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

Creative Commons Attribution 4.0 License
This work is licensed under a Creative Commons Attribution 4.0 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

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.

Download

Share

COinS