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Role of NudE in transporting Golgi outposts during dendrite morphogenesis
Author(s) -
Abellaneda Allison,
Arthur Ashley,
Yang Sihui,
Wildonger Jill
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.884.18
Subject(s) - dynein , golgi apparatus , microbiology and biotechnology , kinesin , dendrite (mathematics) , organelle , axoplasmic transport , biology , morphogenesis , motor protein , dynactin , nude mouse , cytoplasm , microtubule , endoplasmic reticulum , cell culture , biochemistry , genetics , geometry , mathematics , gene
Dynein and kinesin motor proteins are cells' primary method of transporting cargo, but our knowledge of transport regulation is incomplete. Misregulation of transport in neurons causes multiple different human neurological diseases. NudE and Lis1 are protein cofactors that bind to and regulate dynein. We are using the Drosophila melanogaster dendritic arborization (da) neurons as a model to investigate how motor complexes that include NudE transport cargo in developing neurons. Previous work showed that mutations affecting cytoplasmic dynein increase the number of dendritic branches that form close to the cell body and perturb the positioning of organelles within dendrites. Our studies reveal that the loss of NudE disrupts dendrite growth and branching similar to the loss of dynein function. Our preliminary data show that Golgi outposts, which are involved in dendrite growth, are transported with the participation of NudE in dendrites. This leads us to hypothesize that NudE is required for the proper localization of Golgi outposts during dendrite morphogenesis. Our data also reveal that overexpression of Lis1 rescues the dendrite growth and branching defects in neurons lacking NudE, and we are investigating how NudE and Lis1 might coordinately regulate Golgi outpost distribution. Additionally, we are determining if NudE assists in the transport of other vesicles and organelles that are also important for neuronal function. Understanding the basics of how the NudE/Lis1/dynein motor complex acts in da neurons will aid in understanding how transport is regulated and will also provide insight into human diseases caused by motor protein dysfunction.