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Figure 1. Edn1-Ednra signaling mutant STGs project ectopically. ; (a–h) Wholemount Th immunostaining visualizing sympathetic projections from STGs in E15.5 thoraxes (a–d) and hearts (e–h) from Ednra-/- (b, f), Edn1-/- (c, g), Ece1-/- (d, h) and a control (a, e) embryos. Black arrows denote ectopic medial projections from Edn1-Ednra signaling-deficient STGs to the thoracic aorta (b–d), which is associated with reduced cardiac sympathetic innervations (f, g, h) (Manousiouthakis et al., 2014); very rare projections from the STG to the dorsal aorta occur in control embryos (arrow in a). (i) A compiled representation of Th+ area in the medial upper thorax area in E15.5 endothelin signaling component mutant embryos. For the embryos of each litter, the proportion of Th+ pixel area within the upper thoracic body wall area (between C7 and T4 vertebrae) between sympathetic chains was measured. Analysis included results of 5 Ednra litters (7 controls, 10 Ednra-/-), 4 Edn1 litters (9 controls, 9 Edn1-/-), and 7 Ece1 litters (18 controls, 15 Ece1-/-). Error bars; mean ± sd. p=8.49E-22, p=8.22E-25, p=1.71E-19. (j–q) Serial transverse sections of an E15.5 Ednra-/- embryo at the levels corresponding to the white dotted arrows in (b) (from the top: T2 vertebral body, the second rib, T3 vertebral body, and the third rib) were immunostained for Th (brown) and counterstained with hematoxylin (blue). (n–q) Magnified views of bracketed areas in j–m). Red arrows point to ectopic medial projections from STG that are associated with thoracic arteries. dAo, descending aorta; es, esophagus; LA, left atrium; lsvc, left superior vena cava; LV, left ventricle; pia, posterior intercostal artery; RA, right atrium; rsvc, right superior vena cava; RV, right ventricle; stg, stellate ganglion; sv, sinus venosus; T, thoracic segment; tr, trachea; X, Xth cranial nerve. Scale bars, 200 μm (a–d), 100 μm (e–h), 200 μm (j–m), 100 μm (n–q).

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Video 2. Ey-RNAi ectopic adult P-EN morphology Ey-RNAi ectopic old INP born P-EN neurons innervate the same distinct neuropil regions of the central complex.

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Figure 4—figure supplement 2. Quantitative analysis demonstrating the effect of Pgk1 expressed in zebrafish muscle on the growth of axonal motor neurons. ; Zebrafish wild-type (WT) embryos and embryos injected with pZα-Cas9, pZα-Cas9 plus pgk1 sgRNA (reduction of Pgk1 in muscle cells) and pZα-Cas9 plus pgam2 sgRNA (reduction of Pgam2 in muscle cells) were used to count (A) the percentage of embryos which motor axons having retarded growth among the examined number of embryos (n) and (B) the average length of axons. In a parallel experiment, zebrafish WT embryos and embryos injected with pZα-Pgk1 (overexpression of Pgk1 in muscle cells) were used to calculate (C) the percentage of embryos which motor axons having ectopic growth among the examined number of embryos (n), measure (D) the ectopic growth length of axons, and count (E) the number of branches from a single axon. Data were averaged from all examined embryos/axons and presented as mean ±S.D. Student’s t-test was used for statistical analysis(***, significant difference at p

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Figure 6. Reawakening svb expression in the early Drosophila embryo affects segmentation. ; Top panels show in situ hybridization of svb (A–D) and tal (A’–D’) mRNA and anti-Wingless (Wg) immunostaining (A”–D”) at gastrulation stage in control conditions (nullo >GFP) and following the ectopic expression (driven by nullo-Gal4) of wild type Svb (B–B”), Svb-ACT (C–C”) and Svb-3Kmut (D–D”), which mimics or prevents Pri/Ubr3-mediated processing of Svb, respectively. (A’’’–D’’’) show cuticle preparations of control (A’’’), nullo >Svb (B’’’), nullo >Svb ACT (C’’’) and nullo >Svb-3Kmut (D’’’) embryos. (E–F’) panels show immunostaining for the Wingless protein and cuticle preparations of control (E–E’) and svb ectopic expression (nullo >Svb) (F–F’) in a tal null genetic background. tal mutant embryos display characteristic trichome loss and cuticle defects. (G) Quantification of segmental defects for each genotype. Data were analyzed by one-way ANOVA. ***, p-value

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Figure 2—figure supplement 3. Cell cycle induced by the ectopic expression of pcl12 is independent on MAPK-mediated phosphorylation of Crk1. ; Representative images of cultures of strains expressing an ectopic copy of pcl12 (Pcrg1:pcl12) as well as the indicated mutations, used for the graph showed in Figure 2C. Cultures were incubated for 6 hr in inducing conditions for Pcrg1:pcl12 (CMA). Cells carried a constitutively expressed NLS-GFP reporter to detect nuclei and were stained with Calcofluor White (CFW). Note that mutants in MAPK signaling showed an aberrant deposition of CFW staining. Bar: 15 μm.

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Figure 6. Activin signaling is required for patterning and maturation of hair cells. ; (A–B) FST overexpression at E12.5 delays hair cell maturation and causes a mild overproduction of inner hair cells. FST transgenic (R26-FST) embryos and their control (single transgenic) littermates were exposed to dox starting at E12.5 until tissue harvest at E17.5. (A) Shown are the apical surfaces of hair cells located in the base, mid and apex of control and R26-FST transgenic cochlear sensory epithelia. Phalloidin labels actin-rich stereocilia of inner (white arrowhead) and outer hair cells (white bar). Red asterisks mark ectopic inner hair cells. White arrows mark location of missing outer hair cells. Scale bar 50 µm. (B) Graphed are the number of ectopic inner hair cells (IHC) within the most basal segment (0–0.5 mm) and within the entire length (0–4 mm) of control (Ctrl, gray) and FST overexpressing (FST, purple) cochleae. Data expressed as mean ± SEM (n = 3 animals per group, ****p

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Figure 3—figure supplement 1. Cell cycle arrest upon ectopic expression of pcl12 relies on Cdk1 inhibitory phosphorylation, although does not down-regulate Cdc25 levels. ; (A) Schemes of the strains used for the co-expression of an ectopic copy of pcl12 as well as a cdk1 allele refractory to inhibitory phosphorylation. (B) Representative images of cultures of indicated strains. Cultures were incubated for 6 hr in inducing conditions for crg1 promoter (CMA). Cells carried a constitutively expressed NLS-GFP reporter to detect nuclei and were stained with Calcofluor White (CFW) to detect the septa. Bar: 15 μm. (C) Western blot analysis showing the levels of Cdc25 (upper blot) upon ectopic expression of pcl12 in cells growing in inducing conditions (CMA) for the indicated time. Levels of Cdk1 were used as loading control (bottom blot).

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Figure 3—figure supplement 1. Ectopic expression of IRE1 LDTM attenuates apoptotic caspase activation independent of full-length IRE1. ; (A) KMS11 overexpressing an untagged version of LDTM (amino acids 1–470) or parental cells were treated with DMSO or 100 nM Tg for 24 hr. Equal amounts of protein from cell lysates were analyzed by Caspase-Glo 3/7 assay. Graphs depict mean luminescence signal ± SD as a ratio to the DMSO control from three technical replicates. (B) Two independent clones expressing ectopic LDTM (1-470) were isolated (C7 and C13). Cells were treated with different concentrations of Tg for 72 hr and viability was measured by CellTiter-Glo assay. The percentage of viable cells is graphed as an average of three biological replicates ± SD. (C) Parental KMS11 cells or cells stably transfected with a plasmid encoding a CMV-driven LDTM protein, representing a precise cleavage fragment of IRE1 with a Flag tag (1–507F), were treated with DMSO or 0.3 μg/ml SubAB for 3 hr and analyzed by Caspase-Glo 3/7 assay. The graph depicts mean luminescence signal ± SD as a ratio to the DMSO control from three technical replicates. (D) Parental JJN3 cells or JJN3 cells transfected as in C were treated with 100 nM Tg, or 5 μg/ml Tm, or 0.5 μg/ml BfeA for 24 hr, or 0.3 μg/ml SubAB for 3 hr, and analyzed by Caspase-Glo 3/7 assay. The graph depicts mean luminescence signal ± SD as a ratio to the DMSO control from three technical replicates. (E) Fixed MDA-MB-231 cells expressing the flag-tagged LDTM construct were stained with anti-flag (red), anti-calnexin (green), and DAPI. Cells were imaged using a confocal microscope and a z-stack image was acquired to determine localization of LDTM in the ER. An orthogonal projection is shown. (F, G) KMS11 cells expressing DOX-inducible IRE1 shRNA (Parental) were stably transfected with a plasmid encoding a CMV-driven LDTM protein without (1-507) or with a Flag tag (1–507F). The cells were incubated in the absence or presence of 1 μg/ml DOX for 3 days to induce IRE1 shRNA expression. Cells were then treated with DMSO, 100 nM Tg, or 5 μg/ml Tm for 6 hr and equal amounts of protein lysates were analyzed by Caspase-Glo 3/7 assay (F) or WB (G). Data represent at least three independent experiments; graphs depict mean ± SD of three technical replicates.

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Figure 6—figure supplement 2. sad-1 splicing is controlled by distinct RBPs and TFs in ventral nerve cord motor neurons. ; (A) Ectopic expression of mec-8 in excitatory motor neurons (via unc-17 promoter) changes sad-1 splicing in excitatory motor neurons from partial exon inclusion to complete exon inclusion (n = 7/11 animals examined). (B) Ectopic expression of mbl-1 in inhibitory motor neurons (via unc-25 promoter) has similar effects in inhibitory motor neurons (n = 9/13 animals examined). (C) unc-3 mutants exhibit partial (12/25 worms examined) or complete (13/25 worms) loss of sad-1 exon inclusion in excitatory motor neurons. (D) unc-3 mutants exhibit partially-penetrant loss of mbl-1 expression in excitatory motor neurons (25/65 animals exhibit complete loss, 28/65 partial (example displayed), 12/65 no detectable change).

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Figure 5. FST overexpression in the developing cochlea disrupts inner hair cell patterning and delays hair cell maturation. ; FST transgenic (R26-FST) embryos and their control (wild type or single transgenic) littermates were exposed to dox starting at E11.5 until tissue harvest at E18.5. (A) FST overexpression results in ectopic inner hair cells. Shown are cross-sections through the cochlear mid-base of control and R26-FST transgenic embryos. GFP (green) and Myo7a (red) label inner hair cells (IHC, white arrowhead) and outer hair cells (OHC, white bar). Red asterisks mark ectopic inner hair cells. SOX2 (blue) labels supporting cells including inner phalangeal cells (IPH), pillar cells (PC) and Deiters’ cells (DC) indicated by white arrows. Scale bar 50 µm. (B) FST overexpression delays stereocilia formation. Shown are z-stack projections of the luminal surface of control and R26-FST transgenic cochlear sensory epithelia. Phalloidin labels actin-rich stereocilia of inner (white arrowhead) and outer hair cells (white bar). Red asterisks mark ectopic inner hair cells. Yellow arrows mark the location of missing outer hair cells. Scale bar 50 µm. (C–D) Quantification of hair cell (C) and supporting cell (D) density in the base, mid and apex of control (Ctrl, gray bars) and FST overexpressing (FST, purple bars) cochleae. Abbreviations: IHC, inner hair cells; OHC, outer hair cells; IPH, inner phalangeal cells; PC, pillar cells; DC, Deiters’ cells; B, base; M, mid; A, apex. Data expressed as mean ± SEM (n = 3 animals per group, *p≤0.05, **p

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