DNA damage triggers increased mobility of chromosomes in G1-phase cells

Author:

Smith Michael J.1,Bryant Eric E.2,Joseph Fraulin J.1,Rothstein Rodney1

Affiliation:

1. Department of Genetics and Development, Columbia University Irving Medical Center, New York, NY 10032

2. Department of Biological Sciences, Columbia University, New York, NY 10027

Abstract

During S phase in Saccharomyces cerevisiae, chromosomal loci become mobile in response to DNA double-strand breaks both at the break site (local mobility) and throughout the nucleus (global mobility). Increased nuclear exploration is regulated by the recombination machinery and the DNA damage checkpoint and is likely an important aspect of homology search. While mobility in response to DNA damage has been studied extensively in S phase, the response in interphase has not, and the question of whether homologous recombination proceeds to completion in G1 phase remains controversial. Here, we find that global mobility is triggered in G1 phase. As in S phase, global mobility in G1 phase is controlled by the DNA damage checkpoint and the Rad51 recombinase. Interestingly, despite the restriction of Rad52 mediator foci to S phase, Rad51 foci form at high levels in G1 phase. Together, these observations indicate that the recombination and checkpoint machineries promote global mobility in G1 phase, supporting the notion that recombination can occur in interphase diploids.

Publisher

American Society for Cell Biology (ASCB)

Subject

Cell Biology,Molecular Biology

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