Slow elimination of phosphorylated histone γ-H2AX from DNA of terminally differentiated mouse heart cells in situ

被引：27

作者：

Gavrilov, Boris ^{[1
]}

Vezhenkova, Irina ^{[1
]}

Firsanov, Denis ^{[1
]}

Solovjeva, Liudmila ^{[1
]}

Svetlova, Maria ^{[1
]}

Mikhailov, Vyacheslav ^{[1
]}

Tomilin, Nikolai ^{[1
]}

机构：

[1] Russian Acad Sci, Inst Cytol, St Petersburg 194064, Russia

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2006年 / 347卷 / 04期

基金：

俄罗斯基础研究基金会;

关键词：

ionizing radiation; historic H2AX phosphorylation; differentiated heart cells; chromatin remodeling;

D O I：

10.1016/j.bbrc.2006.07.005

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：

Phosphorylation of replacement histone H2AX occurs in megabase chromatin domains around double-strand DNA breaks (DSBs) and this modification (called gamma-H2AX) may serve as a useful marker of genome damage and repair in terminally differentiated cells. Here using immunohistochemistry we studied kinetics of gamma-H2AX formation and elimination in the X-irradiated mouse heart and renal epithelial tissues in situ. Unirradiated tissues have 3-5% gamma-H2AX-positive cells and in tissues fixed 1 h after X-irradiation gamma-H2AX-positive nuclei are induced in a dose-dependent manner approaching 20-30% after 3 Gy of IR. Analysis of mouse tissues at different times after 3 Gy of IR showed that maximal induction of gamma-H2AX in heart is observed 20 min after IR and then is decreased slowly with about half remaining 23 It later. In renal epithelium maximum of the gamma-H2AX-positive cells is observed 40 min after IR and then decreases to control values in 23 h. This indicates that there are significant variations between non-proliferating mammalian tissues in the initial H2AX phosphorylation rate as well as in the rate of gamma-H2AX elimination after X-irradiation, which should be taken into account in the analysis of radiation responses. (c) 2006 Published by Elsevier Inc.

引用

页码：1048 / 1052

页数：5

共 19 条

[1] Radiation sensitivity, H2AX phosphorylation, and kinetics of repair of DNA strand breaks in irradiated cervical cancer cell lines [J].

Banáth, JP ;

MacPhail, SH ;

Olive, PL .

CANCER RESEARCH, 2004, 64 (19) :7144-7149

[2] γ-H2AX dephosphorylation by protein phosphatase 2A facilitates DNA double-strand break repair [J].

Chowdhury, D ;

Keogh, MC ;

Ishii, H ;

Peterson, CL ;

Buratowski, S ;

Lieberman, J .

MOLECULAR CELL, 2005, 20 (05) :801-809

[3] A phosphatase complex that dephosphorylates γH2AX regulates DNA damage checkpoint recovery [J].

Keogh, MC ;

Kim, JA ;

Downey, M ;

Fillingham, J ;

Chowdhury, D ;

Harrison, JC ;

Onishi, M ;

Datta, N ;

Galicia, S ;

Emili, A ;

Lieberman, J ;

Shen, XT ;

Buratowski, S ;

Haber, JE ;

Durocher, D ;

Greenblatt, JF ;

Krogan, NJ .

NATURE, 2006, 439 (7075) :497-501

[4]

Kitada S, 1996, ONCOGENE, V12, P187

[5] A double-strand break repair defect in ATM-deficient cells contributes to radiosensitivity [J].

Kühne, M ;

Riballo, E ;

Rief, N ;

Rothkamm, K ;

Jeggo, PA ;

Löbrich, M .

CANCER RESEARCH, 2004, 64 (02) :500-508

[6] Acetylation by Tip60 is required for selective histone variant exchange at DNA lesions [J].

Kusch, T ;

Florens, L ;

MacDonald, WH ;

Swanson, SK ;

Glaser, RL ;

Yates, JR ;

Abmayr, SM ;

Washburn, MP ;

Workman, JL .

SCIENCE, 2004, 306 (5704) :2084-2087

[7] Organ-specific gene expressions in C57BL/6 mice after exposure to low-dose radiation [J].

Lee, WJ ;

Majumder, ZR ;

Jeoung, DI ;

Lee, HJ ;

Kim, SH ;

Bae, S ;

Lee, YS .

RADIATION RESEARCH, 2006, 165 (05) :562-569

[8] Dephosphorylation of histone γ-H2AX during repair of DNA double-strand breaks in mammalian cells and its inhibition by calyculin A [J].

Nazarov, OB ;

Smirnova, AN ;

Krutilina, RI ;

Svetlova, MP ;

Solovjeva, LV ;

Nikiforov, AA ;

Oei, SL ;

Zalenskaya, IA ;

Yau, PM ;

Bradbury, EM ;

Tomilin, NV .

RADIATION RESEARCH, 2003, 160 (03) :309-317

[9] DNA repair in terminally differentiated cells [J].

Nouspikel, T ;

Hanawalt, PC .

DNA REPAIR, 2002, 1 (01) :59-75

[10] Radiation-induced H2AX phosphorylation and neural precursor apoptosis in the developing brain of mice [J].

Nowak, E ;

Etienne, O ;

Millet, P ;

Lages, CS ;

Mathieu, C ;

Mouthon, MA ;

Boussin, FD .

RADIATION RESEARCH, 2006, 165 (02) :155-164

← 1 2 →