Sen1 and Rrm3 ensure permissive topological conditions for replication termination

Choudhary, Ramveer; Niska-Blakie, Joanna; Adhil, Mohamood; Liberi, Giordano; Achar, Yathish Jagadheesh; Giannattasio, Michele; Foiani, Marco

doi:10.1016/j.celrep.2023.112747

Cited by 4 publications

(2 citation statements)

References 74 publications

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“…Finally, although the global analyses mentioned above indicate that termination sites tend to localise to intergenic regions, Choudhary et al (2023) found that, in yeast, Rrm3 is able to promote fork convergence at termination sites (TERs) which specifically reside within transcription units. In this case, Rrm3 coordinates with the helicase Sen1 to help counteract RNA Polymerase II and RNA-DNA hybrids, thus enabling the full completion of fork convergence and replication.…”

Section: Replication Fork Convergencementioning

confidence: 99%

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A Decade of Discovery—Eukaryotic Replisome Disassembly at Replication Termination

Jones,

Reynolds-Winczura,

Gambus

2024

Biology

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The eukaryotic replicative helicase (CMG complex) is assembled during DNA replication initiation in a highly regulated manner, which is described in depth by other manuscripts in this Issue. During DNA replication, the replicative helicase moves through the chromatin, unwinding DNA and facilitating nascent DNA synthesis by polymerases. Once the duplication of a replicon is complete, the CMG helicase and the remaining components of the replisome need to be removed from the chromatin. Research carried out over the last ten years has produced a breakthrough in our understanding, revealing that replication termination, and more specifically replisome disassembly, is indeed a highly regulated process. This review brings together our current understanding of these processes and highlights elements of the mechanism that are conserved or have undergone divergence throughout evolution. Finally, we discuss events beyond the classic termination of DNA replication in S-phase and go over the known mechanisms of replicative helicase removal from chromatin in these particular situations.

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Section: Replication Fork Convergencementioning

confidence: 99%

“…In this case, Rrm3 coordinates with the helicase Sen1 to help counteract RNA Polymerase II and RNA-DNA hybrids, thus enabling the full completion of fork convergence and replication. In the absence of both factors, RNA Pol II accumulates at TERs and cells express chromosomal fragility [41].…”

Section: Replication Fork Convergencementioning

confidence: 99%

A Decade of Discovery—Eukaryotic Replisome Disassembly at Replication Termination

Jones,

Reynolds-Winczura,

Gambus

2024

Biology

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Sch9S6K controls DNA repair and DNA damage response efficiency in aging cells

Lucca,

Ferrari,

Shubassi

et al. 2024

Cell Reports

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The increase in cell death rates in caloric restricted cells of the yeast helicase mutant rrm3 is Sir complex dependent

Ivessa,

Singh

2023

Sci Rep

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Calorie restriction (CR), which is a reduction in calorie intake without malnutrition, usually extends lifespan and improves tissue integrity. This report focuses on the relationship between nuclear genomic instability and dietary-restriction and its effect on cell survival. We demonstrate that the cell survival rates of the genomic instability yeast mutant rrm3 change under metabolic restricted conditions. Rrm3 is a DNA helicase, chromosomal replication slows (and potentially stalls) in its absence with increased rates at over 1400 natural pause sites including sites within ribosomal DNA and tRNA genes. Whereas rrm3 mutant cells have lower cell death rates compared to wild type (WT) in growth medium containing normal glucose levels (i.e., 2%), under CR growth conditions cell death rates increase in the rrm3 mutant to levels, which are higher than WT. The silent-information-regulatory (Sir) protein complex and mitochondrial oxidative stress are required for the increase in cell death rates in the rrm3 mutant when cells are transferred from growth medium containing 2% glucose to CR-medium. The Rad53 checkpoint protein is highly phosphorylated in the rrm3 mutant in response to genomic instability in growth medium containing 2% glucose. Under CR, Rad53 phosphorylation is largely reduced in the rrm3 mutant in a Sir-complex dependent manner. Since CR is an adjuvant treatment during chemotherapy, which may target genomic instability in cancer cells, our studies may gain further insight into how these therapy strategies can be improved.

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Sen1 and Rrm3 ensure permissive topological conditions for replication termination

Cited by 4 publications

References 74 publications

A Decade of Discovery—Eukaryotic Replisome Disassembly at Replication Termination

A Decade of Discovery—Eukaryotic Replisome Disassembly at Replication Termination

Sch9S6K controls DNA repair and DNA damage response efficiency in aging cells

The increase in cell death rates in caloric restricted cells of the yeast helicase mutant rrm3 is Sir complex dependent

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