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. Author manuscript; available in PMC: 2016 Jul 5.
Published in final edited form as: Adv Exp Med Biol. 2016;916:335–369. doi: 10.1007/978-3-319-30654-4_15

Fig. 3.

Fig. 3

pten haploinsufficiency promotes loss of MYC transgene dependence, (a, c) One representative rag2:MYC-ER; rag2:GFP double-transgenic pten-wild-type zebrafish, shown at time of T-ALL onset (a) and 3 weeks after removal from 4HT (c). (b, d) Representative rag2:MYC-ER; rag2:GFP double-transgenic zebrafish that harbored heterozygous mutations of both ptenA and ptenB, shown at time of T-ALL onset (b) and 3 weeks after removal from 4HT (d). Bar, 1 mm. (e) Quantitation of T-ALL phenotypes after 4HT removal, based on pten genotype. Number of fish with T-ALL analyzed per genotype: ptenA +/+, ptenB +/+, n = 39; ptenA +/+, ptenB +/−, n = 12; ptenA +/−, ptenB +/+, n = 22; ptenA +/−, ptenB +/−, n = 10. (f) Western blot analysis for phosphorylation of S6 ribosomal protein, a marker of Akt pathway activation, in sorted T-ALL cells from five different rag2:MYC-ER pten–wild-type zebrafish in which T-ALL progressed despite MYC downregulation. Units for the molecular mass markers shown are in kD. (Republished with permission from The Rockefeller University Press) [63]