scholarly journals Evidence for Sequential and Increasing Activation of Replication Origins along Replication Timing Gradients in the Human Genome

2011 ◽  
Vol 7 (12) ◽  
pp. e1002322 ◽  
Author(s):  
Guillaume Guilbaud ◽  
Aurélien Rappailles ◽  
Antoine Baker ◽  
Chun-Long Chen ◽  
Alain Arneodo ◽  
...  
2016 ◽  
Vol 26 (3) ◽  
pp. 365-375 ◽  
Author(s):  
Jared M. Peace ◽  
Sandra K. Villwock ◽  
John L. Zeytounian ◽  
Yan Gan ◽  
Oscar M. Aparicio

2012 ◽  
Vol 23 (1) ◽  
pp. 1-11 ◽  
Author(s):  
G. I. Dellino ◽  
D. Cittaro ◽  
R. Piccioni ◽  
L. Luzi ◽  
S. Banfi ◽  
...  

2012 ◽  
Vol 31 (18) ◽  
pp. 3667-3677 ◽  
Author(s):  
Satoshi Yamazaki ◽  
Aii Ishii ◽  
Yutaka Kanoh ◽  
Masako Oda ◽  
Yasumasa Nishito ◽  
...  

2019 ◽  
Author(s):  
Haiyang Zhang ◽  
Meghan V. Petrie ◽  
Yiwei He ◽  
Jared M. Peace ◽  
Irene E. Chiolo ◽  
...  

ABSTRACTChromosomal DNA elements are organized into spatial domains within the eukaryotic nucleus. Sites undergoing DNA replication, high-level transcription, and repair of double-strand breaks coalesce into foci, although the significance and mechanisms giving rise to these dynamic structures are poorly understood. InS. cerevisiae, replication origins occupy characteristic subnuclear localizations that anticipate their initiation timing during S phase. Here, we link localization of replication origins in G1 phase with Fkh1 activity, which is required for their early replication timing. Using a Fkh1-dependent origin relocalization assay, we determine that execution of Dbf4-dependent kinase function, including Cdc45 loading, results in dynamic relocalization of a replication origin from the nuclear periphery to the interior in G1 phase. Origin mobility increases substantially with Fkh1-driven relocalization. These findings provide novel molecular insight into the mechanisms that govern dynamics and spatial organization of DNA replication origins and possibly other functional DNA elements.


2012 ◽  
Vol 26 (18) ◽  
pp. 2050-2062 ◽  
Author(s):  
A. Tazumi ◽  
M. Fukuura ◽  
R. Nakato ◽  
A. Kishimoto ◽  
T. Takenaka ◽  
...  

2020 ◽  
Author(s):  
Haiqing Fu ◽  
Christophe E. Redon ◽  
Koichi Utani ◽  
Bhushan L. Thakur ◽  
Sangmin Jang ◽  
...  

AbstractWe determined replication patterns in cancer cells in which the controls that normally prevent excess replication were disrupted (“re-replicating cells”). Single-fiber analyses suggested that replication origins were activated at a higher frequency in re-replicating cells. However, nascent strand sequencing demonstrated that re-replicating cells utilized the same pool of potential replication origins as normally replicating cells. Surprisingly, re-replicating cells exhibited a skewed initiation frequency correlating with replication timing. These patterns differed from the replication profiles observed in non-re-replicating cells exposed to replication stress, which activated a novel group of dormant origins not typically activated during normal mitotic growth. Hence, disruption of the molecular interactions that regulates origin initiation can activate two distinct pools of potential replication origins: re-replicating cells over-activate flexible origins while replication stress in normal mitotic growth activates dormant origins.


2018 ◽  
Vol 37 (15) ◽  
Author(s):  
Shiho Ogawa ◽  
Sayuri Kido ◽  
Tetsuya Handa ◽  
Hidesato Ogawa ◽  
Haruhiko Asakawa ◽  
...  

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