Fig. S7
- ID
- ZDB-FIG-130118-29
- Publication
- Kaiser et al., 2012 - Amyloid Beta precursor protein and prion protein have a conserved interaction affecting cell adhesion and CNS development
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High doses of MOs affect apoptotic cell death, and Human APP rescues apoptotic cell death. High doses of prp1, appa or appb MO are used here to show their individual effects on apoptotic cell death. Some combinations of these MOs co-injected at low doses show that these MOs can synergize to produce this effect (Fig. 4). Apoptosis levels are increased when appa, appb, or prp1 mRNA is disrupted (A–D). Brightfield images of the area above the yolk sac extension of fish injected with effective doses of control, appb, appa and prp1 (A–D, respectively) MOs. Compared with control fish, prominent anti-activated caspase 3 staining is apparent in appb, appa, or prp1 MO injected fish (A′–D′, respectively). E. Number of caspase 3 positive cells were counted above the yolk sac extension in fish treated as per those in A–D. N = 5. Panels F–K show examples of human APP rescuing the concerted appa plus prp1 knockdown. appb is not able to rescue the phenotype in wildtype fish, nor in transgenic fish labelling the CNS with GFP (H & I, respectively, compare to F & G) as we noted in Fig. 3K and here serves as a negative control. A noticeable lack of GFP was apparent along portions of the CNS (* in panel I). Human APP is able to rescue these phenotypes (J, K). Panels L–N show the yolk-sac extension of fish in F, H & J. L′–N′ show examples of activated caspase labelling during rescue with human APP. The latter treatments were quantified in O. N = 5. * = P<0.05. ** = P<0.01. |