Faculty Opinions recommendation of The Fanconi anemia protein FANCM can promote branch migration of Holliday junctions and replication forks.

2008 ◽  
Author(s):  
Philippe Pasero
Keyword(s):  
Fanconi Anemia ◽  
Holliday Junctions ◽  
Replication Forks ◽  
Branch Migration

scholarly journals The Fanconi Anemia Protein FANCM Can Promote Branch Migration of Holliday Junctions and Replication Forks

2008 ◽  
Vol 29 (1) ◽  
pp. 141-148 ◽  
Author(s):  
Kerstin Gari ◽  
Chantal Décaillet ◽  
Alicja Z. Stasiak ◽  
Andrzej Stasiak ◽  
Angelos Constantinou
Keyword(s):  
Fanconi Anemia ◽  
Holliday Junctions ◽  
Replication Forks ◽  
Branch Migration

scholarly journals DisA Limits RecG Activities at Stalled or Reversed Replication Forks

Cells ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 1357
Author(s):  
Rubén Torres ◽  
Carolina Gándara ◽  
Begoña Carrasco ◽  
Ignacio Baquedano ◽  
Silvia Ayora ◽  
...  
Keyword(s):  
Atp Hydrolysis ◽  
Holliday Junctions ◽  
Genome Integrity ◽  
Stable Complex ◽  
Dna Unwinding ◽  
Replication Forks ◽  
Dna Structures ◽  
Checkpoint Protein

The DNA damage checkpoint protein DisA and the branch migration translocase RecG are implicated in the preservation of genome integrity in reviving haploid Bacillus subtilis spores. DisA synthesizes the essential cyclic 3′, 5′-diadenosine monophosphate (c‑di-AMP) second messenger and such synthesis is suppressed upon replication perturbation. In vitro, c-di-AMP synthesis is suppressed when DisA binds DNA structures that mimic stalled or reversed forks (gapped forks or Holliday junctions [HJ]). RecG, which does not form a stable complex with DisA, unwinds branched intermediates, and in the presence of a limiting ATP concentration and HJ DNA, it blocks DisA-mediated c-di-AMP synthesis. DisA pre-bound to a stalled or reversed fork limits RecG-mediated ATP hydrolysis and DNA unwinding, but not if RecG is pre-bound to stalled or reversed forks. We propose that RecG-mediated fork remodeling is a genuine in vivo activity, and that DisA, as a molecular switch, limits RecG-mediated fork reversal and fork restoration. DisA and RecG might provide more time to process perturbed forks, avoiding genome breakage.

scholarly journals A mutation in helicase motif III ofE.coliRecG protein abolishes branch migration of Holliday junctions

1994 ◽  
Vol 22 (3) ◽  
pp. 308-313 ◽  
Author(s):  
Gary J. Sharples ◽  
Matthew C. Whitby ◽  
Lizanne Ryder ◽  
Robert G. Lloyd
Keyword(s):  
Holliday Junctions ◽  
Branch Migration

Rad54 protein promotes branch migration of Holliday junctions

Nature ◽  
2006 ◽  
Vol 442 (7102) ◽  
pp. 590-593 ◽  
Author(s):  
Dmitry V. Bugreev ◽  
Olga M. Mazina ◽  
Alexander V. Mazin
Keyword(s):  
Holliday Junctions ◽  
Branch Migration

scholarly journals The Bloom syndrome complex senses RPA-coated single-stranded DNA to restart stalled replication forks

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Ann-Marie K. Shorrocks ◽  
Samuel E. Jones ◽  
Kaima Tsukada ◽  
Carl A. Morrow ◽  
Zoulikha Belblidia ◽  
...  
Keyword(s):  
Replication Stress ◽  
Bloom Syndrome ◽  
Holliday Junctions ◽  
Replication Forks ◽  
Single Stranded Dna ◽  
Ssdna Binding ◽  
Ssdna Binding Protein ◽  
Dna Replication Stress ◽  
Dna End Resection ◽  
Stalled Replication Forks

AbstractThe Bloom syndrome helicase BLM interacts with topoisomerase IIIα (TOP3A), RMI1 and RMI2 to form the BTR complex, which dissolves double Holliday junctions to produce non-crossover homologous recombination (HR) products. BLM also promotes DNA-end resection, restart of stalled replication forks, and processing of ultra-fine DNA bridges in mitosis. How these activities of the BTR complex are regulated in cells is still unclear. Here, we identify multiple conserved motifs within the BTR complex that interact cooperatively with the single-stranded DNA (ssDNA)-binding protein RPA. Furthermore, we demonstrate that RPA-binding is required for stable BLM recruitment to sites of DNA replication stress and for fork restart, but not for its roles in HR or mitosis. Our findings suggest a model in which the BTR complex contains the intrinsic ability to sense levels of RPA-ssDNA at replication forks, which controls BLM recruitment and activation in response to replication stress.

Abstract 2112: CA-microsatellite instability as a factor of branch migration impeding in Holliday junctions

2012 ◽  
Author(s):  
Natalia Y. Karpechenko ◽  
Nina G. Dolinnaya ◽  
Vladimir I. Popenko ◽  
Marianna G. Yakubovskaya ◽  
Victoria K. Gasanova
Keyword(s):  
Microsatellite Instability ◽  
Holliday Junctions ◽  
Branch Migration

scholarly journals Active Control of Repetitive Structural Transitions between Replication Forks and Holliday Junctions by Werner Syndrome Helicase

Structure ◽  
2016 ◽  
Vol 24 (8) ◽  
pp. 1292-1300 ◽  
Author(s):  
Soochul Shin ◽  
Jinwoo Lee ◽  
Sangwoon Yoo ◽  
Tomasz Kulikowicz ◽  
Vilhelm A. Bohr ◽  
...  
Keyword(s):  
Active Control ◽  
Werner Syndrome ◽  
Holliday Junctions ◽  
Replication Forks ◽  
Structural Transitions
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