scholarly journals A comparison of G2 phase radiation-induced chromatid break kinetics using calyculin-PCC with those obtained using colcemid block

Mutagenesis ◽  
2007 ◽  
Vol 22 (5) ◽  
pp. 359-362 ◽  
Author(s):  
P. E. Bryant ◽  
H. Mozdarani
1992 ◽  
Vol 60 (2) ◽  
pp. 183-187 ◽  
Author(s):  
Martin F. Lavin ◽  
Priscilla Le Poidevin ◽  
Paul Bates

2011 ◽  
Vol 101 (1) ◽  
pp. 46-50 ◽  
Author(s):  
Andrea Beucher ◽  
Dorothee Deckbar ◽  
Eik Schumann ◽  
Andrea Krempler ◽  
Marlis Frankenberg-Schwager ◽  
...  

1989 ◽  
Vol 10 (10) ◽  
pp. 1911-1916 ◽  
Author(s):  
Katherine K. Sanford ◽  
Ram Parshad ◽  
Floyd M. Price ◽  
Raymond Gantt ◽  
Gary M. Jones ◽  
...  
Keyword(s):  

2010 ◽  
Vol 21 (22) ◽  
pp. 3866-3877 ◽  
Author(s):  
Burcu Inanç ◽  
Helen Dodson ◽  
Ciaran G. Morrison

DNA damage can induce centrosome overduplication in a manner that requires G2-to-M checkpoint function, suggesting that genotoxic stress can decouple the centrosome and chromosome cycles. How this happens is unclear. Using live-cell imaging of cells that express fluorescently tagged NEDD1/GCP-WD and proliferating cell nuclear antigen, we found that ionizing radiation (IR)-induced centrosome amplification can occur outside S phase. Analysis of synchronized populations showed that significantly more centrosome amplification occurred after irradiation of G2-enriched populations compared with G1-enriched or asynchronous cells, consistent with G2 phase centrosome amplification. Irradiated and control populations of G2 cells were then fused to test whether centrosome overduplication is allowed through a diffusible stimulatory signal, or the loss of a duplication-inhibiting signal. Irradiated G2/irradiated G2 cell fusions showed significantly higher centrosome amplification levels than irradiated G2/unirradiated G2 fusions. Chicken–human cell fusions demonstrated that centrosome amplification was limited to the irradiated partner. Our finding that only the irradiated centrosome can duplicate supports a model where a centrosome-autonomous inhibitory signal is lost upon irradiation of G2 cells. We observed centriole disengagement after irradiation. Although overexpression of dominant-negative securin did not affect IR-induced centrosome amplification, Plk1 inhibition reduced radiation-induced amplification. Together, our data support centriole disengagement as a licensing signal for DNA damage-induced centrosome amplification.


1994 ◽  
Vol 76 (1) ◽  
pp. 43-46 ◽  
Author(s):  
Philip Chen ◽  
Áine Farrell ◽  
Karen Hobson ◽  
Adeeb Girjes ◽  
Martin Lavin

2011 ◽  
pp. 667-677 ◽  
Author(s):  
J. CMIELOVÁ ◽  
R. HAVELEK ◽  
A. JIROUTOVÁ ◽  
R. KOHLEROVÁ ◽  
M. SEIFRTOVÁ ◽  
...  

Cellular response to ionizing radiation-induced damage depends on the cell type and the ability to repair DNA damage. Some types of cells undergo apoptosis, whereas others induce a permanent cell cycle arrest and do not proliferate. Our study demonstrates two types of response of embryonic diploid fibroblasts WI-38 to ionizing radiation. In the WI-38 cells p53 is activated, protein p21 increases, but the cells are arrested in G2 phase of cell cycle. Some of the cells die by apoptosis, but in remaining viable cells p16 increases, senescence associated DNA-damage foci occur, and senescence-associated beta-galactosidase activity increases, which indicate stress-induced premature senescence.


Sign in / Sign up

Export Citation Format

Share Document