bims-plator Biomed News
on Plant TOR
Issue of 2026–04–19
six papers selected by
Christian Meyer, INRAE
  1. A conserved translational repression module buffers sugar-inducible root vascular proliferation.
  2. Role of AtCPK5 and AtCPK6 in the regulation of the plant immune response triggered by rhamnolipids in Arabidopsis.
  3. Light as the Master Regulator: Photoreceptor-Mediated Pathways in Hormonal and Epigenetic Switches of Fruit Ripening.
  4. A Plant Virus Glycoprotein Induces Autophagy by Activating the Toll7 Immune Pathway in Its Insect Vector.
  5. Identification of a plasma membrane complex that interacts with phyB to regulate ROS production.
  6. An Arabidopsis receptor-like kinase mediates competitive plant-plant interactions.
  1. Mol Plant. 2026 Apr 13. pii: S1674-2052(26)00113-9. [Epub ahead of print]
    A conserved translational repression module buffers sugar-inducible root vascular proliferation.
    Sangkyu Choi, Hyun Seob Cho, Seungchul Lee, Hoyoung Nam, Garam Lee, Heejae Nam, Sion Bae, Ildoo Hwang.
      Balancing vascular proliferation with sugar availability is essential for optimal carbon allocation; however, the molecular signaling networks integrating sugar status into vascular development remains unclear. Here, using histological, genetic, and pharmacological analyses in the Arabidopsis root, we demonstrate that sugar acts as an instructive signal to drive vascular proliferation. Sugar primes cell proliferation and the gene regulatory networks required for vascular development through the TARGET OF RAPAMYCIN (TOR) pathway. We further uncover that this sugar-driven vascular program incorporates a translational repression module comprising the RNA-binding protein JULGI1 (JUL1) and its target, CLAVATA3/ESR-RELATED41 (CLE41) mRNA. This regulation is mediated by a conserved guanine-rich motif in the CLE41 5' UTR, which enables JUL1 binding and imposes a negative feedback regulation on vascular proliferation. Furthermore, phylogenetic and cross-species analyses indicate that the JUL1-CLE41 module is conserved across cambium-bearing plant lineages. Collectively, these findings establish that sugars directly activate vascular growth, while the JUL1-CLE41 module constrains this response to ensure balanced proliferation under sugar-rich conditions. Our work provides a framework for viewing vascular proliferation as a sugar-responsive developmental process buffered by intrinsic regulatory mechanisms to maintain homeostasis, a principle that may underlie the evolutionary refinement of sugar-responsive vascular growth strategies.
    Keywords:  RNA-binding protein; Sugar; cambial homeostasis; peptide signaling; translational repression; vascular proliferation
    DOI:  https://doi.org/10.1016/j.molp.2026.04.004
  2. PLoS One. 2026 ;21(4): e0346370
    Role of AtCPK5 and AtCPK6 in the regulation of the plant immune response triggered by rhamnolipids in Arabidopsis.
    Juliette Stanek, Olivier Fernandez, Marie Boudsocq, Dina Aggad, Sandra Villaume, Laetitia Parent, Sandrine Dhondt-Cordelier, Jérôme Crouzet, Stéphan Dorey, Sylvain Cordelier.
      Rhamnolipids (RLs) are bacterial glycolipids with potential applications in the biocontrol of plant pathogens. Although RLs are known to activate plant immune responses, the underlying signaling mechanisms remain poorly understood. Calcium-dependent protein kinases (CPKs) are a large family of kinases involved in various functions in plants including signaling of the plant immunity. Here, we investigated the contribution of AtCPK5 and AtCPK6 to RL-triggered immunity in Arabidopsis. RL treatment induced the expression of both AtCPK5 and AtCPK6 genes in Arabidopsis leaves. Functional analyses revealed that RL-induced responses, including reactive oxygen species production and the expression of defense-related genes (AtWRKY46, AtFRK1 and AtPR1), were enhanced in cpk5/6 mutants compared to wild-type plants. The cpk5 mutant exhibited intermediate responses, whereas cpk6 alone had little effect, except on AtFRK1 expression, indicating a predominant role for AtCPK5 in regulating RL-triggered signaling. However, cpk5/6 mutations did not affect RL-induced electrolyte leakage or RL-mediated resistance to Pseudomonas syringae pv. tomato DC3000. Together, these results suggest that AtCPK5 and AtCPK6 negatively modulate RL-triggered immune signaling, while additional components contribute to the regulation of downstream defense responses.
    DOI:  https://doi.org/10.1371/journal.pone.0346370
  3. Physiol Plant. 2026 Mar-Apr;178(2):178(2): e70881
    Light as the Master Regulator: Photoreceptor-Mediated Pathways in Hormonal and Epigenetic Switches of Fruit Ripening.
    Sayan Pal, Abir Das, Malay Kumar Adak.
      Fruit ripening, the penultimate stage before senescence, is exclusively regulated by light, which signals and activates ripening-specific genes. Building on light's regulatory role in development, this review updates on signaling pathways, including phytochrome, cryptochrome, phototropins, and wavelength receptors, that are involved in gene activation during ripening. Understanding CONSTITUTIVE PHOTOMORPHOGENIC 1 (COP1) and ELONGATED HYPOCOTYL 5 (HY5) as the principal hub of light perception and downstream modulation for transcriptome, proteome, and metabolome activities, the synergism of hormonal influence is discussed. The precise wavelengths of light and their effects on major growth hormones, such as ethylene, abscisic acid (ABA), and auxin, are discussed in relation to the progression of ripening metabolism and the regulation of specific transcription factors. This review points out regulatory factors like ETHYLENE RESPONSE FACTOR E4 to alter auxin's promoter binding activity, allowing ethylene sensitivity. The major focus is on ethylene response factors, MADS-box genes, and bZIP proteins for the molecular regulation of ripening-induced fruit coat hydrolysis, aroma production, and respiratory burst. The genetic mutation was elucidated in the context of the RIPENING INHIBITOR (RIN) and NON-RIPENING (NOR) factors in tomato genotypes, which share similar sequences with other crops, such as strawberry. The review also highlights epigenetic control through chromatin remodeling, methylation/demethylation reactions, and histone modifications, providing further insight into the light's influence on the extra-transcriptome affair. Collectively, this review concludes that light is a major molecular switch in pathways of hormonal, genetic, and epigenetic functions, contributing to advances in postharvest preservation.
    Keywords:  chromatin remodeling; hormonal crosstalk; photoreceptor signaling; ripening metabolism; transcription factors
    DOI:  https://doi.org/10.1111/ppl.70881
  4. Mol Plant Pathol. 2026 Apr;27(4): e70259
    A Plant Virus Glycoprotein Induces Autophagy by Activating the Toll7 Immune Pathway in Its Insect Vector.
    Yu-Juan He, Yu-Hua Qi, Can Wang, Gao-Yang Jiao, Zhuang-Xin Ye, Lin Lin, Qian-Zhuo Mao, Gang Lu, Xiao-Wei Wang, Chuan-Xi Zhang, Jian-Ping Chen, Jun-Min Li.
      The Toll7 pathway is crucial in defending against diverse pathogenic microorganisms, including viruses. This study reveals that a plant virus (rice stripe virus, RSV) infection activates Toll7-mediated antiviral response in the insect vector Laodelphax striatellus. We identified a specific interaction between the TIR domain of Toll7 and RSV glycoprotein (Gc). Furthermore, Toll7 silencing significantly enhanced RSV replication and acquisition, suggesting its antiviral role in L. striatellus. Transcriptomic analysis indicated that Toll7 negatively regulates the PI3K-Akt-mTOR pathway, a key autophagy regulator. Toll7 knockdown upregulated the expression of PI3K, Akt and mTOR; simultaneously, autophagy-related genes (Atg3, Atg5, Atg8, Atg9, Torc1 and ULK1) were downregulated and autophagy inhibitor Sqstm1 was upregulated. Conversely, silencing PI3K, Akt or mTOR suppressed RSV replication, highlighting the essential role of this pathway in viral persistence within its vector. These findings demonstrate that Toll7-mediated inhibition of the PI3K-Akt-mTOR pathway activates autophagy, restricting RSV replication in L. striatellus. This study uncovers a conserved Toll7-dependent antiviral mechanism modulating autophagy to inhibit viral infection, offering new insights into the co-evolutionary dynamics between plant viruses and insect vectors.
    Keywords:   Laodelphax striatellus ; PI3K‐Akt–mTOR pathway; Toll7; autophagy; glycoprotein; rice stripe virus
    DOI:  https://doi.org/10.1111/mpp.70259
  5. Plant Physiol. 2026 Apr 15. pii: kiag214. [Epub ahead of print]
    Identification of a plasma membrane complex that interacts with phyB to regulate ROS production.
    Devasantosh Mohanty, Yosef Fichman, María Ángeles Peláez-Vico, Ronald J Myers, Maya Sealander, Ranjita Sinha, Johanna Morrow, Ron Eckstein, Kate Olson, Chunhui Xu, Hong An, Chan Yul Yoo, Jian-Kang Zhu, Chunzhao Zhao, Sara I Zandalinas, Emmanuel Liscum, Ron Mittler.
      Reactive oxygen species (ROS) regulate plant growth, development, and responses to the environment. ROS production by the RESPIRATORY BURST OXIDASE PROTEIN D (RBOHD) protein is regulated by PHYTOCHROME B (phyB), and phyB is phosphorylated by FERONIA, highlighting the possibility that these three proteins interact to regulate ROS levels during stress. We used immunoprecipitation and proximity labelling, followed by split-luciferase and functional validation assays, to study interactions among FERONIA, phyB, and RBOHD under excess light (EL) stress in Arabidopsis (Arabidopsis thaliana). We found that phyB, RBOHD and FERONIA interact, that phosphorylation of phyB by FERONIA, as well as the kinase activity of FERONIA, are required for RBOHD-driven ROS production in response to EL stress, and that CYSTEINE-RICH RECEPTOR LIKE KINASE 10 (CRK10) and PLASMA MEMBRANE INTRINSIC PROTEIN 2;6 (PIP2;6) interact with RBOHD and phyB and are also required for EL-driven RBOHD ROS production. Our findings uncover a putative plasma membrane complex between FERONIA, RBOHD, CRK10, and PIP2;6 that interacts with phyB to regulate ROS production in Arabidopsis in response to stress. This complex could play a canonical role in the integration and regulation of multiple signaling pathways in plants.
    Keywords:  Feronia; Light stress; Phytochrome B; Reactive oxygen species (ROS); Respiratory burst oxygen homolog (RBOH)
    DOI:  https://doi.org/10.1093/plphys/kiag214
  6. J Exp Bot. 2026 Apr 16. pii: erag172. [Epub ahead of print]
    An Arabidopsis receptor-like kinase mediates competitive plant-plant interactions.
    Cyril Libourel, Marie Invernizzi, Fabrice Roux, Mathieu Hanemian, Dominique Roby.
      While competition among plant species is recognized as a major factor affecting crop yield and plant community dynamics, the genetic and molecular mechanisms underlying natural variation of such biotic interactions remain poorly characterized. Here, we report the cloning of a Quantitative Trait Locus previously detected in a Genome-Wide Association Study investigating the competitive response of Arabidopsis thaliana to the presence of the annual bluegrass weed species Poa annua. Using mutant and complementation strategies, we identified ESCAPE 1 (ESC1) as the gene responsible for the natural variation of an escape strategy of A. thaliana in response to the presence of P. annua. ESC1 encodes a proline-rich, extensin-like receptor kinase, also known as PERK13. An RNA-seq experiment revealed that PERK13 functions through different pathways in leaves and roots involving genes associated with responses to biotic and abiotic stresses. Using these RNA-seq together with yeast two-hybrid (Y2H) data, protein-protein interaction network reconstruction revealed two distinct decentralized protein networks in leaves and roots. These findings support the notion of an active response mechanism involved in neighbor detection. The functional validation of ESC1 underlying natural variation in response to competition opens new avenues for a better understanding of the molecular dialogue involved in plant-plant interactions.
    Keywords:   Arabidopsis thaliana ; competitive response; natural variation; plant-plant interactions; receptor-like kinase
    DOI:  https://doi.org/10.1093/jxb/erag172
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