bims-pideca Biomed News
on Class IA PI3K signalling in development and cancer
Issue of 2026–01–11
ten papers selected by
Ralitsa Radostinova Madsen, MRC-PPU



  1. bioRxiv. 2025 Dec 31. pii: 2025.12.30.697122. [Epub ahead of print]
      Primordial germ cells (PGCs) are the first cells specified in the Drosophila embryo and serve as precursors to the germline. Their formation requires suppression of somatic fates, a process achieved by excluding the receptor tyrosine kinase Torso from the posterior pole through degradation mediated by the ubiquitin ligase adaptor Germ Cell-Less (GCL). Although Torso is known to antagonize PGC formation, the underlying mechanism has remained unclear. Here, we combine optogenetic Ras activation and Ras effector loop mutants to show that Ras signaling suppresses PGC formation independently of the canonical Raf/MEK/ERK pathway. We identify an unexpected early role for Torso in activating phosphoinositide 3-kinase (PI3K), generating posterior membrane domains enriched in phosphatidylinositol (3,4,5)-trisphosphate (PIP3). Elevated PI3K activity disrupts PGC formation, while reduced PI3K activity leads to ectopic PGCs. We further demonstrate that GCL remodels the posterior pole membrane by suppressing Torso-dependent PI3K activation. Clearing PIP3 enables Myosin II enrichment, thereby constricting the pole bud for PGC formation. Together, our findings reveal how antagonistic Torso and GCL activities establish the soma-germline boundary by regulating cortical lipid organization.
    DOI:  https://doi.org/10.64898/2025.12.30.697122
  2. Biophys J. 2026 Jan 06. pii: S0006-3495(25)03512-X. [Epub ahead of print]
      RAFs initiate the cascade leading to activation of the extracellular signal-regulated kinases (ERK). In a substantial fraction of cancer cells, RAFs are the least abundant pathway proteins between receptor tyrosine kinases (RTKs) and ERK. In some cases, active RAF kinases are present at the plasma membrane at just hundreds of copies per cell, but the consequences of such limited RAF abundance are unclear. By developing continuum and stochastic computational models of the epidermal growth factor receptor (EGFR)-ERK pathway, we showed that low RAF abundance creates signaling bottlenecks between RTKs and ERK with a potential for stochastic RAF dynamics that can propagate especially to low-abundance downstream pathway proteins. RAF bottlenecks were also predicted to impede ERK activation by oncogenic RAS mutants. Advanced parameter sensitivity and Sloppiness analyses identified RAS activation and RAS-RAF interactions as strong determinants of signaling in low-RAF settings and revealed an efficient model fitting approach. This work provides quantitative insight into a common, but unexplored, regime for EGFR-ERK signaling and a systematic approach to develop and characterize dynamic models of receptor-mediated signaling.
    Keywords:  RAS mutation; Sloppiness analysis; computational modeling; epidermal growth factor receptor; parameter sensitivity; stochastic simulations
    DOI:  https://doi.org/10.1016/j.bpj.2025.12.033
  3. Blood Vessel Thromb Hemost. 2026 Feb;3(1): 100123
      Insulin is produced in the pancreas and regulates blood glucose levels by binding to the insulin receptor (IR) thereby stimulating glucose uptake into cells. Inadequate insulin production or dysregulated IR signaling leads to diabetes. Most research, to date, has focused on enhancing insulin production or correcting impaired IR signaling in tissues of nutrient exchange, for example, muscle or fat. However, the transendothelial trafficking of insulin to target tissues is also crucial in regulating organismal responses to insulin. In fact, this process has been established as the rate-limiting step for glucose disposal. Initially, it was believed that the transendothelial trafficking of insulin was dependent on endothelial IR. Unfortunately, subsequent studies have demonstrated that mice lacking endothelial IR possess minimal changes in insulin sensitivity. These studies have contributed to the widespread belief that endothelial IR does not regulate insulin trafficking and insulin sensitivity. However, recent genetic studies from our laboratory, and others, have shown that enhancing endothelial IR activity improves insulin sensitivity. These studies underscore the crucial role of endothelial IR in regulating insulin trafficking and metabolism. Now that researchers have conclusively demonstrated the presence and function of IR on endothelial cells (ECs) in vivo, it is essential to clarify why this receptor has been so controversial. Additionally, this timely review aims to encourage vascular biology researchers to explore how endothelial IR is regulated and identify new roles for this receptor on ECs.
    DOI:  https://doi.org/10.1016/j.bvth.2025.100123
  4. Cell. 2026 Jan 08. pii: S0092-8674(25)01418-7. [Epub ahead of print]
      The guanosine triphosphate (GTP)-bound state of the heterodimeric Rag GTPases functions as a molecular switch regulating mechanistic target of rapamycin complex 1 (mTORC1) activation at the lysosome downstream of amino acid fluctuations. Under low amino acid conditions, GTPase-activating protein (GAP) activity toward Rags 1 (GATOR1) promotes RagA GTP hydrolysis, preventing mTORC1 activation. KICSTOR recruits and regulates GATOR1 at the lysosome by undefined mechanisms. Here, we resolve the KICSTOR-GATOR1 structure, revealing a striking ∼60-nm crescent-shaped assembly. GATOR1 anchors to KICSTOR via an extensive interface, and mutations that disrupt this interaction impair mTORC1 regulation. The S-adenosylmethionine sensor SAMTOR binds KICSTOR in a manner incompatible with metabolite binding, providing structural insight into methionine sensing via SAMTOR-KICSTOR association. We discover that KICSTOR and GATOR1 form a dimeric supercomplex. This assembly restricts GATOR1 to an orientation that favors the low-affinity active GAP mode of Rag GTPase engagement while sterically restricting access to the high-affinity inhibitory mode, consistent with a model of an active lysosomal GATOR1 docking complex.
    Keywords:  GATOR1; KICSTOR; RAG GTPase; Rag-Ragulator; S-adenosylmethionine; SAMTOR; SZT2; cell metabolism; cryo-EM; mTORC1
    DOI:  https://doi.org/10.1016/j.cell.2025.12.005
  5. Mol Cell. 2026 Jan 07. pii: S1097-2765(25)01015-9. [Epub ahead of print]
      Mechanistic target of rapamycin complex 1 (mTORC1) is a central regulator of cell growth, responding to amino acid availability. While mTORC1 is modulated by amino acid sensors like CASTOR1, the mechanisms driving its dynamic response to fluctuating amino acid levels remain unclear. Here, we investigate the role of CASTOR2, an understudied CASTOR1 homolog, in regulating mTORC1 activity. We show that CASTOR1 and CASTOR2 bind to arginine similarly but differ in their sensitivity: CASTOR1 responds to low arginine levels, whereas CASTOR2 responds to high arginine concentrations. Both proteins interact with the GATOR2 component Mios, inhibiting its binding to GATOR1. Arginine binding to CASTOR1/2 induces conformational changes at the aspartate kinase, chorismate mutase, and TyrA (ACT) domain (ACT2-ACT4) interface, leading to its dissociation from Mios. Functionally, we demonstrate that CASTOR proteins are highly expressed in muscle tissue and, in C2C12 cells, they regulate mTORC1 and myogenesis in response to different arginine availability. These findings highlight how CASTOR proteins function as dual arginine sensors to fine-tune mTORC1 activity.
    Keywords:  CASTOR1; CASTOR2; GATOR1; GATOR2; amino acid sensor; arginine; mTORC1 signaling; myogenesis
    DOI:  https://doi.org/10.1016/j.molcel.2025.12.016
  6. J Cell Biol. 2026 Mar 02. pii: e202506139. [Epub ahead of print]225(3):
      Transcriptional control of lysosome biogenesis is an important mechanism underlying cellular adaptation to stress. It is largely unclear how cell surface changes or signals induce alteration in lysosome numbers. By developing a Caenorhabditis elegans-based heterologous TFE3 activation system, we here identify the non-receptor tyrosine kinases SRC-1/-2 (C. elegans) and FGR (mammals) as critical regulators of lysosome biogenesis. In C. elegans, inactivation of src-1/-2 leads to nuclear enrichment of ectopically expressed TFE3 and increased intensity of lysosomal markers. In mammalian cells, FGR inhibition or deficiency similarly results in TFEB/TFE3-dependent lysosomal increase. FGR acts through AKT2 by promoting the activation of the latter. FGR associates with the plasma membrane but is internalized onto endosomes and reaches lysosomes along the endosome-lysosome pathway following endocytosis. Lysosomal FGR promotes AKT2 recruitment to lysosomes, where it phosphorylates TFEB/TFE3 to prevent their activation. Together, these findings reveal a plasma membrane-to-lysosome signaling axis that is required for endocytosis-associated lysosome homeostasis.
    DOI:  https://doi.org/10.1083/jcb.202506139
  7. Nature. 2026 Jan 07.
      Cancer metastasis is a major contributor to patient morbidity and mortality1, yet the factors that determine the organs where cancers can metastasize are incompletely understood. Here we quantify the absolute levels of 124 metabolites in multiple tissues in mice and investigate how this relates to the ability of breast cancer cells to grow in different organs. We engineered breast cancer cells with broad metastatic potential to be auxotrophic for specific nutrients and assessed their ability to colonize different tissue sites. We then asked how tumour growth in different tissues relates to nutrient availability and tumour biosynthetic activity. We find that single nutrients alone do not define the sites where breast cancer cells can grow as metastases. In addition, we identify purine synthesis as a requirement for tumour growth and metastasis across many tissues and find that this phenotype is independent of tissue nucleotide availability or tumour de novo nucleotide synthesis activity. These data suggest that a complex interplay between multiple nutrients within the microenvironment dictates potential sites of metastatic cancer growth, and highlights the interdependence between extrinsic environmental factors and intrinsic cellular properties in influencing where breast cancer cells can grow as metastases.
    DOI:  https://doi.org/10.1038/s41586-025-09898-9
  8. Trends Cancer. 2026 Jan 02. pii: S2405-8033(25)00311-5. [Epub ahead of print]
      Cancer cells often retain lineage- and tissue of origin-specific programs established prior to malignant transformation. This observation has been elaborated by advances in single-cell and lineage-tracing technologies, which provide high-resolution mapping of these features. Here, we provide an overview of these recent technological developments and examine how the tissue of origin shapes tumor behavior and vulnerabilities. We discuss how the preferential selection of oncogenic drivers by specific tissues leads to distinct genetic alterations across cancers. We then explore the continued dependence of cancer cells on lineage-specific physiological functions and signaling pathways, thereby revealing lineage-dependent therapeutic targets. Finally, we highlight how lineage-specific cell surface marker expression informs precision immunotherapies. Together, these insights are driving a shift toward therapies tailored to the developmental and functional identities of cancer cells.
    Keywords:  cancer specialized function; high-resolution mapping; lineage dependencies; lineage-tracing systems; precision oncology; targeted therapies; tissue-selective oncogenic drivers; tumor antigen repertoire for advanced T cell therapies; tumor tissue of origin
    DOI:  https://doi.org/10.1016/j.trecan.2025.12.004
  9. bioRxiv. 2026 Jan 03. pii: 2026.01.03.697314. [Epub ahead of print]
      RNA velocity is a computational framework for single-cell RNA sequencing (scRNA-seq) that estimates the future transcriptional state of individual cells, thereby capturing the direction and rate of cell state transitions rather than providing a purely static snapshot. Since its introduction in 2018, multiple RNA velocity methods have been developed, differing in their modeling assumptions, required inputs, computational complexity, and robustness. However, there remains limited consensus on how best to evaluate these methods or on which tools are most reliable under specific biological and technical settings. Here, we perform a systematic comparison of 29 velocity inference algorithms across 114 simulated datasets with known ground-truth cell dynamics and 62 real scRNA-seq datasets, and we extend the evaluation to spatial and multi-omics levels where velocity is increasingly applied. We benchmark RNA velocity methods using a unified framework that decomposes performance into four practical dimensions: accuracy, scalability, stability, and usability. Our results show that performance rankings vary substantially across metrics and datasets, indicating no single method is uniformly optimal and that practical deployment is often constrained by feasibility and robustness as much as by accuracy. Based on these results, we provide actionable guidance for selecting RNA velocity tools according to data modality, available priors, and computational constraints. Finally, we identify key bottlenecks that currently limit RNA velocity development and deployment, including scalability to large size of datasets, sensitivity to gene selection, and the lack of genuinely multimodal and spatially explicit velocity models for spot-based technologies.
    DOI:  https://doi.org/10.64898/2026.01.03.697314
  10. bioRxiv. 2025 Dec 23. pii: 2025.12.20.695697. [Epub ahead of print]
      mTORC1 coordinates cellular growth and metabolism by integrating inputs from both amino acids and growth factors, and its activation requires two upstream branches involving the Rag GTPases and the Rheb GTPase. These branches are regulated by distinct GAP complexes: GATOR1 (Depdc5-Nprl2-Nprl3) inhibits RagA/B, and TSC (TSC1-TSC2-TBC1D7) inhibits Rheb. Despite the prevailing view that these pathways converge only at mTORC1 itself, several observations suggest upstream crosstalk. This gap is especially striking in organisms like C. elegans and S. cerevisiae that lack the TSC complex yet maintain fully responsive mTORC1 signaling. How these inputs are dynamically coordinated under complex physiological conditions and in organisms lacking the key components remain unknown. We performed unbiased quantitative proteomics in C. elegans and identified the GATOR1 complex as a previously unrecognized RHEB-1 ( C. elegans ortholog of Rheb) interactor. Through biochemical validation in human cells, we show that nucleotide-free Rheb associates with the Nprl2-Nprl3 subunits of GATOR1, whereas GTP-bound or membrane-detached Rheb mutants fail to bind. Nutrient stress, but not direct pharmacologic inhibition of mTORC1, robustly induced this interaction. In TSC2-null cells, where Rheb is constitutively GTP-loaded, Rheb-Nprl2/3 binding was strongly diminished and was restored by expressing the nucleotide-free Rheb S20N mutant, demonstrating that Rheb's nucleotide state governs this interaction. Pulldown assays confirmed that the Nprl2/3 heterodimer is sufficient for binding nucleotide-free Rheb. Structural modeling using AlphaFold3 consistently positioned Rheb at a conserved site on Nprl3 distinct from the RagA/B GAP-active surface of Nprl2, supporting a non-catalytic mode of association. Together, these findings identify a conserved, nutrient-regulated physical interaction between Rheb and the Nprl2/3 subunits of GATOR1, revealing a previously unrecognized point of convergence between the growth factor and amino acid branches of the mTORC1 pathway. This model provides a direct molecular link between the Rag and Rheb branches, furthering our understanding of how nutrient stress fine-tunes mTORC1 signaling.
    DOI:  https://doi.org/10.64898/2025.12.20.695697