A DNA damage response pathway controlled by Tel1 and the Mre11 complex.
We define a DNA damage checkpoint pathway in S. cerevisiae governed by the ATM homolog Tel1 and the Mre11 complex. In mitotic cells, the Tel1-Mre11 complex pathway triggers Rad53 activation and its interaction with Rad9, whereas in meiosis it acts via Rad9 and the Rad53 paralog Mre4/Mek1. Activation of the Tel1-Mre11 complex pathway checkpoint functions appears to depend upon the Mre11 complex as a damage sensor and, at least in meiotic cells, to depend on unprocessed DNA double-strand breaks (DSBs). The DSB repair functions of the Mre11 complex are enhanced by the pathway, suggesting that the complex both initiates and is regulated by the Tel1-dependent DSB signal. These findings demonstrate that the diverse functions of the Mre11 complex in the cellular DNA damage response are conserved in mammals and yeast.
Pubmed ID: 11430828
June 29, 2001
- Agency: NIGMS NIH HHS, Id: GM56888
- Cell Cycle Proteins
- Checkpoint Kinase 2
- DNA Damage
- DNA Repair
- DNA-Binding Proteins
- Fungal Proteins
- Genes, cdc
- Intracellular Signaling Peptides and Proteins
- Protein Kinases
- Protein-Serine-Threonine Kinases
- Saccharomyces cerevisiae Proteins