Reference Report

Reference
Citation	Schneiderman, J.I., Sakai, A., Goldstein, S., Ahmad, K. (2009). The XNP remodeler targets dynamic chromatin in Drosophila. Proc. Natl. Acad. Sci. U.S.A. 106(34): 14472--14477. (Export to RIS)
FlyBase ID	FBrf0208542
Publication Type	Research paper
PubMed ID	19706533
PubMed Abstract	Heterochromatic gene silencing results from the establishment of a repressive chromatin structure over reporter genes. Gene silencing is often variegated, implying that chromatin may stochastically switch from repressive to permissive structures as cells divide. To identify remodeling enzymes involved in reorganizing heterochromatin, we tested 11 SNF2-type chromatin remodelers in Drosophila for effects on gene silencing. Overexpression of five remodelers affects gene silencing, and the most potent de-repressor is the alpha-thalassaemia mental retardation syndrome X-linked (ATRX) homolog X-linked nuclear protein (XNP). Although the mammalian ATRX protein localizes to heterochromatin, Drosophila XNP is not a general component of heterochromatin. Instead, XNP localizes to active genes and to a major focus near the heterochromatin of the X chromosome. The XNP focus corresponds to an unusual decondensed satellite DNA block, and both active genes and the XNP focus are sites of ongoing nucleosome replacement. We suggest that the XNP remodeler modulates nucleosome dynamics at its target sites to limit chromatin accessibility. Although XNP at active genes may contribute to gene silencing, we find that a single focus is present across Drosophila species and that perturbation of this site cripples heterochromatic gene silencing. Thus, the XNP focus appears to be a functional genetic element that can contribute to gene silencing throughout the nucleus.
DOI	10.1073/pnas.0905816106
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Language of Publication	English
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Publication Type	Journal
Abbreviation	Proc. Natl. Acad. Sci. U.S.A.
Title	Proceedings of the National Academy of Sciences of the United States of America
Publication Year	1915-
ISBN/ISSN	0027-8424
Data from Reference
Aberrations (3)
	Df(3R)Exel6202 Dp(?;2)bw^D In(1)w^m4
Alleles (18)
	brm^f04692 CG4049^f01495 CG5316^d10097 Chd1^EP dom^f00946 Etl1^EP701 Hel89B^d00861 His3.3A^{core.hs.T:Avic\GFP} Ino80^d10097 kis^EY12846 Marcal1^f05123 Mi-2^EY13252 mor^d00861 Scer\GAL4^Act5C.PI Scer\GAL4^GMR.PF XNP⁴⁰³ XNP⁴⁰⁶ XNP^EP635
Constructs (2)
	P{EP} P{hs-His3.3A.core.GFP}
Genes (24)
	brm CG4049 CG5316 CG7376 CG10445 Chd1 Chd3 dom Etl1 Hel89B His3 His3.3A Ino80 Iswi kis lds Marcal1 Mi-2 mor okr RpII215 Scer\GAL4 Su(var)205 XNP
Insertions (12)
	P{EP}Chd1^EP P{EP}Etl1^EP701 P{EP}XNP^EP635 P{EPgy2}EY09137 P{EPgy2}kis^EY12846 P{EPgy2}Mi-2^EY13252 P{XP}Hel89B^d00861 P{XP}Ino80^d10097 PBac{WH}Arl1^f04692 PBac{WH}CG3253^f01495 PBac{WH}dom^f00946 PBac{WH}Marcal1^f05123