Abstract:
:The SeqA protein binds hemi-methylated GATC sites and forms structures that sequester newly replicated origins and trail the replication forks. Cells that lack SeqA display signs of replication fork disintegration. The broken forks could arise because of over-initiation (the launching of too many forks) or lack of dynamic SeqA structures trailing the forks. To confirm one or both of these possible mechanisms, we compared two seqA mutants with the oriCm3 mutant. The oriCm3 mutant over-initiates because of a lack of origin sequestration but has wild-type SeqA protein. Cells with nonfunctional SeqA, but not oriCm3 mutant cells, had problems with replication elongation, were highly dependent on homologous recombination, and exhibited extensive chromosome fragmentation. The results indicate that replication forks frequently break in the absence of SeqA function and that the broken forks are rescued by homologous recombination. We suggest that SeqA may act in two ways to stabilize replication forks: (i) by enabling vital replication fork repair and restarting reactions and (ii) by preventing replication fork rear-end collisions.
journal_name
Nucleic Acids Resjournal_title
Nucleic acids researchauthors
Pedersen IB,Helgesen E,Flåtten I,Fossum-Raunehaug S,Skarstad Kdoi
10.1093/nar/gkx263subject
Has Abstractpub_date
2017-06-20 00:00:00pages
6471-6485issue
11eissn
0305-1048issn
1362-4962pii
3605638journal_volume
45pub_type
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