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Figure 15. Time-lapse photomicroscopy of cells irradiated with X-rays. Wild type cells at the time of irradiation (A) and several hours later (B). Notes that the originally unbudded G1 (A) cells have remained arrested as large budded cells (B) while the budded G2 cell (A) has resumed cell division (B). G1 haploid cells are very inefficient at repairing double strand breaks because of the lack of a template for homologous recombinational repair. rad9 mutants cells at the time of irradiation (C) and several hours later (D). Note that the G1 unbudded rad9 cells (C) do not arrest division but continue dividing producing dead microcolonies (D).

DNA damage checkpoint. Fortunately, my interest in genomic instability coincided with Ted Weinertís interest in studying the regulation of cell division. He thought it likely that all of our cell cycle mutants were identifying genes that contributed to the machinery of cell division and was interested in studying something that was more clearly an example of cell cycle regulation. I had remembered noticing that yeast cells became arrested synchronously in the cell cycle by radiation and mutagens and he began looking at radiation sensitive mutants to see if any were altered for their cell cycle response. He quickly found that some radiation sensitive mutants failed to arrest the cell cycle in response to radiation. He demonstrated that deletion of the RAD9 gene eliminated the regulation of the cell cycle by radiation, demonstrating a regulatory role for this gene and discovered a number of additional genes involved in the DNA damage checkpoint Tedís discovery led to an appreciation of the role of checkpoints in the fidelity of chromosome transmission.