Disease-related phenotypes in a Drosophila model of hereditary spastic paraplegia are ameliorated by treatment with vinblastine
J. Clin. Invest. Genny Orso, et al. 115:3026 doi:10.1172/JCI24694 [Go to this article.]

Figure 5
Neuronal expression of pathological mutant Dspastin K467R and Dspastin RNAi induce an analogous hyperstabilization of microtubules. (A) Images of NMJ immunocytochemistry using an anti-HRP antibody (red; middle panels), a neuronal maker of the presynaptic arbor, and an anti–acetylated α-tubulin antibody (AcTub, green; left panels), present only in stable microtubules (33), demonstrate that nervous system expression of Dspastin K467R induced accumulation of stabilized microtubules, as indicated by the dramatic increase of acetylated α-tubulin signal compared with controls (Elav-Gal4/+ and UAS-Dspastin-K467R/+). (B) Quantification of the data in A revealed that this increase was statistically significant and comparable to that caused by RNAi knockdown of Dspastin. Values were normalized as described in Methods. *P < 0.0001. Scale bar: approximately 10 μM.