In this study, we set out to investigate the role of Fanconi anemia complementation group D2 protein (FANCD2) in developmental stage-specific DNA damage responses in Caenorhabditis elegans. A mutant C. elegans strain containing a deletion in the gene encoding the FANCD2 homolog, FCD-2, exhibited egg-laying defects, precocious oogenesis, and partial defects in fertilization. The mutant strain also had a lower hatching rate than the wild-type after γ-irradiation of embryos, but not after the irradiation of pachytene stage germ cells. This mutation sensitized pachytene stage germ cells to the genotoxic effects of photoactivated psoralen, as seen by a greatly reduced hatching rate and increased chromosomal aberrations. This mutation also enhanced physiological M-phase arrest and apoptosis. Taken together, our data reveal that the C. elegans FANCD2 homolog participates in the repair of spontaneous DNA damage and DNA crosslinks, not only in proliferating cells but also in pachytene stage cells, and it may have an additional role in double-stranded DNA break repair during embryogenesis.
|Number of pages||7|
|Journal||Biochemical and Biophysical Research Communications|
|Publication status||Published - 2007 Jan 12|
Bibliographical noteFunding Information:
Caenorhabditis elegans N2 was obtained from the C. elegans Genetics Center (Minneapolis, MN, USA), which is supported by the National Center for Research Resources. The fcd-2 ( tm1298 ) strain was kindly provided by the National Bioresource Project (Japan). We thank Dr. Yuji Kohara (National Institute of Genetics, Japan) for fcd-2 EST clone yk293c3. This work was supported by Grant R01-2003-000-10396-0 from the Basic Research Program of the Korea Science and Engineering Foundation.
All Science Journal Classification (ASJC) codes
- Molecular Biology
- Cell Biology