A DNA replication origin and a replication fork barrier used in vivo in the circular plasmid pKD1

2001 ◽  
Vol 266 (2) ◽  
pp. 326-335 ◽  
Author(s):  
L. Fabiani ◽  
C. Irene ◽  
M. Aragona ◽  
C. Newlon
1996 ◽  
Vol 93 (4) ◽  
pp. 1498-1503 ◽  
Author(s):  
D. S. Dimitrova ◽  
M. Giacca ◽  
F. Demarchi ◽  
G. Biamonti ◽  
S. Riva ◽  
...  

2016 ◽  
Vol 21 (8) ◽  
pp. 907-914 ◽  
Author(s):  
Masahiro Tatsumi Akiyama ◽  
Taku Oshima ◽  
Onuma Chumsakul ◽  
Shu Ishikawa ◽  
Hisaji Maki

2018 ◽  
Author(s):  
Jean-Michel Arbona ◽  
Arach Goldar ◽  
Olivier Hyrien ◽  
Alain Arneodo ◽  
Benjamin Audit

AbstractThe time-dependent rate I(t) of origin firing per length of unreplicated DNA presents a universal bell shape in eukaryotes that has been interpreted as the result of a complex time-evolving interaction between origins and limiting firing factors. Here we show that a normal diffusion of replication fork components towards localized potential replication origins (p-oris) can more simply account for the I(t) universal bell shape, as a consequence of a competition between the origin firing time and the time needed to replicate DNA separating two neighboring p-oris. We predict the I(t) maximal value to be the product of the replication fork speed with the squared p-ori density. We show that this relation is robustly observed in simulations and in experimental data for several eukaryotes. Our work underlines that fork-component recycling and potential origins localization are sufficient spatial ingredients to explain the universality of DNA replication kinetics.


eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Jean-Michel Arbona ◽  
Arach Goldar ◽  
Olivier Hyrien ◽  
Alain Arneodo ◽  
Benjamin Audit

The time-dependent rate I(t) of origin firing per length of unreplicated DNA presents a universal bell shape in eukaryotes that has been interpreted as the result of a complex time-evolving interaction between origins and limiting firing factors. Here, we show that a normal diffusion of replication fork components towards localized potential replication origins (p-oris) can more simply account for the I(t) universal bell shape, as a consequence of a competition between the origin firing time and the time needed to replicate DNA separating two neighboring p-oris. We predict the I(t) maximal value to be the product of the replication fork speed with the squared p-ori density. We show that this relation is robustly observed in simulations and in experimental data for several eukaryotes. Our work underlines that fork-component recycling and potential origins localization are sufficient spatial ingredients to explain the universality of DNA replication kinetics.


1988 ◽  
Vol 8 (10) ◽  
pp. 4018-4027
Author(s):  
D Lockshon ◽  
D A Galloway

Herpes simplex virus (HSV) types 1 and 2 contain two classes of origins of DNA replication, oriS and oriL, which are closely related. A series of plasmids was constructed which contained specifically altered versions of the HSV type 2 oriS replication origin. Their ability to replicate in an in vivo replicon assay allowed a core origin of 75 base pairs (bp) to be defined. It included both arms of a 56-bp palindrome and from 13 to 20 bp of sequence leftward of the palindrome. The AT-rich sequence at the center of the palindrome was essential. Sequences on either side of the core origin enhanced replication. When additional copies of the -AT-dinucleotide were introduced progressively into the center of the palindrome, an oscillating effect on origin function was observed. These and other data implicate a linear rather than a cruciform conformation of the oriS palindrome in the initiation of HSV replication.


2017 ◽  
Vol 65 (1) ◽  
pp. 117-130 ◽  
Author(s):  
Christoph F. Kurat ◽  
Joseph T.P. Yeeles ◽  
Harshil Patel ◽  
Anne Early ◽  
John F.X. Diffley

1988 ◽  
Vol 8 (10) ◽  
pp. 4018-4027 ◽  
Author(s):  
D Lockshon ◽  
D A Galloway

Herpes simplex virus (HSV) types 1 and 2 contain two classes of origins of DNA replication, oriS and oriL, which are closely related. A series of plasmids was constructed which contained specifically altered versions of the HSV type 2 oriS replication origin. Their ability to replicate in an in vivo replicon assay allowed a core origin of 75 base pairs (bp) to be defined. It included both arms of a 56-bp palindrome and from 13 to 20 bp of sequence leftward of the palindrome. The AT-rich sequence at the center of the palindrome was essential. Sequences on either side of the core origin enhanced replication. When additional copies of the -AT-dinucleotide were introduced progressively into the center of the palindrome, an oscillating effect on origin function was observed. These and other data implicate a linear rather than a cruciform conformation of the oriS palindrome in the initiation of HSV replication.


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