Genome-wide HP1 binding in Drosophila:: Developmental plasticity and genomic targeting signals

被引:83
作者
de Wit, E [1 ]
Greil, F [1 ]
van Steensel, B [1 ]
机构
[1] Netherlands Canc Inst, NL-1066 CX Amsterdam, Netherlands
关键词
D O I
10.1101/gr.3198905
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Heterochromatin protein 1 (HP1) is a major component of heterochromatin. It was reported to bind to a large number of genes and to many, but not all, transposable elements (TEs). The genomic signals responsible for targeting of HP1 have remained elusive. Here, we use whole-genome and computational approaches to identify genomic features that are predictive of HP1 binding in Drosophila melanogaster. We show that genes in repeat-dense regions are more likely to be bound by HP1, particularly in pericentric chromosomal regions. We also demonstrate that TEs are only bound by HP1 if they are flanked by other repeats, suggesting a cooperative mechanism of binding. Genome-wide DamID) mapping of HP1 in larvae and adult flies reveals that repeat-flanked genes typically bind HP1 throughout development, whereas repeat-free genes display developmentally dynamic HP1 association. Furthermore, computational analysis shows that HP1 preferentially binds to transcribed regions of long genes. Finally, we detect low but significant amounts of HP1 along the entire X chromosome in male, but not female, flies, suggesting a link between HP1 and the dosage compensation complex. These results provide insights into the mechanisms of HP1 targeting in the natural genomic context.
引用
收藏
页码:1265 / 1273
页数:9
相关论文
共 53 条
[1]   Dosage compensation: an intertwined world of RNA and chromatin remodelling [J].
Akhtar, A .
CURRENT OPINION IN GENETICS & DEVELOPMENT, 2003, 13 (02) :161-169
[2]   BASIC LOCAL ALIGNMENT SEARCH TOOL [J].
ALTSCHUL, SF ;
GISH, W ;
MILLER, W ;
MYERS, EW ;
LIPMAN, DJ .
JOURNAL OF MOLECULAR BIOLOGY, 1990, 215 (03) :403-410
[3]  
[Anonymous], GENOME BIOL
[4]   Selective recognition of methylated lysine 9 on histone H3 by the HP1 chromo domain [J].
Bannister, AJ ;
Zegerman, P ;
Partridge, JF ;
Miska, EA ;
Thomas, JO ;
Allshire, RC ;
Kouzarides, T .
NATURE, 2001, 410 (6824) :120-124
[5]  
BRAND AH, 1993, DEVELOPMENT, V118, P401
[6]  
Celniker Susan., 2002, GENOME BIOL, V3, DOI [10.1186/gb-2002-3-12-research0079, DOI 10.1186/GB-2002-3-12-RESEARCH0079]
[7]   Maintenance of stable heterochromatin domains by dynamic HP1 binding [J].
Cheutin, T ;
McNairn, AJ ;
Jenuwein, T ;
Gilbert, DM ;
Singh, PB ;
Misteli, T .
SCIENCE, 2003, 299 (5607) :721-725
[8]   Physical and functional association of SU(VAR)3-9 and HDAC1 in Drosophila [J].
Czermin, B ;
Schotta, G ;
Hülsmann, BB ;
Brehm, A ;
Becker, PB ;
Reuter, G ;
Imhof, A .
EMBO REPORTS, 2001, 2 (10) :915-919
[9]   Increased expression of Drosophila Su(var)3-7 triggers Su(var)3-9-dependent heterochromatin formation [J].
Delattre, M ;
Spierer, A ;
Jaquet, Y ;
Spierer, P .
JOURNAL OF CELL SCIENCE, 2004, 117 (25) :6239-6247
[10]   EXPANSIONS OF TRANSGENE REPEATS CAUSE HETEROCHROMATIN FORMATION AND GENE SILENCING IN DROSOPHILA [J].
DORER, DR ;
HENIKOFF, S .
CELL, 1994, 77 (07) :993-1002