Originally published as Genetics Published Articles Ahead of Print on February 1, 2008.
Genetics, Vol. 178, 749-759, February 2008, Copyright © 2008
doi:10.1534/genetics.107.083105
Interplay of Developmentally Regulated Gene Expression and Heterochromatic Silencing in Trans in Drosophila
Brian T. Sage1,
Michael D. Wu and
Amy K. Csink2
Department of Biological Sciences, Carnegie Mellon University, Pittsburgh, Pennsylvania 15213
2 Corresponding author: University of Washington, Department of Biology, 24 Kincaid Hall, Box 351800, Seattle, WA 98195-1800.
E-mail: csink{at}u.washington.edu
The brownDominant (bwD) allele of Drosophila contains a heterochromatic block that causes the locus to interact with centric heterochromatin. This association silences bw+ in heterozygotes (trans-inactivation) and is dependent on nuclear organizational changes later in development, suggesting that trans-inactivation may not be possible until later in development. To study this, a P element containing an upstream activating sequence (UAS)–GFP reporter was inserted 5 kb from the bwD insertion site. Seven different GAL4 driver lines were used and GFP fluorescence was compared in the presence or the absence of bwD. We measured silencing in different tissues and stages of development and found variable silencing of GFP expression driven by the same driver. When UAS–GFP was not expressed until differentiation in the eye imaginal disc it was more easily trans-inactivated than when it was expressed earlier in undifferentiated cells. In contrast to some studies by other workers on silencing in cis, we did not find consistent correlation of silencing with level of expression or evidence of relaxation of silencing with terminal differentiation. We suggest that such contrasting results may be attributed to a potentially different role played by nuclear organization in cis and trans position-effect variegation.
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P. Nisha, J. L. Plank, and A. K. Csink
Analysis of Chromatin Structure of Genes Silenced by Heterochromatin in Trans
Genetics,
May 1, 2008;
179(1):
359 - 373.
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Copyright © 2008 by the Genetics Society of America.