Journal: Neurobiology of disease

Article Title: Inactivation of Hippo and cJun-N-terminal Kinase (JNK) signaling mitigate FUS mediated neurodegeneration in vivo

doi: 10.1016/j.nbd.2020.104837

Figure Lengend Snippet: MAb24B10 (Chaoptin), marks the retinal axons that innervate lamina and medulla regions of the brain. Top panel shows, (A) wild-type larval eye-antennal imaginal disc, and (B) GMR>FUS (C) GMR>FUS R518K, and (D) GMR>FUS R521C showing expression of the retinal axons marked by 24B10 in control and when FUS or mutant FUS (FUS R518K and FUS R521C) are misexpressed in the GMR domain respectively. Activation of Hippo signaling by misexpressing hpo, along with FUS or mutant FUS results in impaired targeting of retinal axons to the brain (E) GMR>FUS+hpo, (F) GMR>FUS R518K+hpo, (G) GMR>FUS R521C+hpo, as compared to the wild-type (A). In-activation of Hippo signaling by misexpressing hpoRNAi, along with FUS and mutant FUS results in restoration of targeting of retinal axons to the brain (H) GMR>FUS+hpoRNAi, (I) GMR>FUS R518K+hpoRNAi, (J) GMR>FUS R521C+hpoRNAi. Note that all transgenes are in heterozygous combination. Magnification of all the eye-antennal imaginal discs is 20X.

Article Snippet: The primary antibodies used were: rabbit anti-FUS (1:500, Bethyl Laboratories, A300-302A), mouse anti-Dlg (1:100, Developmental Studies Hybridoma Bank-DSHB, 4F3), mouse anti-Wg (1:50, DSHB, 4D4), rat anti-Elav (1:100; DSHB, 7E8A10), mouse anti-Chaoptin, MAb24B10 (1:100, DSHB, 24B10) ( Zipursky et al., 1984 ), and rabbit anti-β-galactosidase (1:100, Promega, Z3781).

Techniques: Expressing, Mutagenesis, Activation Assay