Date: 4 March 2026 (Wednesday)
Time: 3:00 pm – 4:00 pm
Venue: Mrs Chen Yang Foo Oi Telemedicine Centre, 2/F, William M.W. Mong Block, 21 Sassoon Road
Host: Professor Michael Hӓusser

Volker Haucke received his PhD summa cum laude in 1997 from the University of Basel, Switzerland. Following postdoctoral studies at Yale he started his own laboratory at the University of Göttingen. Since 2012 Volker Haucke is director at the Leibniz Forschungsinstitut für Molekulare Pharmacologie (FMP), full professor of molecular pharmacology at FU Berlin and a member of the NeuroCure Cluster of Excellence. 

The focus of research in his laboratory is the dissection of the molecular mechanisms of endocytosis and endolysosomal membrane dynamics and its role in the nervous system and in neurological diseases using biochemical and cell biological approaches, electrophysiology, chemical biology, super-resolution and electron microscopy as well as genetics. Among his major discoveries are the identification of novel lipid conversion mechanisms that control exo-endocytosis (1,2), nutrient signaling (3,4), lysosome function (5,6), and presynapse formation via axonal transport of a lysosome-related precursor organelle (7). His lab has identified important pathways for the control of neurotransmission by endocytic proteins (8) and by neuronal autophagy (9) and developed small molecule inhibitors of endocytosis (10). 

Prof. Haucke is an elected member of the European Molecular Biology Organisation (EMBO), the Academy of Europe (AE), the German National Academy of Science Leopoldina, and the Berlin-Brandenburg Academy of Science (BBAW). He has received the Avanti Award of the American Society for Biochemistry and Molecular Biology (ASBMB) 2017, the Feldberg Prize for Research in Physiology and Pharmacology 2020, the Gottfried-Wilhelm-Leibniz Prize 2025, and the Ernst-Schering Prize 2025. 

Selected publications:

1. Bolz, S., et al Haucke, V. (2023) Neuron 111, 3765-3774.e7
2. Ketel, K., et al, Haucke, V. (2016) Nature, 529, 408-412
3. Marat, A.L., et al Haucke, V. (2017) Science, 356, 968-972
4. Jang, W., et al Haucke, V. (2022) Science 378, eabq5209.
5. Ebner, M., et al Haucke, V. (2023) Cell 186, 5328-5346.
6. Lopez-Hernandez, T. et al Haucke, V. (2020) Nat Cell Biol 22, 815-827.
7. Rizalar, F.S., et al Haucke, V. (2023) Science 382 (6667), 223-230.
8. Soykan, T., et al Haucke, V. (2017) Neuron, 93, 854-866
9. Kuijpers, M., et al Haucke, V. (2021) Neuron, 109, 299-313
10. von Kleist, L., et al Haucke, V. (2011) Cell 146, 471-484

Phosphoinositides (PIs) form a minor class of phospholipids with crucial functions in cell physiology, ranging from cell signalling and motility to a role as signposts of compartmental membrane identity and dynamics. In fed cells, phosphatidylinositol 3-phosphates are present at the plasma membrane and within the endosomal system, where they serve as key regulators of both cell signaling and of intracellular membrane dynamics, while PI 4-phosphates delineate the secretory pathway. 

In the first part of my talk I will present our recent insights into the function of specific phosphoinositide lipids in the formation and function of synapses in stem cell-derived human neurons. Nervous system function relies on the polarized architecture of neurons, established by directional transport of pre- and postsynaptic cargoes. While delivery of postsynaptic components depends on the secretory pathway, the identity, composition and ultrastructure of the membrane compartment(s) that supply presynaptic vesicle (SV) proteins is largely unknown. I will discuss our recent advances in our understanding of how key components of the presynaptic machinery for neurotransmitter release are transported and assembled focussing on our studies in genome-engineered human induced pluripotent stem cell-derived neurons. Our findings identify a crucial signaling lipid-dependent mechanism mediating the delivery of SV and active zone proteins to developing synapses. 

In the second part of my talk, I will discuss how the various activities of lysosomes in mediating anabolic growth signaling and the catabolic turnover of macromolecules (e.g. to counteract neurodegeneration) are controlled by signaling membrane lipids, e.g. in response to various kinds of stress such as starvation or membrane damage. Our data unravel a signaling lipid-based network orchestrated by the disease-associated phosphatidylinositol 3-phosphate [PI(3)P] 3-phosphatase MTMR14 that couples lysosomal membrane repair, remodeling, and removal pathways to cellular proteostasis by local control of mechanistic target of Rapamycin complex 1 (mTORC1) activity. We demonstrate that MTMR14 is recruited to damaged lysosomes through a calcium-dependent interaction between its C-terminal disordered domain and scrambled sphingomyelin. This interaction triggers a local signaling lipid switch that represses nutrient signaling and protein translation, while promoting membrane repair. Disruption of this pathway compromises cellular resilience to lysosomal damage. Our findings reveal a lipid-driven circuit that choreographs membrane repair and proteostasis to maintain cellular health.

Related references

1. Witkowska, A. et al Haucke, V.* (2026) Mechanical control of neurotransmission via disordered endocytic protein domain. Nat. Cell Biol, in revision
2. Su, Y. et al Haucke, V.* (2026) A phosphoinositide phosphatase orchestrates the lysosomal damage response. Science, under review
3. Russo, G. et al Haucke, V.*, Krauss, M.* (2026) Nanoscale PI(4,5)P2 synthesis by septin-associated PIPKIg isoforms controls centralspindlin association with the midbody during cytokinesis. Nat Commun 17, 1482. doi.org/10.1038/s41467-026-69224-3 [*co-corresponding last authors]
4. Ebner, M. et al, Haucke, V. (2023) Nutrient regulated control of lysosome function by signaling lipid conversion. Cell 186, 5328-5346. doi: 10.1016/j.cell.2023.09.027
5. Rizalar, F.S. et al Haucke, V. (2023) Phosphatidylinositol 3,5-bisphosphate-controlled vesicle transport directs presynapse assembly. Science 382 (6667), 223-230. DOI: 10.1126/science.adg1075
6. Jang, W. et al Haucke, V. (2022) Endosomal lipid signalling reshapes the endoplasmic reticulum to control mitochondrial function. Science 378, eabq5209 (2022). DOI: 10.1126/science.abq5209 

All are welcome.