Establishment of poly(ADP-ribose) polymerase-deficient mouse embryonic stem cell lines

被引:12
作者
Masutani, M [1 ]
Nozaki, T
Nishiyama, E
Ochiya, T
Nakagama, H
Wakabayashi, K
Suzuki, H
Sugimura, T
机构
[1] Natl Canc Ctr, Res Inst, Div Biochem, Chuo Ku, Tokyo 1040045, Japan
[2] Natl Canc Ctr, Res Inst, Sect Studies Metastasis, Chuo Ku, Tokyo 1040045, Japan
[3] Natl Canc Ctr, Res Inst, Can Prevent Div, Chuo Ku, Tokyo 1040045, Japan
[4] Chugai Pharmaceut Co Ltd, Shizuoka 4120038, Japan
来源
PROCEEDINGS OF THE JAPAN ACADEMY SERIES B-PHYSICAL AND BIOLOGICAL SCIENCES | 1998年 / 74卷 / 10期
关键词
Gene-targeting; poly(ADP-ribose) polymerase; embryonic stem cells;
D O I
10.2183/pjab.74.233
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Many studies revealed that poly(ADP-ribose) polymerase (Parp) is involved in DNA-damage recovery, cell-death induction and maintenance of genomic stability. We generated mouse Parp(+/-) embryonic stem (ES) cell lines by disrupting one allele of Parp exon 1 with a neomycin-resistance gene-cassette and subsequently produced Parp(-/-) ES cells by disrupting the remaining allele with a puromycin-resistance gene-cassette. Parp activity was decreased to half in Parp(+/-) ES cell clones and lost in Parp(-/-) ES cell clones. Growth rates of Parp(+/-) and Parp(-/-) ES cell clones were similar to that of parental J1 ES cells, indicating that Parp is not required for ES cell proliferation. These Parp(-/-) ES cells will be useful to study biological role of poly(ADP-ribosyl)ation reaction.
引用
收藏
页码:233 / 236
页数:4
相关论文
共 12 条
  • [1] ALTHAUS FR, 1987, ADP RIBOSYLATION PRO, P3
  • [2] BERGER NA, 1983, ADP RIBOSYLATION DNA, P219
  • [3] Requirement of poly(ADP-ribose) polymerase in recovery from DNA damage in mice and in cells
    deMurcia, JM
    Niedergang, C
    Trucco, C
    Ricoul, M
    Dutrillaux, B
    Mark, M
    Oliver, FJ
    Masson, M
    Dierich, A
    LeMeur, M
    Walztinger, C
    Chambon, P
    deMurcia, G
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (14) : 7303 - 7307
  • [4] DING RC, 1992, J BIOL CHEM, V267, P12804
  • [5] POSTTRANSLATIONAL MODIFICATION OF POLY(ADP-RIBOSE) POLYMERASE INDUCED BY DNA STRAND BREAKS
    LINDAHL, T
    SATOH, MS
    POIRIER, GG
    KLUNGLAND, A
    [J]. TRENDS IN BIOCHEMICAL SCIENCES, 1995, 20 (10) : 405 - 411
  • [6] CLONING AND FUNCTIONAL EXPRESSION OF POLY(ADP-RIBOSE) POLYMERASE CDNA FROM SARCOPHAGA-PEREGRINA
    MASUTANI, M
    NOZAKI, T
    HITOMI, Y
    IKEJIMA, M
    NAGASAKI, K
    DEPRATI, AC
    KURATA, S
    NATORI, S
    SUGIMURA, T
    ESUMI, H
    [J]. EUROPEAN JOURNAL OF BIOCHEMISTRY, 1994, 220 (02): : 607 - 614
  • [7] MASUTANI M, IN PRESS MOL CELL BI
  • [8] THE ENHANCEMENT OF CYTO-TOXICITY OF N-METHYL-N-NITROSOUREA AND OF GAMMA-RADIATION BY INHIBITORS OF POLY(ADP-RIBOSE) POLYMERASE
    NDUKA, N
    SKIDMORE, CJ
    SHALL, S
    [J]. EUROPEAN JOURNAL OF BIOCHEMISTRY, 1980, 105 (03): : 525 - 530
  • [9] SUPPRESSION OF G1 ARREST AND ENHANCEMENT OF G2 ARREST BY INHIBITORS OF POLY(ADP-RIBOSE) POLYMERASE - POSSIBLE INVOLVEMENT OF POLY(ADP-RIBOSYL)ATION IN CELL-CYCLE ARREST FOLLOWING GAMMA-IRRADIATION
    NOZAKI, T
    MASUTANI, M
    AKAGAWA, T
    SUGIMURA, T
    ESUMI, H
    [J]. JAPANESE JOURNAL OF CANCER RESEARCH, 1994, 85 (11): : 1094 - 1098
  • [10] ROLE OF POLY(ADP-RIBOSE) FORMATION IN DNA-REPAIR
    SATOH, MS
    LINDAHL, T
    [J]. NATURE, 1992, 356 (6367) : 356 - 358