Our genome is damaged by environmental factors such as UV, endogenous reactive oxygen, and chemicals. Because the accumulation of DNA damage can lead to aging and disease such as cancers, DNA repair machinery is essential for the life. In human, it is reported that polymorphisms in DNA repair genes are correlated to cancers. Additionally, WRN, which is a responsible gene of Werner syndrome characterized by the premature aging, is involved in DNA repair. However, it remains unclear which molecules in DNA repair pathway is essential for the genome stability. Therefore, we performed whole genome sequencing of worms with mutations in DNA repair genes and searched for deletions to investigate the risk of gene deletion in each mutant. For the analysis, we used
atm-1;
xpc-1,
cku-80,
cku-80;
ced-3,
pcn-1,
wrn-1 and
ced-4 mutants. XPC-1 is required for recognition of nucleotide excision. ATM-1 and CKU-80 is important for the repair of double strand break. PCN-1 and WRN-1, which is C. elegans homologue of WRN, is involved in the control of cell cycle. When the DNA damage is severe, CED-3 and CED-4 is activated to eliminate the damaged cell. To induce the deletion, all mutants and N2 control are mutagenized by TMP/UV method. As a result, the frequency of deletion in mutagenized
atm-1;
xpc-1 was almost quadruple as much as mutagenized N2. The numbers of deletions per strain in the other mutants except for
wrn-1 were at least twice as much as N2. This indicates that the impairment of genes involved in the both of single and double strand damage increase the risk of gene deletion. Moreover, we found that higher occurrence of deletions in
ced-4 than the other single mutants, suggesting that individuals with mutation in apoptosis pathway entail a greater risk than individuals with genetic defect of non-homologous end joining or cell cycle. The data that displays higher occurrence of deletions in
cku-80;
ced-3 than
cku-80 also support this suggestion. In addition to the number of deletion, the size of deletion is also important for genome stability. The median values of deletion sizes in
pcn-1 and
cku-80 were about 50 bases higher than that in N2. To investigate the average deletion sizes in the mutants after double strand break of DNA, we obtained
dpy-3 mutant alleles using CRISPR system and checked the deletion sizes near target site. In 16 alleles derived from N2, we could identify only small indel, but no deletion, which is larger than 500 bases. However, we could find the large deletions in 5/43, 2/24, 5/33, 3/26 and 2/29 alleles derived from
cku-80,
wrn-1,
pcn-1,
ced-4, and
atm-1;
xpc-1, respectively. This suggests that impairment in DNA repair genes also induce larger deletions than wild type.