Yeast Genetics and Molecular Biology 1998
College Park, Maryland
August 1998


Name: Bertuch, Alison A.
Mailing Address: Molecular and Human Genetics, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA
Email Address: abertuch@bcm.tmc.edu
Phone and Fax numbers: (713)798-3610, (713)798-5386

008

Proteins required for the repair of double strand breaks play two distinct roles in telomere maintenance in yeast.


Alison A. Bertuch , Constance I. Nugent, Lyle O. Ross, Sara K. Evans, Andrew P. Salinger, Vicki Lundblad
Molecular and Human Genetics, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA

Telomere end structure serves to protect chromosome ends from degradation and end-to-end fusions, and to provide the substrate for the telomere replication enzyme, telomerase. In S. cerevisiae , CDC13 is required for both of these functions. To uncover additional genes required for telomere end-protection and/or replication, we performed a screen for mutations that were required in parallel with CDC13 . Surprisingly, mutations were recovered in the Ku70/Ku80 heterodimer and the Mre11/Rad50/Xrs2 complex, both of which are required for double strand break (DSB) repair via the nonhomologous end-joining pathway. We have shown that Ku, previously shown to bind double strand ends in vitro , plays a third role at the telomere, required in parallel with telomerase and Cdc13p. We propose that Ku and Cdc13p function as terminus-binding factors, contributing non-overlapping roles in telomere end-protection. In contrast, the Mre11/Rad50/Xrs2 complex is required for telomerase-mediated telomere replication, possibly via processing DNA ends in preparation for telomerase activity. We are currently asking whether the Mre11/Rad50/Xrs2 complex interacts with either the telomere or telomerase, and whether chromosome end structure is altered in strains mutant in this complex. In addition, a screen for Ku and Mre11/Rad50/Xrs2 separation-of-function mutants is being performed to address whether these repair proteins have differential roles at the telomere versus at DSBs.


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