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ROLE OF THE SERINE-THREONINE KINASE NDR2 IN NEURONAL PRIMARY CILIA FORMATION AND AUTOPHAGY
Anastasia Schöneand 3 co-authors
IBIO Magdeburg Institut für Biologie
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS05-09AM-218
Presentation
Date TBA
Board: PS05-09AM-218
Event Information
Poster Board
PS05-09AM-218
Poster
View posterAbstract
Role of the serine-threonine kinase Ndr2 in neuronal primary cilia formation and autophagy.
The nuclear Dbf2-related kinase 2 (NDR2), a member of the NDR/LATS kinase family, controls neuronal development including axon specification, dendritic growth, as well as synapse formation and plasticity. Recently, NDR2 has been identified as a key organizer of the neuronal primary cilium (NPC), a microtubule-based sensory organelle that coordinates major signalling pathways. In neurons, the primary cilium acts as a central signalling hub supporting cellular maintenance, plasticity and autophagy. Moreover, NPC deteriorate with age and in models of Alzheimer’s and Parkinson’s disease, where NPC dysfunction exacerbates the neuropathology. We here demonstrate an elongation of NPC in hippocampal primary neurons, as well as in the CA1 and CA3 hippocampal region of Ndr2 null mutant mice in vivo. Furthermore, Ndr2 deficiency
uncouples primary cilia length from normal autophagic-endosomal regulation. Given the previous reports NDR2 participation in autophagy, we hypothesize that NDR2 functions as a molecular nexus linking these two homeostatic systems. Therefore, and to examine its role in human neuronal cells, we silence NDR2 in neuronally differentiated human induced pluripotent stem cells. To examine ciliary integrity and cilium-dependent autophagy, we determine ciliation frequency and cilia length and evaluate autophagic flux with LC3 and p62/SQSTM1 analysis. Our data shed light on the role of NDR2 in the interaction of ciliary signalling and autophagy, and their role in defective environmental sensing and proteostasis failure ultimately driving age-related neuronal vulnerability and neurodegeneration.
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