Exchange of genetic information during meiosis occurs in all sexually reproducing species to produce haploid gametes from diploid cells. This process involves tight coordination of a meiotic specific cohesin complex, the synaptonemal complex, and DNA damage repair mechanisms. In this study, we describe a putative myosin heavy chain protein orthologous to human myosin 1, F28D1.2, which we named
atz-1 (Abnormal Transition Zone). Deletion of
atz-1 results in embryonic lethality and a depleted transition zone, accompanied by reduced expression of the meiotic cohesin protein, REC-8.
atz-1 mutants display disorganised and aggregated chromosomal bodies in diakinetic oocytes. In addition to this,
atz-1 mutants are hypersensitive to mild inhibition of DNA damage repair, suggesting that DNA replication in
atz-1 mutants is impaired. Moreover, the
atz-1 mutant phenotype is germline specific and resupplying somatically expressed
atz-1 does not rescue the reproductive defects associated with
atz-1 mutants. Overall, our data suggests that
atz-1 contributes to meiosis and maintains germline chromosomal stability.