Chan Choo Yap

Contradictory Results doi: https://doi.org/10.1101/2023.03.08.531742 Abstract In neurons, degradation of dendritic cargos requires RAB7 and dynein-mediated retrograde transport to somatic lysosomes. In order to test if the dynein adaptor RILP (RAB-interacting lysosomal protein) mediated the recruitment of dynein to late endosomes for retrograde transport in dendrites, we obtained several knockdown reagents previously validated in non-neuronal cells.

A dominant dendrite phenotype caused by the disease-associated G253D mutation in doublecortin (DCX) is not due to its endocytosis defect Chan Choo Yap‡, Laura Digilio‡, Kamil Kruczek§1, Matylda Roszkowska¶2, Xiao-qin Fu‖3, Judy S.

Doublecortin (DCX[1]) is a protein needed for cortical development, and DCX mutations cause cortical malformations in humans. The microtubule-binding activity of DCX is well described and is important for its function, such as supporting neuronal migration and dendrite growth during development. Previous work showed that microtubule binding is not sufficient for DCX-mediated promotion of dendrite growth, and that domains in DCX’s C-terminus are also required.