Radulovic et al. show that phosphatidylinositol 3-phosphate (PI3P), produced by the phosphatidylinositol 3-kinase PIK3C3, is formed on ER domains after lysosome damage. ER domain PI3P helps to recruit...

Mitochondrial ATP production is essential for life. Mitochondrial function depends on the spatio-temporal coordination of nuclear and mitochondrial genome expression, yet how this coordination occurs ...

The ULK1 complex (ULK1C) and the class III phosphatidylinositol 3-kinase complex I (PI3KC3-C1) act together to initiate autophagy. Human ULK1C consists of ULK1 itself, FIP200, and the HORMA domain het...

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The 2026 Gordon Research Conference on Autophagy in Stress, Development and Disease will be held in Ventura, California. Apply today to reserve your spot.

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Cryo-electron microscopy was used to study human mechanistic target of rapamycin complex 1 (mTORC1) activation on lysosomal membranes, showing progressive recruitment by RAG–Ragulator, RHEB and R...

Nature Reviews Molecular Cell Biology, Published online: 04 August 2025; doi:10.1038/s41580-025-00873-wLysosomes degrade cellular components, and their membrane is an important signalling hub. Recent insights into the mechanisms that maintain lysosomal membrane homeostasis — including the interplay between membrane damage, repair, lysophagy and lysosome biogenesis — highlight their importance in physiology, in disease and during ageing.

Republicans on spending committee push back against proposed reorganization and overhead cuts

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This Review examines recently gained insights into the roles of ESCRT complexes in viral infection, immunity, cancer and neurological disease.

Nature Structural & Molecular Biology, Published online: 29 May 2025; doi:10.1038/s41594-025-01557-xAutophagy is initiated by the Unc-51-like kinase protein kinase complex (ULK1C) and class III phosphatidylinositol 3-OH kinase complex I (PI3KC3-C1). Here, the authors reveal the structure of the 2:1:1 core of ULK1C and its complex with PI3KC3-C1. ULK1C transitions to a 2:2:2 complex in the presence of PI3KC3-C1, suggesting a mechanism for autophagy induction.

The first on-demand CRISPR therapy for an infant with a rare metabolic disease developed by the IGI and collaborators around the world.