Infertility can arise when DNA accessibility is misregulated. This regulation is tightly controlled by core histones: H2A, H2B, H3, and H4 and the replacement with histone variants throughout germ line development. In C. elegans, three H2A variants were identified: HTZ-1, HTAS-1 and HIS-35. HTZ-1 is a known regulator of developmental genes while HTAS-1 is a unique component of sperm. However, the role of HIS-35, which differs from core H2A by only one amino acid is unknown. Preliminary data revealed HIS-35 enrichment in sperm and oocytes, thus I hypothesize that HIS-35 participates in germ line development to maximize fertility. To determine HIS-35 effects on fertility, we developed a mutant strain containing a deletion of the
his-35 gene. Our results reported a 35% reduction in progeny, indicative of a role for HIS-35 in fertility. Furthermore,
his-35;
htas-1 double mutants are sterile, which is a phenotype more severe than either individual mutant alone. These results suggest that these H2A variants may compensate for one another to maximize fertility. Since we have demonstrated that HIS-35 is an important fertility factor, we utilized Crispr/Cas9 mediated repair system to create HIS-35::GFP and assess dynamics within the germ line. Surprisingly, HIS-35::GFP is present in almost all tissues and as expected, HIS-35::GFP localizes in both male and hermaphrodite germ lines. In addition, HIS-35::GFP is retained within mature sperm, oocytes and the newly-fertilized embryo. These findings raise the possibility that HIS-35 may be transferring or maintaining epigenetic states of genes needed throughout the developmental events of gametogenesis, fertilization and embryogenesis. Defining HIS-35 incorporation within these processes provides a basis for how H2A variants regulate DNA accessibility in different tissue types.