Current Genetics, volume 65, issue 2, pages 429-434
ChECing out Rif1 action in freely cycling cells
2
Institute of Genetics and Genomics of Geneva (iGE3), Geneva, Switzerland
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3
Biology of Infection Unit, Institut Pasteur, Paris, France
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Publication type: Journal Article
Publication date: 2018-11-19
Journal:
Current Genetics
Quartile SCImago
Q1
Quartile WOS
Q3
Impact factor: 2.5
ISSN: 01728083, 14320983
General Medicine
Genetics
Abstract
In buddying yeast, like all eukaryotes examined so far, DNA replication is under temporal control, such that some origins fire early and some late during S phase. This replication timing program is established in G1 phase, where chromatin states are thought to prevent binding of key-limiting initiation factors at late-firing origins. Although many factors are involved in replication initiation, a new player, Rif1, has recently entered the scene, with a spate of papers revealing a global role for the protein in the control of replication initiation timing from yeasts to humans. Since budding yeast Rif1 was known to bind only to telomeric and silent mating loci regions, it remained controversial whether Rif1 acts directly at replication origins or instead influences origin activity indirectly. In this perspective, we discuss our recent finding that Rif1 binds directly to the replication origins that it controls. In this study, we also found that Rif1’s regulatory activity at origins is best revealed by an assay (sort-seq) that measures replication in unperturbed, freely cycling cultures, as opposed to commonly used protocols in which cells are first blocked in the G1 phase of the cell cycle by mating pheromone, then released into a synchronous S phase. Finally, we discuss how the sequestration of Rif1 at telomeres, through an interaction with the arrays of Rap1 molecules bound there, plays an important role in limiting Rif1’s action primarily to telomere-proximal replication origins.
Citations by journals
1
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eLife
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1 publication, 16.67%
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Genes
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1 publication, 16.67%
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Nature Communications
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1 publication, 16.67%
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1 publication, 16.67%
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1
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Citations by publishers
1
2
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Springer Nature
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Springer Nature
2 publications, 33.33%
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Elsevier
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Elsevier
2 publications, 33.33%
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eLife Sciences Publications
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eLife Sciences Publications
1 publication, 16.67%
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Multidisciplinary Digital Publishing Institute (MDPI)
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Multidisciplinary Digital Publishing Institute (MDPI)
1 publication, 16.67%
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1
2
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- We do not take into account publications that without a DOI.
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- Statistics recalculated weekly.
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Hafner L. et al. ChECing out Rif1 action in freely cycling cells // Current Genetics. 2018. Vol. 65. No. 2. pp. 429-434.
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Hafner L., Shore D., Mattarocci S. ChECing out Rif1 action in freely cycling cells // Current Genetics. 2018. Vol. 65. No. 2. pp. 429-434.
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TY - JOUR
DO - 10.1007/s00294-018-0902-0
UR - https://doi.org/10.1007%2Fs00294-018-0902-0
TI - ChECing out Rif1 action in freely cycling cells
T2 - Current Genetics
AU - Hafner, Lukas
AU - Shore, David
AU - Mattarocci, Stefano
PY - 2018
DA - 2018/11/19 00:00:00
PB - Springer Nature
SP - 429-434
IS - 2
VL - 65
SN - 0172-8083
SN - 1432-0983
ER -
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@article{2018_Hafner,
author = {Lukas Hafner and David Shore and Stefano Mattarocci},
title = {ChECing out Rif1 action in freely cycling cells},
journal = {Current Genetics},
year = {2018},
volume = {65},
publisher = {Springer Nature},
month = {nov},
url = {https://doi.org/10.1007%2Fs00294-018-0902-0},
number = {2},
pages = {429--434},
doi = {10.1007/s00294-018-0902-0}
}
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Hafner, Lukas, et al. “ChECing out Rif1 action in freely cycling cells.” Current Genetics, vol. 65, no. 2, Nov. 2018, pp. 429-434. https://doi.org/10.1007%2Fs00294-018-0902-0.