Sign up for Table of Contents Alerts.

Email this page

Print this page

Reports

Activation of the Budding Yeast Securin Pds1 But Not Rad53 Correlates with Double-Strand Break-Associated G₂/M Cell Cycle Arrest in a mec1 Hypomorphic Mutant

Mingzeng Sun and Michael Fasullo

Purchase article for $19

Subscribe to this journal for $129/year

Budding yeast Mec1, encoded by the yeast ATR/ATM homolog, negatively regulates cell cycle progression by activating Rad53 (Chk2) and Chk1, two parallel downstream checkpoint pathways. Chk1 phosphorylates Pds1 (securin), which prevents Pds1 degradation. We determined whether activation of both downstream pathways is required to establish G2 arrest in response to double-strand breaks (DSBs). In a hypomorphic mec1 mutant, Rad53 activation was not required to establish G₂ arrest triggered by a single HO endonuclease-generated DSB. However, Pds1 phosphorylation did correlate with G₂ arrest and mec1-21 pds1 cells did not arrest in G₂ after exposure to ionizing radiation. The G₂ checkpoint genes, CHK1 and PDS1, did confer radiation resistance in mec1-21, indicating that CHK1-mediated pathway is functional in the mec1 hypomorph. Thus, phosphorylation of Pds1 but not Rad53 correlates with G₂ arrest in response to DSBs in the mec1 hypomorphic mutant.

Authors

Mingzeng Sun

Ordway Research Institute; Albany NY USA

Michael Fasullo

Ordway Research Institute and School of Public Health, SUNY; Albany NY, USA

Purchase article for $19

Subscribe to this journal for $129/year