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Fig. 4. FoxO overexpression phenotype depends upon Akt phosphorylation status. (A) Uninjected control embryo at stage 13. (B) Bilateral injection of 500 pg FoxO3 RNA does not reveal major phenotypic alterations. (C, D) Bilateral injection of 250 pg (C) or 500 pg FoxO3-TM RNA (D) prevents blastopore closure. (E) Uninjected control embryo at stage 11.5. (F) Bilateral injection of 400 pg FoxO4 prevents blastopore formation. (G) Bilateral injection of 300 pg IGF-1. (H) Co-injection 300 pg IGF-1 and 400 pg FoxO4 RNA restores blastopore formation. (I) Bilateral injection of 400 pg IGF-2. (J) Embryo, co-injected with 400 pg FoxO4 and 400 pg IGF-2 RNA, is rescued to wild type. (K) Bilateral injection of 500 pg Akt-1 RNA. (L) Embryo, co-injected with 400 pg FoxO4 and 500 pg Akt-1 RNA, is rescued to wild type. (M) Embryo, co-injected with 400 pg FoxO3-TM and 500 pg Akt-1 RNA, stage 11.5. The wild type phenotype cannot be restored. (N) Bilateral injection of 200 pg FoxO6 prevents blastopore formation. (O) Embryo, co-injected with 200 pg FoxO6 and 500 pg Akt-1. Blastopore formation fails. (P) Uninjected control embryo, stage 19. (Q) Bilateral injection of 500 pg Akt-1 RNA. (R) Embryo, co-injected with 400 pg FoxO4 and 500 pg Akt-1 RNA. Akt-1 prevents formation of the FoxO4 phenotype and allows neural plate formation. All bilateral injections were performed at 2-cell stage. (S) HeLa cells transfected with GFP, FoxO3-GFP, FoxO3-TM-GFP and FoxO6-GFP fusion-constructs. Percentages of blastopore closure are given in supplementary Table S3.

Image published in: Schuff M et al. (2010)

Copyright © 2010. Image reproduced with permission of the Publisher, Elsevier B. V.

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