Skip to main content
letter
. 2018 Aug;103(8):e336–e340. doi: 10.3324/haematol.2018.191338

Figure 1.

Figure 1.

GATA1s mutation is essential for the development of transient abnormal myelopoiesis (TAM). (A) Schematic representation of the GATA1 locus, the translation of wild-type (WT) GATA1 product in normal fetal hematopoiesis (top), and the translation of GATA1s after the introduction of mutations as seen in TAM (middle) or as generated using CRISPR-Cas9 genome editing (bottom). (B) The efficacies of 4 different sgRNAs targeting exon 2 of GATA1 as assessed using a fluorescence-based reporter assay. The sgRNAs selected for later studies are marked red and blue. (C-F) K562 cells lentivirally transduced with GATA1-targeting (GATA1.1 and GATA1.2) or control (Luc.1) sgRNAs. (C) Western blot of GATA1 and GATA1s proteins in WT K562 cells and in two representative GATA1s-K562 clones (#1 and #2; used in subsequent experiments). (D) Number of WT and GATA1s-K562 cells (clone #1 and #2) grown in liquid culture. (E) Flow cytometric analysis of WT and GATA1s-K562 cells (clone #1 and #2) for expression of the indicated cell surface markers. (F) Expression of CD235a represented as mean fluorescence intensity (MFI), in WT K562 cells and GATA1s-K562 clone #1 and #2.