Figure 1.

A UTX-interacting region of Trr is sufficient to rescue Trr-null viability. (A) The diagram depicts full-length Trr coding sequence and the various deletion constructs assayed for complementation with the trr[1] lethal allele. Green check marks designate which constructs rescue trr[1] viability according to the complementation assay illustrated in Supplemental Figure S1. (B) Western blots for H3K4-methylation confirm bulk H3K4me1 decrease in the del4 rescue line, which lack the catalytic SET domain. (C) Immunoprecipitation of the Del5-GFP fragment in Drosophila S2 cells copurifies UTX, but not LPT. (D) Immunofluorescence microscopy in larval wing imaginal discs confirms the “minimal” Del5 fragment is sufficient to stabilize UTX in the absence of full-length TRR. Endogenous TRR is depleted by RNAi in the posterior compartment (GFP-labeled), leading to reductions in H3K4me1. However, UTX levels are not affected upon expression of Del5, which is insensitive to Trr-RNAi.