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Faculty
Tanya Paull
Professor in Molecular Genetics & Microbiology
Howard Hughes Medical Institute Investigator

Email: tpaull@utexas.edu
Website
Main Office: MBB 2.448
Phone: (512) 232-7802

Alternate Office: MBB 2.448
Alt. Phone: (512) 232-7803

Mailing Address
The University of Texas at Austin
Institute for Cellular and Molecular Biology (ICMB)
2500 Speedway Stop A4800
Austin ,TX 78712-1191

Tanya Paull


Research Summary

Research in the lab is focused on the DNA damage response in eukaryotic cells, specifically the checkpoint activation and DNA repair responses that occur immediately after the introduction of chromosomal double-strand breaks. Several components of these DNA damage response systems have been implicated as tumor suppressors in mammalian organisms, thus establishing these factors as major targets in the progression from normal to unregulated cell growth.

Current studies in the lab are primarily focused on the biochemical activities of a complex of proteins, Mrell/Rad50/Nbs1 (M/R/N), which are critical components in the repair of DNA double-strand breaks. We study the activities of recombinant M/R/N complexes in vitro to characterize its functions on different types of DNA substrates and recombination intermediates. In addition, in vivo assays in S. cerevisiae are utilized to identify functions of the complex and the effects of mutant complexes in cells. Our overall goal is to decipher the functions of each of these factors at a molecular level in order to understand how they cooperate to guard cells against genetic rearrangements and transformation.

The M/R/N complex works in concert with the Ataxia-Telangiectasia-Mutated (ATM) protein kinase that phosphorylates many downstream targets responsible for checkpoint activation and DNA damage signaling in eukaryotes. We have previously shown that MRN recruits ATM to broken DNA ends and activates its kinase activity at these sites. We are currently investigating the mechanisms through which ATM is activated, how post-translational modifications affect this process, and how other ATM-interacting factors influence its regulation. We have also recently found that ATM can be activated in an MRN-independent manner through direct oxidation. This pathway is important for cellular control of antioxidant functions and for global responses of human cells to reactive oxygen species. The mechanism and targets of ATM activation through this pathway are currently being investigated.

 

 

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