ArticleMolecular and cellular biology2004
Mdt1, a novel Rad53 FHA1 domain-interacting protein, modulates DNA damage tolerance and G(2)/M cell cycle progression in Saccharomyces cerevisiae.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 44 citations in OpenAlex.
- Article
- The Yeast DNA Damage Checkpoint Kinase Rad53 Targets the Exoribonuclease, Xrn1.G3 (Bethesda, Md.) · 2018Article
- Phosphoproteome dynamics of Saccharomyces cerevisiae under heat shock and cold stress.Molecular systems biology · 2015Article
- Prion-promoted phosphorylation of heterologous amyloid is coupled with ubiquitin-proteasome system inhibition and toxicity.Molecular microbiology · 2014Article
- Use of quantitative mass spectrometric analysis to elucidate the mechanisms of phospho-priming and auto-activation of the checkpoint kinase Rad53 in vivo.Molecular & cellular proteomics : MCP · 2014Article
- Yeast hEST1A/B (SMG5/6)-like proteins contribute to environment-sensing adaptive gene expression responses.G3 (Bethesda, Md.) · 2013Article
- The yeast copper response is regulated by DNA damage.Molecular and cellular biology · 2013Article
- An N-terminal acidic region of Sgs1 interacts with Rpa70 and recruits Rad53 kinase to stalled forks.The EMBO journal · 2012Article
- ATM substrate Chk2-interacting Zn2+ finger (ASCIZ) Is a bi-functional transcriptional activator and feedback sensor in the regulation of dynein light chain (DYNLL1) expression.The Journal of biological chemistry · 2012Article
- Saccharomyces cerevisiae Dbf4 has unique fold necessary for interaction with Rad53 kinase.The Journal of biological chemistry · 2012Article
- A strategy for interaction site prediction between phospho-binding modules and their partners identified from proteomic data.Molecular & cellular proteomics : MCP · 2010Article
- Dual functions of ASCIZ in the DNA base damage response and pulmonary organogenesis.PLoS genetics · 2010Article
- Life in the midst of scarcity: adaptations to nutrient availability in Saccharomyces cerevisiae.Current genetics · 2010Review
- CDC5 inhibits the hyperphosphorylation of the checkpoint kinase Rad53, leading to checkpoint adaptation.PLoS biology · 2010Article
- A genome-wide deletion mutant screen identifies pathways affected by nickel sulfate in Saccharomyces cerevisiae.BMC genomics · 2009Article
- Characterization of the rapamycin-sensitive phosphoproteome reveals that Sch9 is a central coordinator of protein synthesis.Genes & development · 2009Article
- Mechanistic insights into phosphoprotein-binding FHA domains.Accounts of chemical research · 2008Review
- Mdt1 facilitates efficient repair of blocked DNA double-strand breaks and recombinational maintenance of telomeres.Molecular and cellular biology · 2007Article
- Mechanisms of checkpoint kinase Rad53 inactivation after a double-strand break in Saccharomyces cerevisiae.Molecular and cellular biology · 2007Article
- Critical role of DNA checkpoints in mediating genotoxic-stress-induced filamentous growth in Candida albicans.Molecular biology of the cell · 2007Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
The Rad53 kinase plays a central role in yeast DNA damage checkpoints. Rad53 contains two FHA phosphothreonine-binding domains that are required for Rad53 activation and possibly downstream signaling. Here we show that the N-terminal Rad53 FHA1 domain interacts with the RNA recognition motif, coiled-coil, and SQ/TQ cluster domain-containing protein Mdt1 (YBl051C). The interaction of Rad53 and Mdt1 depends on the structural integrity of the FHA1 phosphothreonine-binding site as well as threonine-305 of Mdt1. Mdt1 is constitutively threonine phosphorylated and hyperphosphorylated in response to DNA damage in vivo. DNA damage-dependent Mdt1 hyperphosphorylation depends on the Mec1 and Tel1 checkpoint kinases, and Mec1 can directly phosphorylate a recombinant Mdt1 SQ/TQ domain fragment. MDT1 overexpression is synthetically lethal with a rad53 deletion, whereas mdt1 deletion partially suppresses the DNA damage hypersensitivity of checkpoint-compromised strains and generally improves DNA damage tolerance. In the absence of DNA damage, mdt1 deletion leads to delayed anaphase completion, with an elongated cell morphology reminiscent of that of G(2)/M cell cycle mutants. mdt1-dependent and DNA damage-dependent cell cycle delays are not additive, suggesting that they act in the same pathway. The data indicate that Mdt1 is involved in normal G(2)/M cell cycle progression and is a novel target of checkpoint-dependent cell cycle arrest pathways.
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