Characterization of nurf-1 mutations in suppressing of top-2-induced embryonic lethality in C. elegans.


  • Simran Kaur, Biological Sciences, University of Delaware

Faculty Mentor(s)

  • Amiee Jaramillo-Lambert, Biological Sciences, University of Delaware


    Meiosis, a specialized form of cell division, orchestrates the transformation of diploid cells into haploid gametes. It initiates with a singular round of DNA replication, succeeded by two rounds of chromosome segregation known as meiosis I and meiosis II. During meiosis I, homologous chromosomes segregate, while meiosis II involves the separation of sister chromatids. Consequently, this process engenders non-identical gametes, specifically eggs and sperm. The successful execution of meiosis I hinges on precise homologous chromosome pairing and complete segregation. Prior investigations have illuminated the vital role of the highly-conserved, ATP-dependent enzyme Topoisomerase II in mediating homologous chromosome segregation during meiosis I. Our research has unveiled a loss-of-function mutation in C. elegans Topo II, designated as top-2(it7). This deleterious mutation results in sperm production lacking nuclei and culminates in embryonic lethality post-fertilization. A previous study identified 11 suppressor lines associated with top-2, and under conditions of 24 degrees Celsius, the top-2 mutant exhibited near negligible viability of embryos. Nonetheless, each of the identified suppressor lines displayed variable degrees of rescue in terms of embryonic lethality. Notably, a missense mutation in nurf-1 along with a missense mutation with mep-1, both chromatin remodelers, co-suppressed the top-2 embryonic lethality. The goal of this study is to characterize the role of nurf-1 in spermatogenesis.