Replication continues in DNA-damaged embryos (top) unless translesion synthesis is blocked (bottom).

On page 999, Holway et al. reveal that worm embryos would rather risk genomic mutation than disturb the timing of cell division. DNA damage–induced checkpoints, the group finds, are silenced during early embryogenesis.

The need for the silencing arises because of the importance of timing in embryogenesis. At the worm's two-cell stage, for instance, a two-minute lag between the division times of the two cells is needed for germ line formation. Embryogenesis fails if this lag is extended, as would be expected upon DNA damage.

Holway and colleagues found, however, that genomic damage from UV or MMS treatments did not stall division in worm embryos. In somatic cells, DNA lesions block the progress of replication forks, whose stalling initiates the damage checkpoint. But replication forks advanced directly through the lesions in the...

The Rockefeller University Press
2006
The Rockefeller University Press
2006
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