Document Type
Article
Publication Date
12-2018
Journal Title
Molecular and Cellular Neuroscience
Issue Number
93
First Page
10
Last Page
17
Version
Publisher PDF: the final published version of the article, with professional formatting and typesetting
Creative Commons License
This work is licensed under a CC BY License.
Disciplines
Biology | Cell Biology | Laboratory and Basic Science Research | Molecular and Cellular Neuroscience
Abstract
Expansions of polygutamine-encoding stretches in several genes cause neurodegenerative disorders including Huntington's Disease and Spinocerebellar Ataxia type 3. Expression of the human disease alleles in Drosophila melanogaster neurons recapitulates cellular features of these disorders, and has therefore been used to model the cell biology of these diseases. Here, we show that polyglutamine disease alleles expressed in Drosophila photoreceptors disrupt actin structure at rhabdomeres, as other groups have shown they do in Drosophila and mammalian dendrites. We show this actin regulatory pathway works through the small G protein Rac and the actin nucleating protein Form3. We also find that Form3 has additional functions in photoreceptors, and that loss of Form3 results in the specification of extra photoreceptors in the eye
Digital USD Citation
Vu, Annie; Humphries, Tyler; Vogel, Sean; and Haberman, Adam, "Polyglutamine repeat proteins disrupt actin structure in Drosophila photoreceptors." (2018). Biology: Faculty Scholarship. 30.
https://digital.sandiego.edu/biology_facpub/30
Included in
Biology Commons, Cell Biology Commons, Laboratory and Basic Science Research Commons, Molecular and Cellular Neuroscience Commons
Notes
Published in final form at:
Vu, Annie, Tyler Humphries, Sean Vogel, Adam Haberman. Polyglutamine repeat proteins disrupt actin structure in Drosophila photoreceptors. Molecular and Cellular Neuroscience, 93. 2018. doi: 10.1016/j.mcn.2018.08.005.