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Mutations in SID2, a Novel Gene in Saccharomyces cerevisiae, Cause Synthetic Lethality With sic1 Deletion and May Cause a Defect During S Phase
Matthew D. Jacobsona,b, Claudia X. Muñozb, Kirstin S. Knoxb, Beth E. Williamsb, Lenette L. Lub, Frederick R. Crossa, and Elizabeth A. Vallenba The Rockefeller University, New York, New York 10021
b Department of Biology, Swarthmore College, Swarthmore, Pennsylvania 19081
Corresponding author: Elizabeth A. Vallen, Department of Biology, Swarthmore College, Swarthmore, PA 19081., evallen1{at}swarthmore.edu (E-mail)
Communicating editor: M. D. ROSE
were isolated. In this screen, we identified a novel gene, SID2, which encodes an essential protein that appears to be required for DNA replication or repair. sid2-1 sic1 strains and sid2-21 temperature-sensitive strains arrest preanaphase as large-budded cells with a single nucleus, a short spindle, and an 
2C DNA content. RAD9, which is necessary for the DNA damage checkpoint, is required for the preanaphase arrest of sid2-1 sic1 cells. Analysis of chromosomes in mutant sid2-21 cells by field inversion gel electrophoresis suggests the presence of replication forks and bubbles at the arrest. Deleting the two S phase cyclins, CLB5 and CLB6, substantially suppresses the sid2-1 sic1 inviability, while stabilizing Clb5 protein exacerbates the defects of sid2-1 sic1 cells. In synchronized sid2-1 mutant strains, the onset of replication appears normal, but completion of DNA synthesis is delayed. sid2-1 mutants are sensitive to hydroxyurea indicating that sid2-1 cells may suffer DNA damage that, when combined with additional insult, leads to a decrease in viability. Consistent with this hypothesis, sid2-1 rad9 cells are dead or very slow growing even when SIC1 is expressed.
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