It had been known since the early 90's that steroid receptors are transcription factors and will positively regulate transcription of specific genes when ligand binds the receptor. It had also been known that the thyroid receptor has a co-receptor that acts to inhibit transcription in the absence of thyroxin.
In the paper by Shubiger and Truman, they conclude that USP is the co-factor that works with the ecdysone receptor and is required both for ligand-induced activation of transcription of the early genes, and also for repression of transcription of the late genes in the absence of ligand.
Why did they use mosaic analysis to study this problem?
Why was it critical to study ecdysone-induced development of the wing disc in vivo and in disc culture?
When wing discs with mosaic clones that were usp-/- were grown in culture in the absence of ecdysone, the investigators said in the paper that they were "surprised" to find that late genes in the mutant patches were still expressed. Why were they surprised? What did this tell them about the regulation of late gene expression?