Centrosomes are microtubule-based organelles consisting of a pair of barrel-shaped centrioles surrounded by electron dense pericentriolar material. The core components of the centrosome duplication pathway are highly conserved between humans and Caenorhabditis elegans (C. elegans). This makes C. elegans an ideal organism to study duplication mechanisms. Centrosome duplication is a tightly regulated process in which each mother centriole gives birth to a single daughter, yielding two centrosomes prior to cell division. During mitosis, each centrosome functions to organize a pole of the bipolar spindle which enables accurate segregation of the chromosomes upon cell division. When centrosome duplication goes awry, aneuploidy can ensue. This is a hallmark of cancer cells. In this study, we determined the function of a putative RNA-binding protein called RBM-3.2 in C. elegans. To study the localization pattern of RBM-3.2 in C. elegans embryos, a MAP-tagged RBM-3.2 expressing transgenic worm strain was generated using the MoSSCI method. MAP::RBM-3.2 localizes to the centrosomes, the nuclear envelope, the nucleus, the spindle microtubules and the cytoplasmic granules in early C. elegans embryos during various cell cycle stages. To further dissect the function of C. elegans RBM-3.2, a rbm-3.2(ok688) deletion allele in which the entire rbm-3.2 open reading frame is deleted was obtained from the Caenorhabditis Genetics Center. The back-crossed rbm-3.2(ok688) deletion allele exhibited vulval defects that could be rescued by expressing the MAP::RBM-3.2 transgene in this strain. These data indicate that RBM-3.2 is required for normal vulval development in C. elegans. The effect of rbm-3.2 on ZYG-1-mediated centrosome duplication was then evaluated by generating rbm-3.2(ok688) I; zyg-1(it25) II double mutants. zyg-1(it25) single mutants exhibited close to 100% embryonic lethality at 23.5°C due to a failure of centrosome duplication. However, in the rbm-3.2(ok688) I; zyg-1(it25) II double mutants, about 21% of the embryos survived. These data indicate that RBM-3.2 suppresses the centrosome duplication defects of the zyg-1(it25) mutants thereby partially restoring their viability. Thus, our data implicate RBM-3.2 as an inhibitor of ZYG-1-mediated centrosome duplication. Further experiments will evaluate the mechanism by which RBM-3.2 regulates centrosome duplication.

rbm-3.2 negatively regulates centrosome duplication in C. elegans

Macromolecular Chemistry: The Second Century

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ACS Spring 2020 National Meeting & Expo

The official archive and repository for all ACS Meetings & Expositions abstracts and select posters or presentations.