p53-dependent upregulation of PIG3 transcription by γ-ray irradiation and its interaction with KAP1 in responding to DNA damage

详细信息    查看全文

• 作者：Xia Qin (1)
  ShiMeng Zhang (1)
  Bing Li (1)
  XiaoDan Liu (1)
  XingPeng He (2)
  ZengFu Shang (1)
  QinZhi Xu (1)
  ZengQiang Zhao (1)
  QiNong Ye (3)
  PingKun Zhou (1) (2)
  
• 关键词：PIG3 ; KAP1 ; p53 ; DNA damage response ; inducible expression ; large ; scale chromatin remodeling
• 刊名：Chinese Science Bulletin
• 出版年：2011
• 出版时间：October 2011
• 年：2011
• 卷：56
• 期：30
• 页码：3162-3171
• 全文大小：1146KB
• 参考文献：1. Polyak K, Xia Y, Zweier J L, et al. A model for p53-induced apoptosis. Nature, 1997, 389: 300-05 CrossRef
  2. Rao P V, Krishna C M, Zigler Jr J S. Identification and characterization of the enzymatic activity of zeta-crystallin from guinea pig lens. A novel NADPH: Quinone oxidoreductase. J Biol Chem, 1992, 267: 96-02
  3. Porte S, Valencia E, Yakovtseva E A, et al. Three-dimensional structure and enzymatic function of proapoptotic human p53-inducible quinone oxidoreductase PIG3. J Biol Chem, 2009, 284: 17194-7205 CrossRef
  4. Lee J H, Kang Y, Khare V, et al. The p53-inducible gene 3 ( / PIG3) contributes to early cellular response to DNA damage. Oncogene, 2009, 29: 1431-450 CrossRef
  5. Flatt P M, Polyak K, Tang L J, et al. p53-dependent expression of PIG3 during proliferation, genotoxic stress, and reversible growth arrest. Cancer Lett, 2000, 156: 63-2 CrossRef
  6. Szak S T, Mays D, Pietenpol J A. Kinetics of p53 binding to promoter sites / in vivo. Mol Cell Biol, 2001, 21: 3375-386 CrossRef
  7. Tanaka T, Ohkubo S, Tatsuno I, et al. hCAS/CSE1L associates with chromatin and regulates expression of select p53 target genes. Cell, 2007, 130: 638-50 CrossRef
  8. Long X H, Zhao Z Q, He X P, et al. Dose-dependent expression changes of early response genes to ionizing radiation in human lymphoblastoid cells. Int J Mol Med, 2007, 19: 607-15
  9. Contente A, Dittmer A, Koch M C, et al. A polymorphic microsatellite that mediates induction of PIG3 by p53. Nat Genet, 2002, 30: 315-20 CrossRef
  10. Nomdedeu J F, Perea G, Estivill C, et al. Loss of heterozygosity of the polymorphic PIG3 microsatellite with low frequency in / de novo acute myeloid leukemias. Leukemia, 2004, 18: 1148-149 CrossRef
  11. Nomdedeu J F, Perea G, Estivill C, et al. Microsatellite instability may involve the pentanucleotide repeat of the PIG3 promoter in bcr/abl acute lymphoblastic leukemia. Leukemia Res, 2008, 32: 186-88 CrossRef
  12. Qin X, Zhang S M, Xu Q Z, et al. Establishment of a technology detecting chromatin remodeling based on GFP fluorescence imaging (in Chinese). Prog Biochem Biophys, 2011, 38: 558-62 CrossRef
  13. Tumbar T, Sudlow G, Belmont A S. Large-scale chromatin unfolding and remodeling induced by VP16 acidic activation domain. J Biol Chem, 1999, 145: 1341-354
  14. Scheffner M, Werness B A, Huibregtse J M, et al. The E6 oncoprotein encoded by human papillomavirus types 16 and 18 promotes the degradation of p53. Cell, 1990, 63: 1129-136 CrossRef
  15. Scheffner M, Huibregtse J M, Vierstra R D, et al. The HPV-16 E6 and E6-AP complex functions as a ubiquitin-protein ligase in the ubiquitination of p53. Cell, 1993, 75: 495-05 CrossRef
  16. Ziv Y, Bielopolski D, Galanty Y, et al. Chromatin relaxation in response to DNA double-strand breaks is modulated by a novel ATM and KAP-1 dependent pathway. Nat Cell Biol, 2006, 8: 870-76 CrossRef
  17. Noon A T, Shibata A, Rief N, et al. 53BP1-dependent robust localized KAP-1 phosphorylation is essential for heterochromatic DNA double-strand break repair. Nat Cell Biol, 2010, 12: 177-84 CrossRef
  18. Tsukuda T, Fleming A B, Nickoloff J A, et al. Chromatin remodelling at a DNA double-strand break site in Saccharomyces cerevisiae. Nature, 2005, 438: 379-83 CrossRef
  19. Morrison A J, Highland J, Krogan N J, et al. INO80 and γ-H2AX interaction links ATP-dependent chromatin remodeling to DNA damage repair. Cell, 2004, 119: 767-75 CrossRef
  20. Goodarzi A A, Noon A T, Deckbar D, et al. ATM signaling facilitates repair of DNA double-strand breaks associated with heterochromatin. Mol Cell, 2008, 31: 167-77 CrossRef
  21. Ura K, Araki M, Saeki H, et al. ATP-dependent chromatin remodeling facilitates nucleotide excision repair of UV-induced DNA lesions in synthetic dinucleosomes. EMBO J, 2001, 20: 2004-014 CrossRef
  22. Bao Y, Shen X. Chromatin remodeling in DNA double-strand break repair. Curr Opin Genet Dev, 2007, 17: 126-31 CrossRef
  23. Peng G, Yim E K, Dai H, et al. BRIT1/MCPH1 links chromatin remodelling to DNA damage response. Nat Cell Biol, 2009, 11: 865-72 CrossRef
  24. Wang C, Ivanov A, Chen L, et al. MDM2 interaction with nuclear corepressor KAP1 contributes to p53 inactivation. EMBO J, 2005, 24: 3279-290 CrossRef
  
• 作者单位：Xia Qin (1)
  ShiMeng Zhang (1)
  Bing Li (1)
  XiaoDan Liu (1)
  XingPeng He (2)
  ZengFu Shang (1)
  QinZhi Xu (1)
  ZengQiang Zhao (1)
  QiNong Ye (3)
  PingKun Zhou (1) (2)
  
  1. Department of Radiation Toxicology and Oncology, Beijing Institute of Radiation Medicine, Beijing, 100850, China
  2. College of Public Health, University of South China, Hengyang, 421000, China
  3. Beijing Institute of Biotechnology, Beijing, 100850, China
  
• ISSN：1861-9541

文摘

PIG3 (p53-inducible gene 3), originally identified as one of a set of genes induced by p53 before the onset of apoptosis, was assumed to contribute to early cellular response to DNA damage. Here, we studied the relation between p53 status and the increased expression of PIG3 by ionizing radiation (IR), and the related clues regarding the involvement of PIG3 in the cellular response to IR-induced DNA damage signaling. We demonstrated that the pentanucleotide microsatellite sequence was responsible for the p53-dependent induction of PIG3 transcription after irradiation, while sequence upstream of PIG3 promoter could maintain the basal level of expression which was not inducible by irradiation. The interaction of PIG3 and the KRAB-ZFP-associated protein 1 (KAP1), a DNA damage response protein, was revealed. PIG3 nucleus foci were formed 15 min after γ-ray irradiation, and which were found to partially colocalize with the phospho-KAP-1 foci as well as γ-H2AX foci. Although the lac operator tagged EGFP based reporter system revealed that PIG3 does not remodel chromatin in large scale in the cells under normal growing condition, it indeed prompted the chromatin relaxation in the cellular response to DNA damage signaling. All these data suggest that PIG3 is involved in IR-induced DNA damage response, and which maybe partially attribute to its interaction with KAP1.