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Originally published as Genetics Published Articles Ahead of Print on November 15, 2004.
Genetics, Vol. 169, 783-794, February 2005, Copyright © 2005
doi:10.1534/genetics.104.037085
Bonus, a Drosophila TIF1 Homolog, Is a Chromatin-Associated Protein That Acts as a Modifier of Position-Effect Variegation
R. B. Beckstead*,1,
S. S. Ner
,
K. G. Hales
,
T. A. Grigliatti,
B. S. Baker
and
H. J. Bellen*,2
* Department of Molecular and Human Genetics, Howard Hughes Medical Institute, Baylor College of Medicine, Houston, Texas 77030
Department of Zoology, University of British Columbia, Vancouver, British Columbia V6T 1Z4, Canada
Department of Biology, Davidson College, Davidson, North Carolina 28036
Department of Biological Sciences, Stanford University, Stanford, California 94305
2 Corresponding author: Howard Hughes Medical Institute, Baylor College of Medicine, 1 Baylor Plaza T628, Houston, TX 77030.
E-mail: hbellen{at}bcm.tmc.edu
Bonus, a Drosophila TIF1 homolog, is a nuclear receptor cofactor required for viability, molting, and numerous morphological events. Here we establish a role for Bonus in the modulation of chromatin structure. We show that weak loss-of-function alleles of bonus have a more deleterious effect on males than on females. This male-enhanced lethality is not due to a defect in dosage compensation or somatic sex differentiation, but to the presence of the Y chromosome. Additionally, we show that bonus acts as both an enhancer and a suppressor of position-effect variegation. By immunostaining, we demonstrate that Bonus is associated with both interphase and prophase chromosomes and through chromatin immunoprecipitation show that two of these sites correspond to the histone gene cluster and the Stellate locus.
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