Mrc1 and Tof1 promote replication fork progression and recovery independently of Rad53

Helene Tourriere; Gwennaëlle Versini; Violeta Cordón-Preciado; Constance Alabert; Philippe Pasero

doi:10.1016/j.molcel.2005.07.028

Mrc1 and Tof1 promote replication fork progression and recovery independently of Rad53

Helene Tourriere, Gwennaëlle Versini, Violeta Cordón-Preciado, Constance Alabert, Philippe Pasero (Lead / Corresponding author)

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224 Citations (Scopus)

Abstract

The yeast checkpoint factors Mrc1p and Tof1p travel with the replication fork and mediate the activation of the Rad53p kinase in response to a replication stress. We show here that both proteins are required for normal fork progression but play different roles at stalled forks. Tof1p is critical for the activity of the rDNA replication fork barrier (RFB) but plays a minor role in the replication checkpoint. In contrast, Mrc1p is not necessary for RFB activity but is essential to mediate the replication stress response. Interestingly, stalled forks did not collapse in mrc1Δ cells exposed to hydroxyurea (HU) as they do in rad53 mutants. However, forks failed to restart when mrc1Δ cells were released from the block. The critical role of Mrc1p in HU is therefore to promote fork recovery in a Rad53p-independent manner, presumably through the formation of a stable fork-pausing complex.

Original language	English
Pages (from-to)	699-706
Number of pages	8
Journal	Molecular Cell
Volume	19
Issue number	5
DOIs	https://doi.org/10.1016/j.molcel.2005.07.028
Publication status	Published - 2 Sept 2005

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title = "Mrc1 and Tof1 promote replication fork progression and recovery independently of Rad53",

abstract = "The yeast checkpoint factors Mrc1p and Tof1p travel with the replication fork and mediate the activation of the Rad53p kinase in response to a replication stress. We show here that both proteins are required for normal fork progression but play different roles at stalled forks. Tof1p is critical for the activity of the rDNA replication fork barrier (RFB) but plays a minor role in the replication checkpoint. In contrast, Mrc1p is not necessary for RFB activity but is essential to mediate the replication stress response. Interestingly, stalled forks did not collapse in mrc1Δ cells exposed to hydroxyurea (HU) as they do in rad53 mutants. However, forks failed to restart when mrc1Δ cells were released from the block. The critical role of Mrc1p in HU is therefore to promote fork recovery in a Rad53p-independent manner, presumably through the formation of a stable fork-pausing complex.",

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T1 - Mrc1 and Tof1 promote replication fork progression and recovery independently of Rad53

AU - Tourriere, Helene

AU - Versini, Gwennaëlle

AU - Cordón-Preciado, Violeta

AU - Alabert, Constance

AU - Pasero, Philippe

PY - 2005/9/2

Y1 - 2005/9/2

N2 - The yeast checkpoint factors Mrc1p and Tof1p travel with the replication fork and mediate the activation of the Rad53p kinase in response to a replication stress. We show here that both proteins are required for normal fork progression but play different roles at stalled forks. Tof1p is critical for the activity of the rDNA replication fork barrier (RFB) but plays a minor role in the replication checkpoint. In contrast, Mrc1p is not necessary for RFB activity but is essential to mediate the replication stress response. Interestingly, stalled forks did not collapse in mrc1Δ cells exposed to hydroxyurea (HU) as they do in rad53 mutants. However, forks failed to restart when mrc1Δ cells were released from the block. The critical role of Mrc1p in HU is therefore to promote fork recovery in a Rad53p-independent manner, presumably through the formation of a stable fork-pausing complex.

AB - The yeast checkpoint factors Mrc1p and Tof1p travel with the replication fork and mediate the activation of the Rad53p kinase in response to a replication stress. We show here that both proteins are required for normal fork progression but play different roles at stalled forks. Tof1p is critical for the activity of the rDNA replication fork barrier (RFB) but plays a minor role in the replication checkpoint. In contrast, Mrc1p is not necessary for RFB activity but is essential to mediate the replication stress response. Interestingly, stalled forks did not collapse in mrc1Δ cells exposed to hydroxyurea (HU) as they do in rad53 mutants. However, forks failed to restart when mrc1Δ cells were released from the block. The critical role of Mrc1p in HU is therefore to promote fork recovery in a Rad53p-independent manner, presumably through the formation of a stable fork-pausing complex.

U2 - 10.1016/j.molcel.2005.07.028

DO - 10.1016/j.molcel.2005.07.028

M3 - Article

SN - 1097-2765

VL - 19

SP - 699

EP - 706

JO - Molecular Cell

JF - Molecular Cell

IS - 5

ER -

Mrc1 and Tof1 promote replication fork progression and recovery independently of Rad53

Abstract

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