Figure 1.
In vivo CRISPR-Cas9 screening identifies an essential role for Glut1 in MLL::AF9–driven AML. (A) Schematic representation of the experimental design for the pooled in vivo CRISPR screen in MLL::AF9 c-Kit+ leukemia cells (n = 9 mice). (B) Bar plot of normalized median fold change of sgRNAs for the 20 genes with the strongest depletion scores in the screen. Fold change in sgRNA representation in leukemic cells harvested from the bone marrow was calculated as the number of reads after 12 days in vivo (final time point [Tf]) relative to input representation (initial time point [T0]). (C) Waterfall plot showing the normalized fold change of individual sgRNAs for the top regulator Glut1 and 3 known regulators of MLL::AF9 AML (Hoxa9, Cxcr4, and Cd47). A fold change of 10 was used to define depleted sgRNAs, denoted with a dotted line. Illustration in panel A created using BioRender. See also supplemental Figure 1 and supplemental Table 3.

In vivo CRISPR-Cas9 screening identifies an essential role for Glut1 in MLL::AF9–driven AML. (A) Schematic representation of the experimental design for the pooled in vivo CRISPR screen in MLL::AF9 c-Kit+ leukemia cells (n = 9 mice). (B) Bar plot of normalized median fold change of sgRNAs for the 20 genes with the strongest depletion scores in the screen. Fold change in sgRNA representation in leukemic cells harvested from the bone marrow was calculated as the number of reads after 12 days in vivo (final time point [Tf]) relative to input representation (initial time point [T0]). (C) Waterfall plot showing the normalized fold change of individual sgRNAs for the top regulator Glut1 and 3 known regulators of MLL::AF9 AML (Hoxa9, Cxcr4, and Cd47). A fold change of 10 was used to define depleted sgRNAs, denoted with a dotted line. Illustration in panel A created using BioRender. See also supplemental Figure 1 and supplemental Table 3.

Close Modal
This Feature Is Available To Subscribers Only

or Create an Account

Close Modal
Close Modal