A pseudoenzyme sensor of trehalose-6-phosphate directly represses the metabolic integrator SnRK1 in plants.

October 14, 2026| Source: Cell

Trehalose-6-phosphate (T6P) is a central metabolic signal linking sugar availability to plant growth, carbon utilization, and productivity, yet its sensing and signaling mechanisms remain elusive. Using chemical biology and functional approaches, we identify the noncatalytic pseudoenzyme Class-II T6P synthase (TPS-II) as a T6P sensor in Arabidopsis. In the apo state, TPS-II dimerizes to form an autoinhibitory inter-subunit interaction. T6P binding to the N-terminal TPS-like domain triggers a conformational change that releases the C-terminal domain, enabling interaction with the central metabolic integrator SNF1-related protein kinase 1 (SnRK1) to repress its kinase activity. Loss of TPS-II genes activates catabolic and stress-responsive programs while suppressing anabolic gene expression, consistent with constitutive SnRK1 activity. Conservation of this T6P-TPS-II-SnRK1 signaling axis throughout the plant kingdom highlights its fundamental role in coupling carbon availability to metabolic homeostasis. These findings resolve a long-standing question in sugar signaling and provide a framework for improving crop carbon-use efficiency.

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The honey bee stinger: An unusual pump with collapsible double pistons.

Most stinging animals deliver venom by contracting muscles around a venom reservoir, but honey bees employ a fundamentally different strategy. The stingers of worker bees have the unique ability to autotomize, separating from the body, to continue to sting independently. Despite more than a century of anatomical descriptions, the mechanics of venom pumping have remained unresolved due to the challenges of observing them in action. We recorded high-speed videos of active, autotomized stingers, co

Health & MedicineOctober 20, 2026

Chronic cigarette smoke exposure induces distinct stem cell states driving genetic driver-specific non-small cell lung cancer subtypes.

Cigarette smoke-induced chronic inflammation (CI) potentiates development of non-small cell lung cancer (NSCLC) by mediating genetic and epigenetic events. Using normal lung organoids (LOs), we define how chronic cigarette smoke condensate (CSC) exposure drives two separate stem cell populations to evolve premalignant states harboring progressive epigenetic and linked transcriptomic abnormalities in the absence of major driver mutations. These dynamics facilitate evolution of an immune evasive s

Health & MedicineOctober 20, 2026

Cell identity competes with surface tension to determine stromal organization in tumor spheroids beyond the CAF shell paradigm.

Cancer-associated fibroblasts (CAFs) are often found forming a peripheral stromal barrier around tumors. Here, this paradigm is challenged using microfabricated 3D cancer-CAF spheroid models combined with quantitative magnetic force tensiometry. A surface tension atlas is established for eight cancer cell lines, three CAF populations, and heterotypic tumor-CAF assemblies, spanning nearly two orders of magnitude. Surface tension is first shown to govern spheroid morphology and modulate drug respo

Health & MedicineOctober 14, 2026

Sexual dimorphism in epidermal stem cell dynamics.

The epidermis is a stratified epithelium comprising proliferative basal cells and differentiated suprabasal cells that are continuously renewed throughout life. Conflicting theories have been proposed regarding the heterogeneity of the basal cell layer, with some studies proposing that all proliferative cells have self-renewal potential during homeostasis 1-5 . Meanwhile, others posit a model in which stem cell differentiation occurs through an intermediate transit-amplifying-like progenitor sta

Health & MedicineOctober 14, 2026

Engineered TYK2 dependence enables myeloid-selective IL-10 receptor agonism.

Interleukin-10 (IL-10) is a central anti-inflammatory cytokine that suppresses immune responses in myeloid cells but can also activate T cells, limiting its therapeutic use in chronic inflammatory diseases owing to narrow efficacy windows and dose-limiting toxicities 1-5 . Here we show that myeloid and T cells differ in their dependence on JAK-family kinase pairing for IL-10 signalling and function. We took advantage of this differential kinase dependence to engineer a tetravalent nanobody-based