2024-03-29T06:53:13Zhttp://digital.csic.es/dspace-oai/requestoai:digital.csic.es:10261/958702016-02-18T03:03:15Zcom_10261_124com_10261_1col_10261_503
2014-04-25T09:07:19Z
urn:hdl:10261/95870
Multiple DNA repair pathways contribute to cell lethality in checkpoint mutants
Segurado, Mónica
Diffley, John F. X.
Trabajo presentado al Midterm Review Meeting; Checkpoints, DNA Damage Response and Cancer, celebrado en Milán el 3 de noviembre de 2005.
The checkpoint kinases Mec1 and Rad53 play an essential role in stabilizing stalled
DNA replication forks. We have initiated a genetic screen to identify mutants that
render checkpoint-defective yeast cells more resistant to fork-stalling agents (e.g.
hydroxyurea, MMS, etc). We have screened the entire library for mutants with
heightened resistance to hydroxyurea when the checkpoint has been compromised with
caffeine. From this, we have identified mutants in several repair pathways, and
therefore, we decided to check for caffeine plus hydroxyurea resistance in several
members of the main repair pathways. Our conclusions indicate that different repair
pathways contribute to lethality in checkpoint mutants.
We have also found that there is a significant Increase in HU-resistance when
combining different repair mutants in rad53-null background. However, none of these
multiple mutants is able to rescue viability completely, indicating that there are other
requirements to maintain fork stability in the absence of rad53.
2014-04-25T09:07:19Z
2014-04-25T09:07:19Z
2005
comunicación de congreso
Midterm Review Meeting (2005)
http://hdl.handle.net/10261/95870
eng
closedAccess