![Functional domains of AML1-ETO are critical for its activity in Drosophila blood cells. (A) Schematic representation of the AML1-ETO domains and mutations. Interaction sites of AML1-ETO with DNA, CBFβ (light blue lines), and HDAC1-3, Sin3A, N-CoR/SMRT, ETO, and SON (dark blue lines) are indicated below the protein scheme. (B) UAS constructs encoding wild-type AML1-ETO and its mutant variants (indicated on panel) were expressed under control of hmlΔ-Gal4. hmlΔ-Gal4,UAS-GFP heterozygous were used as wild-type control (WT control). In contrast to intact AML1-ETO, mutant forms with altered DNA-binding (R174Q), CBFβ-binding [Y113A/T161A (YT)], or both DNA- and CBFβ-binding [R174Q/Y113A/T161A (YTR)] domains failed to induce proliferation of hemocytes (n = 10, P < .001). Truncated AML1-ETO(NHR3X) and (NHR2X) proteins were less active in inducing hemocyte proliferation than intact protein (n = 10, P < .001). The AML1-ETO(NHR2X542,m7) mutant with disrupted HHR, NHR3, and MYND domains was unable to induce hemocyte proliferation.](https://ash.silverchair-cdn.com/ash/content_public/journal/blood/116/22/10.1182_blood-2010-03-276998/6/zh89991060210002.jpeg?Expires=1722194784&Signature=MxI5G2usMo~e7fIF~YeixhMcOSfOKKX3X9VurEuJP6jh~5ZeFUy2XwemCvRWDjwUsgwT-OL3xjx2febHjW3DyTfJDMbwDjtB3FpxpwMY38R~cmzL-i9lGNrnTRa6rUEzJaAvSRJsXgFVBJ2mFDV4cTaf8yeb2OPolji0SVCYpcS0YKzUFGt4~Yi-HSUQ~y2uXGhaV2ffeZgcMc8yUmJUc1~zh1W5Fie1SGA1~BSMUj7SU49A-0pufIBlDdOulKYlLgPOgYsg~7P04TTT7PyMl1Pm39oGPiemih1rEkIHDBkprL9O~qEUjAewboh1AziVqmZlQObNI8B~W4RfUHjXBw__&Key-Pair-Id=APKAIE5G5CRDK6RD3PGA)
Functional domains of AML1-ETO are critical for its activity in Drosophila blood cells. (A) Schematic representation of the AML1-ETO domains and mutations. Interaction sites of AML1-ETO with DNA, CBFβ (light blue lines), and HDAC1-3, Sin3A, N-CoR/SMRT, ETO, and SON (dark blue lines) are indicated below the protein scheme. (B) UAS constructs encoding wild-type AML1-ETO and its mutant variants (indicated on panel) were expressed under control of hmlΔ-Gal4. hmlΔ-Gal4,UAS-GFP heterozygous were used as wild-type control (WT control). In contrast to intact AML1-ETO, mutant forms with altered DNA-binding (R174Q), CBFβ-binding [Y113A/T161A (YT)], or both DNA- and CBFβ-binding [R174Q/Y113A/T161A (YTR)] domains failed to induce proliferation of hemocytes (n = 10, P < .001). Truncated AML1-ETO(NHR3X) and (NHR2X) proteins were less active in inducing hemocyte proliferation than intact protein (n = 10, P < .001). The AML1-ETO(NHR2X542,m7) mutant with disrupted HHR, NHR3, and MYND domains was unable to induce hemocyte proliferation.
