiology. During evolution, TOR both maintains the highly conserved TOR complex compositions, and cellular and molecular functions, but also evolves distinctive roles and strategies to modulate cell growth, proliferation, metabolism, survival, and stress responses in eukaryotes. Here, we review recent discoveries on the plant TOR signaling network. We present an overview of plant TOR complexes, analyze the signaling landscape of the plant TOR signaling network from the upstream signals that regulate plant TOR activation to the downstream effectors involved in various biological processes, and compare their conservation and specificities within different biological contexts. Finally, we summarize the impact of dysregulation of TOR signaling on every stage of plant growth and development, from embryogenesis and seedling growth, to flowering and senescence. [ABSTRACT FROM AUTHOR]

ABSTRACT Target of rapamycin (TOR) is a very critical protein in plants, which connects with biological process, glycometabolism, life span, and photosynthesis. Here, the evolutionary relationship, conserved motif, gene structure and cis-acting elements of TOR were analyzed. Promoter cis-acting elements analysis indicated various cis-acting elements respond to light, auxin, ABA and multiple signal pathway. Transcriptome sequencing and the co-expression network of VvTOR, sugar and abscisic acid (ABA) related genes from Vitis vinifera L. Cabernet Sauvignon berries indicated that VvTOR might participate in sugar and ABA signaling. The expression of VvTOR in grape suspension cells analyzed by quantitative real-time PCR showed that VvTOR responded to ABA and glucose treatment. These results predicted the potential functions of VvTOR in glucose metabolism and ABA signal pathway.

Nutrition shapes a broad range of life-history traits, ultimately impacting animal fitness. A key fitness-related trait, female fecundity is well known to change as a function of diet. In particular, the availability of dietary protein is one of the main drivers of egg production, and in the absence of essential amino acids egg laying declines. However, it is unclear whether all essential amino acids have the same impact on phenotypes like fecundity. Using a holidic diet, we fed adult female Drosophila melanogaster diets that contained all necessary nutrients except one of the 10 essential amino acids and assessed the effects on egg production. For most essential amino acids, depleting a single amino acid induced as rapid a decline in egg production as when there were no amino acids in the diet. However, when either methionine or histidine were excluded from the diet, egg production declined more slowly. Next, we tested whether GCN2 and TOR mediated this difference in response across amino acids. While mutations in GCN2 did not eliminate the differences in the rates of decline in egg laying among amino acid drop-out diets, we found that inhibiting TOR signalling caused egg laying to decline rapidly for all drop-out diets. TOR signalling does this by regulating the yolk-forming stages of egg chamber development. Our results suggest that amino acids differ in their ability to induce signalling via the TOR pathway. This is important because if phenotypes differ in sensitivity to individual amino acids, this generates the potential for mismatches between the output of a pathway and the animal’s true nutritional status.

The purpose of this study was to estimate the effects of two diets on the growth, body composition, intestinal microbiota and gene expression of juvenile silver sillago, Sillago sihama. Silver sillago was fed a diet with either protein 400 g/kg (P40 group) or protein 500 g/kg (P50 group). 180 healthy fish (average wt. 0.83 ± 0.01 g) were equally distributed in two treatments in triplicates with 30 fish per tank. Following an 8‐week feeding study, the results showed that the protein efficiency ratio (PER) was significantly higher in the P40 group than that in the P50 group (p <.05). Among the morphological parameters, condition factor (CF) was significantly higher in the P40 group and the hepatosomatic indices (HSI) was significantly higher in the P50 group. Whole‐body moisture was significantly higher in the P40 group than that in the P50 group, while whole‐body ash was just the opposite of moisture. From histological sections of the liver, the P50 group had large lipid deposits in the liver. In the fish liver, lipoprotein (LPL) expression was significantly decreased in the P50 group, while heat shock protein 70 (HSP70) was significantly increased in the P50 group. At the phylum level, the relative abundance of Bacteroidetes and Verrucomicrobia was significantly lower in the P40 group. At the family level, the abundance of Lachnospiraceae and Halomonadaceae was lower in the P40 group. The most significantly changed pathways between the two groups were metabolism and environmental information processing. In conclusion, the P50 group was superior to the P40 group in all growth parameters and intestinal flora structure; however, the high‐protein level of the diet can lead to the deposition of excess lipids in the liver and create some metabolic stress. [ABSTRACT FROM AUTHOR]