Recruitment of the male-specific lethal (MSL) dosage compensation complex to an autosomally integrated roX chromatin entry site correlates with an increased expression of an adjacent reporter gene in male Drosophila

Drosophila dosage compensate (equalize X-linked gene products) by doubling the transcription of most X-linked genes in males. The MSL (male-specific l ethal) ribonucleoprotein complex consisting of at least five proteins and t wo non-coding RNAs (roX1 and roX2) is essential for this transcription resp onse. Recently it has been shown that the X-linked roX1 and roX2 genes each contain at least one chromatin entry site for the MSL complex. In this stu dy we show that insertion of either roX1 or roX2 DNA sequences, upstream of an insulated lacZ reporter gene controlled with the constitutive armadillo promoter (arm-lacZ), results in a significant elevation of expression of l acZ in males. However, full compensation, that is a precise doubling of lac Z expression in males relative to females, was only observed in some lines carrying autosomal insertions of either roX1-arm-lacZ or roX2-arm-lacZ tran sgenes. Furthermore, we found that a 419-base pair fragment of roX1 that co ntains an MSL binding site was sufficient to cause a modest elevation of ex pression of lacZ in males, but this response was significantly less than ob tained with a full-length roX1 cDNA. This is the first direct demonstration that insertion of an MSL chromatin entry site on an autosome results in el evated expression in males of genes near the entry site.