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A correction to this article has been published: Holway et al., J. Cell Biol. 178 (5) 887
Published online 20 March 2006. doi:10.1083/jcb.200512136
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 172, Number 7, 999-1008
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Article

Checkpoint silencing during the DNA damage response in Caenorhabditis elegans embryos



Antonia H. Holway1, Seung-Hwan Kim1, Adriana La Volpe2, and W. Matthew Michael1

1 The Biological Laboratories, Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138
2 Istituto di Genetica e Biofisica "Adriano Buzzati-Traverso," Consiglio Nazionale delle Ricerche, 80125 Naples, Italy

Correspondence to W. Matthew Michael: mmichael{at}fas.harvard.edu

In most cells, the DNA damage checkpoint delays cell division when replication is stalled by DNA damage. In early Caenorhabditis elegans embryos, however, the checkpoint responds to developmental signals that control the timing of cell division, and checkpoint activation by nondevelopmental inputs disrupts cell cycle timing and causes embryonic lethality. Given this sensitivity to inappropriate checkpoint activation, we were interested in how embryos respond to DNA damage. We demonstrate that the checkpoint response to DNA damage is actively silenced in embryos but not in the germ line. Silencing requires rad-2, gei-17, and the polh-1 translesion DNA polymerase, which suppress replication fork stalling and thereby eliminate the checkpoint-activating signal. These results explain how checkpoint activation is restricted to developmental signals during embryogenesis and insulated from DNA damage. They also show that checkpoint activation is not an obligatory response to DNA damage and that pathways exist to bypass the checkpoint when survival depends on uninterrupted progression through the cell cycle.

Abbreviations used in this paper: HU, hydroxyurea; MMS, methanesulphonate; PCNA, proliferating cell nuclear antigen; RNAi, RNA interference.


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