TMEM55B promotes anterograde transport and distal axonal distribution of LAMP1-positive organelles

TMEM55B loss in cortical neurons and mouse brains disrupts LAMP1-positive lysosome positioning, causing abnormal clustering and tubulation, and impairs bidirectional transport in distal axons.

• Why it matters: Lysosomal trafficking is essential for post-mitotic neuron survival, yet how axonal LAMP1-positive organelles are positioned and transported in vivo remains unclear.
• What they did: The study generated viable Tmem55b knockout mice and depleted TMEM55B in primary rat neurons to measure lysosomal tubulation and transport, linking defects to disrupted JIP4 function.
• The result: TMEM55B deficiency did not cause neurodegeneration, behavioral deficits, or reduced lifespan in mice, while C. elegans Y71H2AM.2 mutants and Tmem55a/b double-knockouts support conserved, JIP4-dependent lysosome distribution roles.