Haploinsufficiency of the D melanogaster CUX1 homologue, cut, leads to melanotic tumor formation and hemocyte hyperproliferation in vivo.ct knockdown was performed by crossing flies expressing ct RNAi in a construct containing a UAS promoter and GFP tag with flies expressing the GAL4 driver under the hemocyte-specific hml promoter. Two different ct targeting constructs were tested: ct^{RNAi A} and ct^{RNAi B}. (A) ct^{RNAi A} but not wild-type (w¹¹¹⁸;hml-GAL,UAS-GFP/+), Drosophila third instar larvae develop melanotic tumors (indicated by the arrow). (B) ct knockdown leads to increased numbers of hemocytes. Circulating hemocytes bled from wild-type, nonspecific RNAi, ct^{RNAi A}, and ct^{RNAi B} developing larvae were stained with Hoechst and quantified (mean ± SEM). (C) Haploinsufficient levels of ct are confirmed by quantitative RT-PCR of ct from hemocyte RNA. One representative experiment of 3 is shown.