Anoushka Swain

Maintaining genome integrity remains a key priority for all living organisms. Researchers continue to explore why and how genome integrity fails, and what can be done to prevent chromosomal abnormalities. A key part of maintaining genome integrity is ensuring the faithful repair of damaged DNA. When unrepaired, DNA damage can lead to cancer, mutations, and overall genomic instability (Grossman, 1976). Double-stranded breaks (DSBs), the breakage of both strands of DNA, are one type of DNA damage. However, DSBs are necessary for the exchange of genetic information known as homologous recombination, a process required for normal chromosomal exchanges during meiosis; although, improper and untimely repair of these breaks can have consequences on organisms’ reproduction (Jeggo & Löbrich, 2007). Mutations in let-418, a gene in Caenorhabditis elegans and a paralog that is homologous to the human CHD4 gene (Turcotte et al., 2018), have previously been shown to increase infertility and inhibit DSB repair (Turcotte et al., 2018). An important region of the LET-418 protein is its ATPase domain. The role of the ATPase domain of LET-418/CHD4 in DNA repair has yet to be determined. Through CRISPR/Cas-9 mechanisms, we obtained C. elegans with a deletion of the ATPase domain. We discovered that a deletion of the ATPase domain results in zygotic sterility and germline disorganization.  In all, we deemed the ATPase domain to have a significant role in the progression of the germ line and is assumed to be essential for double-stranded break repair.