Comparison of the promoters of the mouse (APEX) and human (APE) apurinic endonuclease genes

被引:17
作者
Harrison, L
Ascione, AG
Takiguchi, Y
Wilson, DM
Chen, DJ
Demple, B
机构
[1] Harvard Univ, Sch Publ Hlth, Dept Canc Cell Biol, Boston, MA 02115 USA
[2] Los Alamos Natl Lab, Div Life Sci, DNA Damage & Repair Grp, Los Alamos, NM USA
来源
MUTATION RESEARCH-DNA REPAIR | 1997年 / 385卷 / 03期
关键词
DNA repair; abasic site; transcription; development; redox regulation;
D O I
10.1016/S0921-8777(97)00053-0
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
We investigated the minimal promoter of APEX, which encodes mouse apurinic DNA repair endonuclease. A 1.85-kb fragment with APEX upstream sequences and similar to 290 bp of the transcribed region linked to a chloramphenicol acetyltransferase (CAT) reporter gene was assayed by transient transfection in NIH-3T3 cells. The minimal APEX promoter was comprised of similar to 190 bp of upstream and similar to 170 bp of transcribed DNA (exon 1 and most of intron 1). This similar to 360-bp region contains two CCAAT boxes and other consensus protein binding sites, but no TATA box. Deletion of the 5'-most CCAAT box decreased activity similar to 5-fold. The second CCAAT box (situated in exon 1) may play an independent role in APEX expression. Transcription start sites have been identified downstream of the second CCAAT box, and DNase I footprinting demonstrated NIH-3T3 nuclear proteins binding this region, including an Sp1 site located between the CCAAT boxes. Electrophoretic mobility-shift assays indicated binding by purified Sp1. Mouse proteins did not bind three myc-like (USF) sites in the APEX promoter, in contrast to the APE promoter. The APEX and APE promoter had similar activity in Hela cells, but in mouse cells, the murine promoter had similar to 5-fold higher activity than did the human promoter, Both the APEX and APE promoters exhibited bidirectional activity in their cognate cells. (C) 1997 Elsevier Science B.V.
引用
收藏
页码:159 / 172
页数:14
相关论文
共 42 条
[31]   IDENTIFICATION OF RESIDUES IN THE HUMAN DNA-REPAIR ENZYME HAP1 (REF-1) THAT ARE ESSENTIAL FOR REDOX REGULATION OF JUN DNA-BINDING [J].
WALKER, LJ ;
ROBSON, CN ;
BLACK, E ;
GILLESPIE, D ;
HICKSON, ID .
MOLECULAR AND CELLULAR BIOLOGY, 1993, 13 (09) :5370-5376
[32]   A ROLE FOR THE HUMAN DNA-REPAIR ENZYME HAP1 IN CELLULAR-PROTECTION AGAINST DNA-DAMAGING AGENTS AND HYPOXIC STRESS [J].
WALKER, LJ ;
CRAIG, RB ;
HARRIS, AL ;
HICKSON, ID .
NUCLEIC ACIDS RESEARCH, 1994, 22 (23) :4884-4889
[33]   INCISION ACTIVITY OF HUMAN APURINIC ENDONUCLEASE (APE) AT ABASIC SITE ANALOGS IN DNA [J].
WILSON, DM ;
TAKESHITA, M ;
GROLLMAN, AP ;
DEMPLE, B .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1995, 270 (27) :16002-16007
[34]   Differential expression of the apurinic apyrimidinic endonuclease (APE/ref-1) multifunctional DNA base excision repair gene during fetal development and in adult rat brain and testis [J].
Wilson, TM ;
Rivkees, SA ;
Deutsch, WA ;
Kelley, MR .
MUTATION RESEARCH-DNA REPAIR, 1996, 362 (03) :237-248
[35]   REDOX ACTIVATION OF FOS JUN DNA-BINDING ACTIVITY IS MEDIATED BY A DNA-REPAIR ENZYME [J].
XANTHOUDAKIS, S ;
MIAO, G ;
WANG, F ;
PAN, YCE ;
CURRAN, T .
EMBO JOURNAL, 1992, 11 (09) :3323-3335
[36]   The redox/DNA repair protein, Ref-1, is essential for early embryonic development in mice [J].
Xanthoudakis, S ;
Smeyne, RJ ;
Wallace, JD ;
Curran, T .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1996, 93 (17) :8919-8923
[37]   THE REDOX AND DNA-REPAIR ACTIVITIES OF REF-1 ARE ENCODED BY NONOVERLAPPING DOMAINS [J].
XANTHOUDAKIS, S ;
MIAO, GG ;
CURRAN, T .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1994, 91 (01) :23-27
[38]   ACTIVATION OF AP-1 AND OF A NUCLEAR REDOX FACTOR, REF-1, IN THE RESPONSE OF HT29 COLON-CANCER CELLS TO HYPOXIA [J].
YAO, KS ;
XANTHOUDAKIS, S ;
CURRAN, T ;
ODWYER, PJ .
MOLECULAR AND CELLULAR BIOLOGY, 1994, 14 (09) :5997-6003
[39]   APOPTOSIS IN HUMAN ADENOCARCINOMA HT29 CELLS INDUCED BY EXPOSURE TO HYPOXIA [J].
YAO, KS ;
CLAYTON, M ;
ODWYER, PJ .
JOURNAL OF THE NATIONAL CANCER INSTITUTE, 1995, 87 (02) :117-122
[40]  
YOSHIMURA K, 1991, J BIOL CHEM, V266, P9140