学术探索
学术期刊
新闻热点
数据分析
智能评审

JBP2, a SWI2/SNF2-like protein, regulates de novo telomeric DNA glycosylation in bloodstream form Trypanosoma brucei

被引：23
作者：
Kieft, Rudo
Brand, Verena
Ekanayake, Dilrukshi K.
Sweeney, Kate
DiPaolo, Courtney
Reznikoff, William S.
Sabatini, Robert [1 ]
机构：
[1] Univ Georgia, Dept Biochem & Mol Biol, Athens, GA 30602 USA
[2] Univ Wisconsin, Dept Biochem, Madison, WI 53705 USA
来源：
MOLECULAR AND BIOCHEMICAL PARASITOLOGY | 2007年 / 156卷 / 01期
关键词：
Trypanasoma brucei; base J; DNA modification; antigenic variation;
D O I：
10.1016/j.molbiopara.2007.06.010
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：
Synthesis of the modified thymine base, beta-D-glucosyl-hydroxymethyluraciI or J, within telomeric DNA of Trypanosoma brucei correlates with the bloodstream form specific epigenetic silencing of telomeric variant surface glycoprotein genes involved in antigenic variation. In order to analyze the function of base J in the regulation of antigenic variation, we are characterizing the regulatory mechanism of J biosynthesis. We have recently proposed a model in which chromatin remodeling by a SW12/SNF2-like protein (JBP2) regulates the developmental and de novo site-specific localization of J synthesis within bloodstream form trypanosome DNA. Consistent with this model, we now show that JBP2 (-/-) bloodstream form trypanosomes contain five-fold less base J and are unable to stimulate de novo J synthesis in newly generated telomeric arrays. (C) 2007 Elsevier B.V. All rights reserved.
引用
收藏
页码：24 / 31
页数：8
相关论文
共 14 条
[1]   ACTIVATION OF TRYPANOSOME SURFACE GLYCOPROTEIN GENES INVOLVES A DUPLICATION-TRANSPOSITION LEADING TO AN ALTERED 3' END [J].
BERNARDS, A ;
VANDERPLOEG, LHT ;
FRASCH, ACC ;
BORST, P ;
BOOTHROYD, JC ;
COLEMAN, S ;
CROSS, GAM .
CELL, 1981, 27 (03) :497-505
[2]   β-D-glucosyl-hydroxymethyluracil, a novel base in African trypanosomes and other Kinetoplastida [J].
Borst, P ;
van Leeuwen, F .
MOLECULAR AND BIOCHEMICAL PARASITOLOGY, 1997, 90 (01) :1-8
[3]   CONTROL OF ANTIGENIC VARIATION IN AFRICAN TRYPANOSOMES [J].
BORST, P ;
GOMMERSAMPT, JH ;
LIGTENBERG, MJL ;
RUDENKO, G ;
KIEFT, R ;
TAYLOR, MC ;
BLUNDELL, PA ;
VANLEEUWEN, F .
COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY, 1993, 58 :105-114
[4]   The modified base J is the target for a novel DNA-binding protein in kinetoplastid protozoans [J].
Cross, M ;
Kieft, R ;
Sabatini, R ;
Wilm, M ;
de Kort, M ;
van der Marel, GA ;
van Boom, JH ;
van Leeuwen, F ;
Borst, P .
EMBO JOURNAL, 1999, 18 (22) :6573-6581
[5]   J-binding protein increases the level and retention of the unusual base J in trypanosome DNA [J].
Cross, M ;
Kieft, R ;
Sabatini, R ;
Dirks-Mulder, A ;
Chaves, I ;
Borst, P .
MOLECULAR MICROBIOLOGY, 2002, 46 (01) :37-47
[6]   Regulation of trypanosome DNA glycosylation by a SWI2/SNF2-like protein [J].
DiPaolo, C ;
Kieft, R ;
Cross, M ;
Sabatini, R .
MOLECULAR CELL, 2005, 17 (03) :441-451
[7]   Repression of polymerase I-mediated gene expression at Trypanosoma brucei telomeres [J].
Glover, L ;
Horn, D .
EMBO REPORTS, 2006, 7 (01) :93-99
[8]   BETA-D-GLUCOSYL-HYDROXYMETHYLURACIL - A NOVEL MODIFIED BASE PRESENT IN THE DNA OF THE PARASITIC PROTOZOAN TRYPANOSOMA-BRUCEI [J].
GOMMERSAMPT, JH ;
VANLEEUWEN, F ;
DEBEER, ALJ ;
VLIEGENTHART, JFG ;
DIZDAROGLU, M ;
KOWALAK, JA ;
CRAIN, PF ;
BORST, P .
CELL, 1993, 75 (06) :1129-1136
[9]   Recognition of base J in duplex DNA by J-binding protein. [J].
Sabatini, R ;
Meeuwenoord, N ;
van Boom, JH ;
Borst, P .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (02) :958-966
[10]   Expression of the human DNA glycosylase hSMUG1 in Trypanosoma brucei causes DNA damage and interferes with J biosynthesis [J].
Ulbert, S ;
Cross, M ;
Boorstein, RJ ;
Teebor, GW ;
Borst, P .
NUCLEIC ACIDS RESEARCH, 2002, 30 (18) :3919-3926
12