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.

多个基因中多聚谷氨酰胺编码序列的扩展会导致神经退行性疾病，包括亨廷顿病和脊髓小脑共济失调 3 型。黑腹果蝇神经元中人类疾病等位基因的表达概括了这些疾病的细胞特征，因此已被用于模拟这些疾病的细胞生物学疾病。在这里，我们展示了在果蝇光感受器中表达的多聚谷氨酰胺疾病等位基因破坏了横纹肌的肌动蛋白结构，正如其他研究小组在果蝇中所做的那样和哺乳动物的树突。我们展示了这种肌动蛋白调节途径通过小 G 蛋白 Rac 和肌动蛋白成核蛋白 Form3 起作用。我们还发现 Form3 在光感受器中具有额外的功能，并且 Form3 的丢失导致眼睛中额外的光感受器的规范。