Phosphorylation of MLL by ATR is required for execution of mammalian S-phase checkpoint

Han Liu, Shugaku Takeda, Rakesh Kumar, Todd D. Westergard, Eric J. Brown, Tej K. Pandita, Emily H.-Y. Cheng and James J.-D. Hsieh ()
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Han Liu: Washington University School of Medicine
Shugaku Takeda: Washington University School of Medicine
Rakesh Kumar: University of Texas Southwestern Medical Center
Todd D. Westergard: Washington University School of Medicine
Eric J. Brown: University of Pennsylvania School of Medicine
Tej K. Pandita: University of Texas Southwestern Medical Center
Emily H.-Y. Cheng: Washington University School of Medicine
James J.-D. Hsieh: Washington University School of Medicine

Nature, 2010, vol. 467, issue 7313, 343-346

Abstract: Linking leukaemia and DNA repair The S-phase checkpoint in mitosis, activated by DNA damage, maintains genome stability by allowing the cell time to repair the damage before it progresses through the cell cycle. Liu et al. now report that the MLL (mixed lineage leukaemia) gene, frequently translocated in leukaemia, is part of the S-phase checkpoint. When DNA is damaged, MLL is phosphorylated by the checkpoint kinase ATR, causing it to accumulate on chromatin and to methylate histone H3 at lysine residue 4. This histone modification blocks activation of late replication origins. MLL translocations disrupt this pathway and promote genomic instability.

Date: 2010
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DOI: 10.1038/nature09350

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