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The DNA replication checkpoint response stabilizes stalled replication forks
It is shown that hydroxyurea-treated rad53 mutants accumulate unusual DNA structures at replication forks, and it is proposed that Rad53 prevents collapse of the fork when replication pauses.
The DNA Damage Checkpoint Response Requires Histone H2B Ubiquitination by Rad6-Bre1 and H3 Methylation by Dot1*
- M. Giannattasio, Federico Lazzaro, P. Plevani, M. Muzi-Falconi
- BiologyJournal of Biological Chemistry
- 18 March 2005
It is demonstrated that ubiquitination of histone H2B on lysine 123 by the Rad6-Bre1 complex, is necessary for activation of Rad53 kinase and cell cycle arrest and results suggest that histone modifications may have a role in checkpoint function by modulating the interactions of Rad9 with chromatin and active Mec1 kinase.
Mutations in the mitochondrial protease gene AFG3L2 cause dominant hereditary ataxia SCA28
This work identifies AFG3L2 as a novel cause of dominant neurodegenerative disease and indicates a previously unknown role for this component of the mitochondrial protein quality control machinery in protecting the human cerebellum against neurodegenersation.
Regulation of the replication initiator protein p65cdc18 by CDK phosphorylation.
- P. Jallepalli, G. W. Brown, M. Muzi-Falconi, D. Tien, T. Kelly
- BiologyGenes & development
- 1 November 1997
Cyclin-dependent kinases (CDKs) promote the initiation of DNA replication and prevent reinitiation before mitosis, presumably through phosphorylation of key substrates at origins of replication. In…
Phosphorylation of the Budding Yeast 9-1-1 Complex Is Required for Dpb11 Function in the Full Activation of the UV-Induced DNA Damage Checkpoint
The data suggest that Dpb11 is held in proximity to damaged DNA through an interaction with the phosphorylated 9-1-1 complex, leading to Mec1-dependent phosphorylation of Rad9, and it is found that the replication factor Dpb 11 is the keystone of this second pathway.
DNA damage checkpoint in budding yeast
- M. Longhese, M. Foiani, M. Muzi-Falconi, G. Lucchini, P. Plevani
- BiologyThe EMBO journal
- 1 October 1998
The yeast Saccharomyces cerevisiae has been invaluable in dissecting genetically the DNA damage checkpoint pathway and recent results on posttranslational modifications and protein–protein interactions of some key factors provide new insights into the architecture of checkpoint protein complexes and their order of function.
Histone methyltransferase Dot1 and Rad9 inhibit single-stranded DNA accumulation at DSBs and uncapped telomeres
It is suggested that both Rad9 and histone H3 methylation allow transmission of the damage signal to checkpoint kinases, and keep resection of damaged DNA under control influencing, both positively and negatively, checkpoint cascades and contributing to a tightly controlled response to DNA damage.
Srs2 DNA helicase is involved in checkpoint response and its regulation requires a functional Mec1‐dependent pathway and Cdk1 activity
It is found that the Srs2 DNA helicase, which is involved in DNA repair and recombination, is phosphorylated in response to intra‐S DNA damage in a checkpoint‐dependent manner, suggesting that the checkpoint pathway might modulate Cdk1 activity in responseto DNA damage.
RNase H and Postreplication Repair Protect Cells from Ribonucleotides Incorporated in DNA
The 9-1-1 Checkpoint Clamp Physically Interacts with Polζ and Is Partially Required for Spontaneous Polζ-dependent Mutagenesis in Saccharomyces cerevisiae*
- S. Sabbioneda, Brenda K. Minesinger, M. Giannattasio, P. Plevani, M. Muzi-Falconi, S. Jinks-Robertson
- BiologyJournal of Biological Chemistry
- 18 November 2005
This work demonstrates an in vivo and in vitro physical interaction between the Mec3 and Ddc1 subunits of the 9-1-1 clamp and the Rev7 subunit of the Polζ TLS polymerase, and suggests that, in addition to its checkpoint signaling role, the9-1,1 clamp may physically regulate Polε-dependent mutagenesis by controlling the access of Polη to damaged DNA.