bims-plator 2026-05-24 papers

bims-plator

Biomed News

on Plant TOR

Issue of 2026–05–24
nine papers selected by
Christian Meyer, INRAE

Linking sugar sensing to immunity in plants via O-glycosylation.
Unlocking translational control of specialized metabolism in plants through 5'UTR structure.
Citric acid alters Arabidopsis root morphology and development through ROS-dependent and ROS-independent mechanisms.
Rewiring the unfolded protein response for plant growth recovery from stress.
PQ-loop repeat-containing 2 (PQLC2) regulates mTORC1 lysosomal localization and autophagic flux.
Systemic and Local Regulation of Root Growth by Vascular Trehalose 6-Phosphate is Correlated With Re-allocation of Primary Metabolites Between Shoots and Roots.
Targeted metabolomics of organic and amino acids in giraffe milk during mid- to late-lactation.
Byakangelicin alleviates metabolic dysfunction-associated steatohepatitis by selective inhibition of non-canonical MTORC1 signaling pathway.
Isolation and characterization of Saccharomyces cerevisiae mutants with ornithine accumulation for value-added craft beer brewing.

bioRxiv. 2026 May 10. pii: 2026.05.04.722566. [Epub ahead of print]

Linking sugar sensing to immunity in plants via O-glycosylation.

Yalikunjiang Aizezi, Yang Bi, Hongliang Zhang, Jung-Gun Kim, Ajeet Chaudhary, Cao Son Trinh, Qingxi J Shen, Shou-Ling Xu, Mary Beth Mudgett, Zhi-Yong Wang.

Interaction with microbes can reprogram metabolism and alter nutrient availability in plant cells. How metabolic cues modulate immune responses remains unknown. Here, we show that sugar-sensing O -glycosylation of immune-signaling kinases mediates metabolic regulation of immunity. Under sugar-replete conditions, the MAP kinase kinases (MKK4 and MKK5), key components of pattern-triggered immunity (PTI), are glycosylated by O -GlcNAc and O -fucose in their activation loops and thus cannot be activated by upstream kinases, thereby restricting PTI. Pathogen infection or sugar starvation reduces O -glycosylation of MKK4/5 and enhances immune signaling; these effects are reversed by GDP-fucose treatment, demonstrating that reduced sugar availability decreases O -fucosylation and enhances immune signaling in infected cells. Chemical inhibition of O -fucosylation enhances immunity and pathogen resistance in both Arabidopsis and tomato. Our findings establish O -glycosylation of MKKs as a metabolic rheostat that fine-tunes immune responses according to sugar availability during plant-microbe interactions, providing a new strategy for improving crop health.

DOI: https://doi.org/10.64898/2026.05.04.722566
Sci Adv. 2026 May 22. 12(21): eaeb6806

Unlocking translational control of specialized metabolism in plants through 5'UTR structure.

Makou Lin, Doosan Shin, Jie Hao, Masood Jan, Minkyu Park, Veronica Perez, Benjamin Breuer, Ying Wang, Jeongim Kim.

Plant-specialized metabolites are essential for plant fitness and human health, with their biosynthesis pathways tightly regulated at multiple levels. However, the translational regulation of their biosynthesis remains poorly understood. Here, we reveal a 5' untranslated region (5'UTR)-mediated translational mechanism that controls glucosinolate production in Arabidopsis. A forward genetic screen exploring the metabolic interaction between auxin and glucosinolates identified two dominant Arabidopsis alleles, each carrying a single-nucleotide substitution located 13-base pair apart within the 5'UTR of MYB28, a master regulator of aliphatic glucosinolate biosynthesis. These mutations markedly increase MYB28 protein abundance without affecting transcript levels, leading to enhanced glucosinolate production. Mutational profiling of the 5'UTR revealed that alterations in RNA tertiary structure influence translation efficiency, establishing a link between RNA conformation and metabolic output. Our findings uncover a previously uncharacterized layer of posttranscriptional regulation in plant-specialized metabolism and highlight the 5'UTR as a potential target for precision breeding to enhance crop performance and nutritional quality.

DOI: https://doi.org/10.1126/sciadv.aeb6806
Plant Physiol. 2026 May 06. pii: kiag194. [Epub ahead of print]201(1):

Citric acid alters Arabidopsis root morphology and development through ROS-dependent and ROS-independent mechanisms.

Tao Zhang, Jesus T Peng, Jie Chu, Shihong Luo, Jihyeon Lee, Diana Belén Sánchez Rodríguez, Katreena Gundran, Xuan Xia, Adriana Garay-Arroyo, Jocelyn A Richardson, Alexandra J Dickinson.

Citric acid is an integral component of primary metabolism and cellular energetics and plays extensive roles in other cellular processes, such as signaling, chelating, and exudation. Here, we characterized the unique effects that citric acid has on Arabidopsis (Arabidopsis thaliana) root structure and development. In particular, we investigated how citric acid modifies 2 root types in opposing ways: by inhibiting primary root growth while promoting anchor root growth. To understand the mechanisms driving these different growth patterns within the same organism, we analyzed nutrient and transcriptomic responses to citric acid treatment in anchor roots and primary roots. High-spatial resolution elemental analysis revealed that root meristems and the root-hypocotyl junction are regions of strong nutrient enrichment, but that citric acid treatment has little effect on nutrient levels in these regions. Transcriptional analysis revealed major differences between primary roots and anchor roots in response to citric acid. In particular, citric acid acted as a reactive oxygen species (ROS) scavenger through increased Class III peroxidase transcription, effectively reducing H2O2 levels both in vitro and in vivo. Altering the ROS balance at the root-hypocotyl junction was sufficient to induce anchor root formation. Citric acid treatment also differentially upregulated lignin biosynthesis, lignin assembly, and ETHYLENE RESPONSE FACTOR 115 expression in primary roots and anchor roots. ETHYLENE RESPONSE FACTOR 115 regulates the quiescent center and root columella, and we found that citric acid treatment induces developmental defects in this tissue. Overall, this study reveals that a vital organic acid produced and secreted at relatively high concentrations has both widespread and specific effects on plant development and root architecture.

DOI: https://doi.org/10.1093/plphys/kiag194
Plant Commun. 2026 May 20. pii: S2590-3462(26)00232-4. [Epub ahead of print] 101924

Rewiring the unfolded protein response for plant growth recovery from stress.

Dae Kwan Ko, Raz Danieli, Federica Brandizzi.

  The unfolded protein response (UPR) is a highly coordinated signaling network that mitigates endoplasmic reticulum (ER) stress, a condition induced by diverse environmental challenges in plants. Over the past two decades, substantial progress has been made in elucidating the molecular and genetic mechanisms of ER stress sensing and signal transduction in plants, largely through studies in the model Arabidopsis thaliana. These advances have established the UPR as a central regulator of proteostasis and underscored its broader relevance to plant growth, development, and crop productivity under stress conditions. Despite this progress, critical knowledge gaps remain, particularly concerning the downstream biological processes required for growth recovery once ER stress is subsided and how these processes are coordinated by UPR regulators. Recent systems-level and integrative studies have begun to reveal critical roles of UPR signaling in pathways governing growth re-establishment and homeostasis of nutrient allocation and energy metabolism. In this review, we highlight recent findings on the functional roles of the plant UPR in recovery from ER stress, with a focus on mechanisms mediated by the UPR regulators and downstream biological pathways that enable the transition from stress mitigation to growth restoration. Although this research area is still emerging, accumulating evidence supports a model in which the UPR functions as a dynamic regulatory network that actively coordinates post-stress physiological recovery and plant fitness.

Keywords:  ER stress; environmental stress; nutrient sensing; root growth; stress recovery; unfolded protein response

DOI:  https://doi.org/10.1016/j.xplc.2026.101924
Eur J Cell Biol. 2026 May 19. pii: S0171-9335(26)00015-4. [Epub ahead of print]105(3): 151544

PQ-loop repeat-containing 2 (PQLC2) regulates mTORC1 lysosomal localization and autophagic flux.

Yun-Ji Jeung, Minsu Jang, Jiwon Ahn, Ok-Seon Kwon, Seung-Hyun Kim, Jae-Eun Kwon, Yunho Park, Seung Pil Jang, Kajung Ryu, Kyung-Sook Chung.

  PQ-loop repeat-containing 2 (PQLC2) is a lysosomal transporter for cationic amino acid that plays a critical role in regulating intracellular amino acid levels. However, its role in lysosomal biogenesis and autophagy remains poorly understood. Here, we investigate the impact of PQLC2 loss on lysosomal function and autophagic flux using PQLC2 knockdown and knockout cell models. PQLC2-deficient cells exhibited enhanced nuclear translocation of transcription factor EB (TFEB), a key regulator of lysosome, accompanied by increased expression of TFEB-lysosomal and autophagy target genes. In addition, genes related to mechanistic target of rapamycin complex 1 (mTORC1), a negative regulator of TFEB, were destabilized, leading to reduced lysosomal recruitment and impaired mTORC1 signaling. Loss of PQLC2 also resulted in lysosomal dysfunction, including defective lysosomal acidification, decreased cathepsin activity, and lysosomal enlargement. Furthermore, autophagosome maturation and autophagic flux were disrupted in PQLC2-deficient cells, as evidenced by p62 accumulation and decreased LC3-II levels. Collectively, our results highlight that PQLC2 is essential for regulating mTORC1-dependent lysosomal function and autophagy, underscoring its potential role in maintaining cellular homeostasis.

Keywords:  Cathepsins; Lysosomal dysfunction; MTOR localization; MTORC1 stability; PQLC2

DOI:  https://doi.org/10.1016/j.ejcb.2026.151544
Plant Cell Environ. 2026 May 21.

Systemic and Local Regulation of Root Growth by Vascular Trehalose 6-Phosphate is Correlated With Re-allocation of Primary Metabolites Between Shoots and Roots.

Moritz Göbel, Jacqueline Foster, Philipp Westhoff, Noemi Skorzinski, Hannah L Lepper, Maria F Njo, Markus Schmid, Tom Beeckman, Miloš Tanurdžić, Anna Amtmann, Franziska Fichtner.

  Trehalose 6-phoshpate (Tre6P) is a key signalling molecule that reflects carbon status and integrates it with developmental decision making. Tre6P has been demonstrated to regulate various developmental processes, including vegetative growth, shoot branching, flowering, and root branching. Here, we investigate how vasculature-derived Tre6P influences root system architecture by expressing heterologous Tre6P synthase or Tre6P phosphatase (TPP) specifically in the plant vasculature. Plants with elevated vascular-derived Tre6P levels had smaller root systems, reduced sucrose levels, and lower root metabolite levels, whereas vascular TPP overexpression had the opposite effect. Using reciprocal grafting experiments, we identified shoot-derived vascular Tre6P to be the main driver of these systemic responses. In lines with increased Tre6P in the shoot vasculature, the shoot-to-root metabolite ratios were consistently increased, indicating that Tre6P modulates metabolite allocation and utilisation to balance carbon partitioning between shoot and root growth. Our data further suggest that vascular Tre6P contributed to optimising the carbon-to-nitrogen ratio to support growth and fitness. Besides this systemic function, this study shows that root-derived Tre6P also plays a critical local role in modulating root development. Collectively, our results demonstrate that Tre6P in the vasculature functions both systemically and locally to coordinate metabolic status with root growth and architecture.

Keywords:  resource allocation; root development; sugar partitioning; sugar signalling; trehalose 6‐phosphate

DOI:  https://doi.org/10.1111/pce.70599
Metabolomics. 2026 May 16. pii: 76. [Epub ahead of print]22(3):

Targeted metabolomics of organic and amino acids in giraffe milk during mid- to late-lactation.

G Osthoff, S Mason, E Davoren, F Deacon.

   BACKGROUND: At the end of lactation (mammary involution), dynamic changes in milk components occur in all mammals. The time to reach complete cessation varies among taxa and species. The involution of cows, sheep, and goats (Bovidae) has been reported, but limited information is available on giraffes.
OBJECTIVES: Characterise organic acids and amino acids in the milk of giraffes at involution.
METHODS: Milk was obtained from five giraffes. A LC-MS/MS metabolomics approach was followed, and statistical analysis of the data was done using MetaboAnalyst 6.0.
RESULTS: There were 38 organic acids and 45 amino acids measured in the giraffe milk. The organic acids indicate a decrease in Krebs cycle intermediates. Lower citrate levels are associated with lower lactose levels, indicating reduced osmotic regulation. Lower uracil and orotic acid indicate decreased pyrimidine synthesis and eventual nucleotide synthesis. Increased amino acid content is not devoted to protein synthesis, but to other functions, specifically as antioxidants, redox buffering, and cytoprotection. Increased histidine, serine and methionine promote protein degradation and one-carbon metabolism. Lysine catabolites lead to decreased levels of energy metabolites and to stress adaptation. Aromatic amino acids modulate the supply of immune and neuroactive metabolites.
CONCLUSIONS: During involution, the regulation of organic acids suggests reduced Krebs cycle activity, indicating a transition from high biosynthetic to catabolic activity. Likewise, amino acids have other functions, specifically antioxidant, redox-buffering, and cytoprotection.

Keywords:  Amino acids; Giraffe; Lactation; Mammary involution; Milk; Organic acids; Ruminant; Targeted metabolomics

DOI:  https://doi.org/10.1007/s11306-026-02455-z
Autophagy. 2026 May 18.

Byakangelicin alleviates metabolic dysfunction-associated steatohepatitis by selective inhibition of non-canonical MTORC1 signaling pathway.

Xiliang Du, Zhiyuan Fang, Guowen Liu, Li Wang, Lingxue Ju, Wenwen Gao, Yuxiang Song, Lin Lei, Xinwei Li.

  Metabolic dysfunction-associated steatohepatitis (MASH) is emerging as a leading cause of chronic liver disease. MTOR (mechanistic target of rapamycin kinase) complex 1 (MTORC1) is a potential therapeutic target, whereas suppression of total MTORC1 activity can lead to unwanted effects. Here, we found that byakangelicin (Bya), a natural compound, selectively inhibited MTORC1-mediated phosphorylation of TFEB (transcription factor EB), without affecting canonical MTORC1 substrates. Knockout of hepatic Tfeb blocked the alleviation effects of Bya on hepatic steatosis, inflammation, insulin resistance, and fibrosis in mice, while reintroduction of TFEB restored these effects. We identified Bya directly bound to MET370 and PHE552 of FLCN (folliculin), suppressing the function of the FLCN-FNIP1 (folliculin interacting protein 1)/FNIP2 complex, which in turn inhibited MTORC1-mediated cytoplasmic sequestration of TFEB. Mutation of FLCN (M370A and F552A) in the liver abolished Bya-induced protection against MASH. Thus, Bya is a promising therapeutic natural compound for MASH, and selective inhibition of MTORC1 is a potential approach to treat this disease.

Keywords:  Autophagy; FLCN; TFEB; fatty liver; natural compound

DOI:  https://doi.org/10.1080/15548627.2026.2676072
J Ind Microbiol Biotechnol. 2026 May 20. pii: kuag013. [Epub ahead of print]

Isolation and characterization of Saccharomyces cerevisiae mutants with ornithine accumulation for value-added craft beer brewing.

Akira Nishimura, Shota Isogai, Koya Yamada, Ryoya Tanahashi, Hiroshi Takagi.

  Ornithine is a non-proteinogenic amino acid with various health benefits, making it a promising target for functional food development. In this study, we developed the yeast Saccharomyces cerevisiae strains with elevated intracellular ornithine and identified the genetic mutation responsible for this trait. An ornithine-rich mutant was successfully isolated by chemical mutagenesis and selection for resistance to canavanine, a toxic arginine analog. Whole-genome sequencing revealed a heterozygous point mutation in the ARG6 gene encoding N-acetylglutamate kinase, a key enzyme in ornithine biosynthesis. This mutation caused a Gly351Asp substitution located in a conserved linker region between functional domains. Introduction of this substitution, along with introducing alternative amino acids at the same site, consistently increased ornithine levels in various strain backgrounds. Structural modeling suggested that this substitution could affect the enzyme conformation or inter-domain interactions. These results establish a practical non-genetically modified breeding strategy for enhancing ornithine production in yeast, which will facilitate the development of ornithine-enriched fermented beverages such as craft beer.

Keywords:   ARG6 ; Saccharomyces cerevisiae ; Craft beer; Ornithine

DOI:  https://doi.org/10.1093/jimb/kuag013