Faculty Opinions recommendation of DNA Damage-Induced Nucleosome Depletion Enhances Homology Search Independently of Local Break Movement.

Author(s):  
Antony Carr
Keyword(s):  
2020 ◽  
Vol 80 (2) ◽  
pp. 311-326.e4 ◽  
Author(s):  
Anaïs Cheblal ◽  
Kiran Challa ◽  
Andrew Seeber ◽  
Kenji Shimada ◽  
Haruka Yoshida ◽  
...  
Keyword(s):  

2019 ◽  
Vol 30 (21) ◽  
pp. 2620-2625 ◽  
Author(s):  
Michael J. Smith ◽  
Eric E. Bryant ◽  
Fraulin J. Joseph ◽  
Rodney Rothstein

During S phase in Saccharomyces cerevisiae, chromosomal loci become mobile in response to DNA double-strand breaks both at the break site (local mobility) and throughout the nucleus (global mobility). Increased nuclear exploration is regulated by the recombination machinery and the DNA damage checkpoint and is likely an important aspect of homology search. While mobility in response to DNA damage has been studied extensively in S phase, the response in interphase has not, and the question of whether homologous recombination proceeds to completion in G1 phase remains controversial. Here, we find that global mobility is triggered in G1 phase. As in S phase, global mobility in G1 phase is controlled by the DNA damage checkpoint and the Rad51 recombinase. Interestingly, despite the restriction of Rad52 mediator foci to S phase, Rad51 foci form at high levels in G1 phase. Together, these observations indicate that the recombination and checkpoint machineries promote global mobility in G1 phase, supporting the notion that recombination can occur in interphase diploids.


2004 ◽  
Vol 171 (4S) ◽  
pp. 416-416
Author(s):  
Tamer M. Said ◽  
Shyam Allamaneni ◽  
Kiran P. Nallella ◽  
Rakesh K. Sharma ◽  
Sijo J. Parekattil ◽  
...  

Nature ◽  
2020 ◽  
Vol 579 (7800) ◽  
pp. 499-500
Author(s):  
Irene Gallina ◽  
Julien P. Duxin
Keyword(s):  

1999 ◽  
Vol 96 (1) ◽  
pp. 143-146 ◽  
Author(s):  
J.-P. Pouget ◽  
J.-L. Ravanat ◽  
T. Douki ◽  
M.-J. Richard ◽  
J. Cadet

2010 ◽  
Vol 49 (S 01) ◽  
pp. S64-S68
Author(s):  
E. Dikomey

SummaryIonising irradiation acts primarily via induction of DNA damage, among which doublestrand breaks are the most important lesions. These lesions may lead to lethal chromosome aberrations, which are the main reason for cell inactivation. Double-strand breaks can be repaired by several different mechanisms. The regulation of these mechanisms appears be fairly different for normal and tumour cells. Among different cell lines capacity of doublestrand break repair varies by only few percents and is known to be determined mostly by genetic factors. Knowledge about doublestrand break repair mechanisms and their regulation is important for the optimal application of ionising irradiation in medicine.


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