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Fig. 1. Schematic of RD- and ETO-related proteins. (A) The RD proteins (blue)
contain the RD, which binds DNA and interacts with CBFß/Bro/Bgb, and a
C-terminal VWRPY motif. ETO and Nervy (green) share four conserved domains
[NHR 1-4; NHR 4 is the zinc-finger (ZF) domain]. enR (red) is from the
Engrailed protein and includes its repressor domain. (B) Wild-type AML1 (blue)
interacts with CBFß (purple) and can bind either transcriptional
activators (yellow triangle) or repressors (red hexagon) to regulate gene
expression. There are two models to describe how AML1-ETO (blue+green) could
be interfering with endogenous AML1 target gene expression to cause leukemia.
First, AML1-ETO, which recruits transcriptional repressors through its C
terminus, could repress the expression of all AML1 targets
(constitutive-repressor model). Alternatively, AML1-ETO might titrate away
AML1 co-factors, such as CBFß, preventing AML1 from activating and
repressing gene expression (dominant-negative model). In contrast to the
predictions of the constitutive repressor model, negatively regulated targets
would be de-repressed in the dominant-negative model. (C) A wild-type
ommatidium contains eight photoreceptors (1-8; circles), four cone cells (c;
ovals), eleven pigment cells (not shown) and three bristles (not shown).
lz (blue), which expressed in photoreceptors 1, 6 and 7 and the cone
cells, regulates the expression of svp (green), Drosophila
Pax2 (red) and dpn (yellow) as indicated.
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