Tid1/Rdh54 translocase is phosphorylated through a Mec1- and Rad53-dependent manner in the presence of DSB lesions in budding yeast

Ferrari, Matteo; Nachimuthu, Benjamin Tamilselvan; Donnianni, Roberto A.; Klein, Hannah L.; Pellicioli, Achille

doi:10.1016/j.dnarep.2013.02.004

Cited by 17 publications

(19 citation statements)

References 30 publications

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“…In another example, which supports a key role for Mec1 in the control of HR, phosphorylation of multiple S/T‐Q residues in Sae2, a pro‐resection factor homologous to human CtIP, contributes to Mec1‐mediated GCR suppression (Liang et al , ). Furthermore, Mec1 phosphorylates the strand exchange factor Rad55, and Rad53 promotes the phosphorylation and DNA binding of the Tid1/Rdh54 translocase (Fig ; Bashkirov et al , ; Ferrari et al , ; Herzberg et al , ). Mec1 also phosphorylates Rad51 at serine 192, likely supporting its ATPase activity and capacity for strand invasion (Fig ; Flott et al , ).…”

Section: Introductionmentioning

confidence: 99%

DNA damage kinase signaling: checkpoint and repair at 30 years

2019

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From bacteria to mammalian cells, damaged DNA is sensed and targeted by DNA repair pathways. In eukaryotes, kinases play a central role in coordinating the DNA damage response. DNA damage signaling kinases were identified over two decades ago and linked to the cell cycle checkpoint concept proposed by Weinert and Hartwell in 1988. Connections between the DNA damage signaling kinases and DNA repair were scant at first, and the initial perception was that the importance of these kinases for genome integrity was largely an indirect effect of their roles in checkpoints, DNA replication, and transcription. As more substrates of DNA damage signaling kinases were identified, it became clear that they directly regulate a wide range of DNA repair factors. Here, we review our current understanding of DNA damage signaling kinases, delineating the key substrates in budding yeast and humans. We trace the progress of the field in the last 30 years and discuss our current understanding of the major substrate regulatory mechanisms involved in checkpoint responses and DNA repair.

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Section: Introductionmentioning

confidence: 99%

DNA damage kinase signaling: checkpoint and repair at 30 years

2019

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“…So far, only Rdh54 has been excluded as a likely functional target of the MCN (Niu et al 2009). Notably, Rdh54 phosphorylation during vegetative growth is implicated in checkpoint adaptation (Ferrari et al 2013).…”

Section: Suppression Of Intersister Recombinationmentioning

confidence: 99%

The Meiotic Checkpoint Network: Step-by-Step through Meiotic Prophase

Subramanian

Hochwagen

2014

Cold Spring Harbor Perspectives in Biology

174

178

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The generation of haploid gametes by meiosis is a highly conserved process for sexually reproducing organisms that, in almost all cases, involves the extensive breakage of chromosomes. These chromosome breaks occur during meiotic prophase and are essential for meiotic recombination as well as the subsequent segregation of homologous chromosomes. However, their formation and repair must be carefully monitored and choreographed with nuclear dynamics and the cell division program to avoid the creation of aberrant chromosomes and defective gametes. It is becoming increasingly clear that an intricate checkpointsignaling network related to the canonical DNA damage response is deeply interwoven with the meiotic program and preserves order during meiotic prophase. This meiotic checkpoint network (MCN) creates a wide range of dependent relationships controlling chromosome movement, chromosome pairing, chromatin structure, and double-strand break (DSB) repair. In this review, we summarize our current understanding of the MCN. We discuss commonalities and differences in different experimental systems, with a particular emphasis on the emerging design principles that control and limit cross talk between signals to ultimately ensure the faithful inheritance of chromosomes by the next generation.

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“…In line with this, Tid1 is recruited to DSBs within 1 hr of break-induction in a Rad51-dependent manner (Kwon et al, 2008). Tid1 is also phosphorylated in response to DNA damage in somatic cells (Ferrari et al, 2013), but it remains unclear how phosphorylation of Tid1 alters Tid1's interaction with Rad51 or its translocation activity. Phosphorylation of Rad54, for instance, suppresses interaction between Rad54 and Rad51 during meiotic recombination (Niu et al, 2009).…”

Section: Model: Tid1 As a Roadblock To Rad54mentioning

confidence: 89%

“…Tid1 translocation on dsDNA also prevents non-recombinogenic binding of Rad51 to dsDNA (Shah et al, 2010). Tid1's ATPase activity is required to turn off Rad53 activation and for checkpoint adaptation (Ferrari et al, 2013). Thus, a secondary role of Tid1 and its ATPase activity downstream in mitotic repair remains yet to be delineated.…”

Section: Physiological Relevance Of D-loop Modulation By Tid1mentioning

confidence: 99%

“…In somatic cells, Rdh54 is phosphorylated in response to DNA damage by Mec1 (Ferrari et al, 2013) and is recruited to DSBs in a Rad51-dependent manner (Kwon et al, 2008;Lisby et al, 2004). Rdh54 also interacts with Rad51 (Santa Maria et al, 2013b) and can promote the DNA strand exchange activity of Rad51 in vitro (Nimonkar et al, 2012;Petukhova et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

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Rdh54/Tid1 Inhibits Rad51-Rad54-Mediated D-loop Formation and Limits D-loop Length

Shah

Hartono

Som

et al. 2020

Preprint

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Displacement loops (D-loops) are intermediates formed during homologous recombination that play a pivotal role in the fidelity of repair. Rdh54 (a.k.a. Tid1), a Rad54 paralog in Saccharomyces cerevisiae, is well-known for its role with Dmc1 recombinase during meiotic recombination. Yet contrary to Dmc1, Rdh54 is also present in somatic cells where its function is less understood.While Rdh54 enhances the Rad51 DNA strand invasion activity in vitro, it is unclear how it interplays with Rad54-mediated invasions. Here, we show that Rdh54 inhibits D-loop formation by Rad51 and Rad54 in an ATPase-independent manner. Using a novel D-loop Mapping Assay, we further demonstrate that Rdh54 uniquely restricts the lengths of Rad54-mediated D-loops. The alterations in D-loop properties appear to be important for cell survival and mating-type switch in haploid yeast, whereas Rdh54 expression is suppressed in diploids. We propose that Rdh54 and Rad54 compete for potential binding sites within the Rad51 filament, where Rdh54 acts as a physical roadblock to Rad54's translocation activity, limiting D-loop formation and D-loop length.

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Tid1/Rdh54 translocase is phosphorylated through a Mec1- and Rad53-dependent manner in the presence of DSB lesions in budding yeast

Cited by 17 publications

References 30 publications

DNA damage kinase signaling: checkpoint and repair at 30 years

DNA damage kinase signaling: checkpoint and repair at 30 years

The Meiotic Checkpoint Network: Step-by-Step through Meiotic Prophase

Rdh54/Tid1 Inhibits Rad51-Rad54-Mediated D-loop Formation and Limits D-loop Length

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