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The Saccharomyces cerevisiae 14-3-3 proteins Bmh1 and Bmh2 directly influence the DNA damage-dependent functions of Rad53.

http://www.ncbi.nlm.nih.gov/pubmed/17299042

In this study, we mutated autophosphorylation sites in Rad53 based on their conservation with previously identified autophosphorylation sites in the mammalian Rad53 ortholog, Chk2. As with wild-type Rad53, the autophosphorylation mutant, rad53-TA, undergoes Mec1/Tel1-dependent interactions with Rad9 and Dun1 in response to genotoxic stress. Whereas rad53-TA in vitro kinase activity is severely impaired, the rad53-TA strains are not completely deficient for cell-cycle checkpoint functions, indicating that the mutant kinase retains a basal level of function. We describe a genetic interaction among Rad53, Dun1, and the 14-3-3 proteins Bmh1 and Bmh2 and present evidence that 14-3-3 proteins directly facilitate Rad53 function in vivo. The data presented account for the previously observed checkpoint defects associated with 14-3-3 mutants in Saccharomyces pombe and Saccharomyces cerevisiae. The 14-3-3 functional interaction appears to modulate Rad53 activity, reminiscent of 14-3-3's effect on human Raf1 kinase and distinct from the indirect mode of regulation by 14-3-3 observed for Chk1 or Cdc25.

Pubmed ID: 17299042 RIS Download

Mesh terms: 14-3-3 Proteins | Binding Sites | Cell Cycle Proteins | Checkpoint Kinase 2 | DNA Damage | Gene Dosage | Immunoprecipitation | Mutant Proteins | Phenotype | Phosphopeptides | Protein Binding | Protein-Serine-Threonine Kinases | Saccharomyces cerevisiae | Saccharomyces cerevisiae Proteins | Suppression, Genetic

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Associated grants

  • Agency: NIGMS NIH HHS, Id: GM 56888
  • Agency: NIGMS NIH HHS, Id: GM 59413
  • Agency: NIGMS NIH HHS, Id: R01 GM059413

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