Identification of Pathways Required for the Coordination of Late Mitotic Events in Animal Cells
Abstract
Telomeres are specialized chromatin structures that protect chromosomes ends from the DNA repair pathways. Telomeres are re-formed after each round of DNA replication. The molecular details of telomere maturation have been well characterized. Many of the details of this process resemble the repair of double strand breaks (DSBs) by the homologous recombination pathway. For this reason, it has been hard to discover what distinguishes telomeres from double stand break lesions. The first step in telomere maturation is the resection of the blunt double stranded end to form a 3? overhang, called a G-tail. This is a critical part of telomere maturation, as it prevents repair of telomeres through nonhomologous end joining. Experiments described here have led to the identification an exonuclease, Rat1p, which is required for G-tail formation. Impairing Rat1p activity in dividing cells causes telomeres to become fused through the non-homologous end joining pathway. The identification of Rat1p was unexpected as this protein has been previously characterized as an exoribonuclease with roles in RNA processing and degradation. I have discovered that Rat1p is also able to degrade DNA substrates in the direction required for G-tail formation. In addition, Rat1p was found to associate with telomere chromatin during late S-phase.
Document Details
- Document Type
- Technical Report
- Publication Date
- Aug 01, 2006
- Accession Number
- ADA507164
Entities
People
- Bridget Baumgartner
Organizations
- Baylor College of Medicine