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dvdy21372-DVDY21372FigS1.tif19169K Supplementary Figure S1. A1-A4:ELAV is only transiently expressed in embryonic glial cells. Neuromeres A1 to A3 of late stage 16 (St16) embryos of arepo -Gal4 line driving a membranebound UAS- mCD8::gfp ; single confocal sections (0.7μm in thickness) at different ventral (A1) and dorsal (A2) levels. In A3 and A4 only the ELAV signal is shown. No ELAV can be detected in late embryonic glial cells (depicted with white arrows).B:Western blot of protein extracts from embryos collected over night. Anti-ELAV antibody from rat (E-R; line A) and mouse (E-M; line C; both commercially available [DSHB]) detect one band at approximately 50kDa corresponding to ELAV protein size (M, molecular weight marker). As a control the secondary antibodies directed against rat (B) or mouse (D) show no signal. As loading control (asterisk) a monoclonal anti-Actin antibody was used (molecular weight of Actin is approximately 40KDa).C1-C3:The small interstitial deletion mutationelav 5 was used to test both antibodies in situ. In this mutation, the complete coding sequence ofelavis deleted (Robinow and White, 1991). Both antibodies (anti-ELAV-mouse in red (C1, C2) and anti-ELAV-rat in green (C1, C3)) detect no protein in stage 15 embryos only non-specific background staining is visible demonstrating their specificity for epitopes of the ELAV protein. In comparison, the anti-Repo antibody (C1 in blue) shows a clear signal. This also shows, that a cross reaction of anti-ELAV antibodies with the anti-Repo antibody can be excluded. Maximal projection of a confocal stack (single section 0.7μm in thickness) showing a flat preparation of a complete embryo.D1, D2:The UAS- mCD8::gfptransgenic line shows no leaky GFP expression. D1 shows a maximum projection; D2 shows a single confocal section of the same stage 15 embryo (0.7μm in thickness).
dvdy21372-DVDY21372FigS2.tif15973K Supplementary Figure S2.G2-arrested NBs do not show elevated levels of ELAV translation.A1-B2:Instringloss of function embryos (B1, B2) NBs are arrested in the G2 phase. At stage 12 levels of ELAV protein are not elevated compared to wild type NBs at stage 11 (A1, A2; same pictures as Fig.3 C3, C4). This argues for posttranscriptional regulation which blocks theelavtranslation in NBs. Single confocal sections (0.8μm in thickness) are shown, anterior is up.C1-D2: elavloss of function embryos show slight mispositioning of glial cells. In elav mutants at stage 17 (D1, D2) some glial cells are mispositioned (compare C1, C2 for wild type stage 17), e.g., peripheral glia or longitudinal glia (white arrows in C2 and D2). Glial dislocalization may be a secondary effect due to a disrupted axonal pattern (as revealed by the FasII staining in C1, D1; red and yellow arrows). Maximum projection of confocal serial sections are shown, anterior is up.
dvdy21372-DVDY21372FigS3.tif39393K Supplementary Figure S3. A1-A6:Glial cells labelled byelav C1555 -Gal4 driven CD8::GFP (yellow arrows) at late stage 16. In addition to identified glial cells indicated in Fig. 4C1-C3 further glial cells can be distinguished, including one or two peripheral glial cells. B1-C6:Theelav.L2 -Gal4 driver line shows the same pattern of expression, as the enhancer trap lineelav C1555 -Gal4.B1-B3:At late stage 11 (St11l) single mitotically active NBs (yellow arrows) show double staining for Mira (red) and CD8::GFP (green) revealing that theelav.L2 -Gal4 line is driving reporter gene expression in NBs. Glial cells (white arrows) also express the GFP.C1-C6:Glial cells still show GFP-expression at stage 16. All pictures show single confocal sections (0.7μm in thickness).

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