Mobile D-loops are a preferred substrate for the Bloom's syndrome helicase

被引:187
作者
Bachrati, Csanad Z.
Borts, Rhona H.
Hickson, Ian D. [1 ]
机构
[1] Univ Oxford, John Radcliffe Hosp, Weatherall Inst Mol Med, Canc Res UK Labs, Oxford OX3 9DS, England
[2] Univ Leicester, Dept Genet, Leicester LE1 7RH, Leics, England
关键词
D O I
10.1093/nar/gkl258
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
The Bloom's syndrome helicase, BLM, is a member of the highly conserved RecQ family, and possesses both DNA unwinding and DNA strand annealing activities. BLM also promotes branch migration of Holliday junctions. One role for BLM is to act in conjunction with topoisomerase III alpha to process homologous recombination (HR) intermediates containing a double Holliday junction by a process termed dissolution. However, several lines of evidence suggest that BLM may also act early in one or more of the recombination pathways to eliminate illegitimate or aberrantly paired DNA joint molecules. We have investigated whether BLM can disrupt DNA displacement loops (D-loops), which represent the initial strand invasion step of HR. We show that mobile D-loops created by the RecA recombinase are a highly preferred substrate for BLM with the invading strand being displaced from the duplex. We have identified structural features of the D-loop that determine the efficiency with which BLM promotes D-loop dissociation. We discuss these results in the context of models for the role of BLM as an 'anti-recombinase'.
引用
收藏
页码:2269 / 2279
页数:11
相关论文
共 44 条
  • [1] Drosophila BLM in double-strand break repair by synthesis-dependent strand annealing
    Adams, MD
    McVey, M
    Sekelsky, JJ
    [J]. SCIENCE, 2003, 299 (5604) : 265 - 267
  • [2] RecQ helicases: suppressors of tumorigenesis and premature aging
    Bachrati, CZ
    Hickson, ID
    [J]. BIOCHEMICAL JOURNAL, 2003, 374 : 577 - 606
  • [3] Replication protein A physically interacts with the Bloom's syndrome protein and stimulates its helicase activity
    Brosh, RM
    Li, JL
    Kenny, MK
    Karow, JK
    Cooper, MP
    Kureekattil, RP
    Hickson, ID
    Bohr, VA
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (31) : 23500 - 23508
  • [4] MANIFOLD INCREASE IN SISTER CHROMATID EXCHANGES IN BLOOMS SYNDROME LYMPHOCYTES
    CHAGANTI, RS
    SCHONBERG, S
    GERMAN, J
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1974, 71 (11) : 4508 - 4512
  • [5] The Bloom's syndrome helicase promotes the annealing of complementary single-stranded DNA
    Cheok, CF
    Wu, L
    Garcia, PL
    Janscak, P
    Hickson, ID
    [J]. NUCLEIC ACIDS RESEARCH, 2005, 33 (12) : 3932 - 3941
  • [6] THE BLOOMS-SYNDROME GENE-PRODUCT IS HOMOLOGOUS TO RECQ HELICASES
    ELLIS, NA
    GRODEN, J
    YE, TZ
    STRAUGHEN, J
    LENNON, DJ
    CIOCCI, S
    PROYTCHEVA, M
    GERMAN, J
    [J]. CELL, 1995, 83 (04) : 655 - 666
  • [7] THE YEAST TYPE-I TOPOISOMERASE TOP3 INTERACTS WITH SGS1, A DNA HELICASE HOMOLOG - A POTENTIAL EUKARYOTIC REVERSE GYRASE
    GANGLOFF, S
    MCDONALD, JP
    BENDIXEN, C
    ARTHUR, L
    ROTHSTEIN, R
    [J]. MOLECULAR AND CELLULAR BIOLOGY, 1994, 14 (12) : 8391 - 8398
  • [8] BLOOM-SYNDROME - A MENDELIAN PROTOTYPE OF SOMATIC MUTATIONAL DISEASE
    GERMAN, J
    [J]. MEDICINE, 1993, 72 (06) : 393 - 406
  • [9] The Werner syndrome protein is a DNA helicase
    Gray, MD
    Shen, JC
    KamathLoeb, AS
    Blank, A
    Sopher, BL
    Martin, GM
    Oshima, J
    Loeb, LA
    [J]. NATURE GENETICS, 1997, 17 (01) : 100 - 103
  • [10] RecQ DNA helicase is a suppressor of illegitimate recombination in Escherichia coli
    Hanada, K
    Ukita, T
    Kohno, Y
    Saito, K
    Kato, J
    Ikeda, H
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (08) : 3860 - 3865