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Papers In Press, published online ahead of print June 11, 2001
Molecular BioSciences, Massey University, Palmerston North 5320
Corresponding Author: M.J.Scott{at}massey.ac.nz
Drosophila dosage compensate (equalise X-linked gene products) by doubling the transcription of most X-linked genes in males. The MSL ribonucleoprotein complex consisting of at least 5 proteins and 2 non-coding RNAs (roX1 and roX2) is essential for this transcription response. Recently it has been shown that both the X-linked roX1 and roX2 genes each contain at least one chromatin entry site for the MSL complex. In this study 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 lacZ in males. However, full compensation, that is a precise doubling of lacZ expression in males relative to females, was only observed in some lines carrying autosomal insertions of either roX1-arm-lacZ or roX2-arm-lacZ transgenes. Further we found that a 419 bp fragment of roX1 that contains an MSL binding site was sufficient to cause a modest elevation of expression of lacZ in males but this response was significantly less than obtained 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 elevated expression in males of genes near the entry site.
J. Biol. Chem, 10.1074/jbc.M103008200
Submitted on April 5, 2001
Revised on June 7, 2001
Accepted on June 11, 2001
Recruitment of the 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
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