Fig 1: MARK4 increase tau‐induced neurodegeneration more strongly than other MARKs. (a,b) Representative images of paraffin sections of fly retina stained with hematoxylin and eosin. (a) Representative images of the retina expressing MARK1, 2, 3, or 4 driven by GMR‐GAL4 without human tau expression. The control flies expressed GFP driven by GMR‐GAL4. (b). Representative images of fly retina co‐expressing MARK 1, 2, 3, or 4 with human tau. Neurodegeneration was identified by the presence of vacuoles (arrows). Scale bar = 20 μm. (c) Quantification of vacuole areas in the lamina (**p < .01,***p < .001, ****p < .0001; Dunnett's multiple comparison test, n = 5). Expression of MARK1, 2, 3, or 4 without tau did not cause neurodegeneration (Kruskal–Wallis test, n = 5–7, p = .2514). (d) Comparison of the contributions of MARK1‐4 to tau‐induced neurodegeneration (**p < .01; Tukey's multiple comparison test, n = 5). Flies were at 10 days post‐eclosion.
Fig 2: Marks differentially regulate tau levels and migration patterns in transgenic Drosophila melanogaster. (a) Domain structure of mammalian MARK family proteins and timeline of experiments. (b) Human MARK1‐4 tagged with Myc were expressed under the control of a UAS promoter driven by GMR‐GAL4. Protein levels were analyzed by western blotting with an anti‐Myc antibody normalized by Actin as a loading control (*p < .05, **p < .01; Tukey's multiple comparison test, n = 3). Flies were at 3 days post‐eclosion. (c–e) Western blotting of fly head lysates with anti‐total tau (T46) revealed different profiles and levels of tau protein co‐expressed with MARKs. (c) Total tau representative blot images, (d) analysis of total tau levels (*p < .05, **p < .01; Dunnett's multiple comparison test, n = 4), and (e) the ratio of upper and lower tau bands (*p < .05; Dunnett's multiple comparison test, n = 3). Flies were at 3 days post‐eclosion.
Supplier Page from DNASU for MARK1 (Homo sapiens) in pDNR-Dual (Creator donor/master vector)