BACKGROUND: The centrosome is composed of a centriole pair and pericentriolar material (PCM). By marking the site of PCM assembly, the centrioles define the number of centrosomes present in the cell. The PCM, in turn, is responsible for the microtubule (MT) nucleation activity of centrosomes. Therefore, in order to assemble a functional bipolar mitotic spindle, a cell needs to control both centriole duplication and PCM recruitment. To date, however, the molecular mechanisms that govern these two processes still remain poorly understood. RESULTS: Here we show that SPD-2 is a novel component of the C. elegans centrosome. SPD-2 localizes to the centriole throughout the cell cycle and accumulates on the PCM during mitosis. We show that SPD-2 requires SPD-5 for its accumulation on the PCM and that in the absence of SPD-2, centrosome assembly fails. We further show that centriole duplication is also defective in spd-2(RNAi) embryos, but not in spd-5(RNAi) embryos, where PCM recruitment is efficiently blocked. CONCLUSIONS: Taken together, our results suggest that SPD-2 may link PCM recruitment and centriole duplication in C. elegans. SPD-2 shares homology with a human centrosome protein, suggesting that this key component of the C. elegans centrosome is evolutionarily conserved.
BACKGROUND: The centrosome is composed of a centriole pair and pericentriolar material (PCM). By marking the site of PCM assembly, the centrioles define the number of centrosomes present in the cell. The PCM, in turn, is responsible for the microtubule (MT) nucleation activity of centrosomes. Therefore, in order to assemble a functional bipolar mitotic spindle, a cell needs to control both centriole duplication and PCM recruitment. To date, however, the molecular mechanisms that govern these two processes still remain poorly understood. RESULTS: Here we show that SPD-2 is a novel component of the C. elegans centrosome. SPD-2 localizes to the centriole throughout the cell cycle and accumulates on the PCM during mitosis. We show that SPD-2 requires SPD-5 for its accumulation on the PCM and that in the absence of SPD-2, centrosome assembly fails. We further show that centriole duplication is also defective in spd-2(RNAi) embryos, but not in spd-5(RNAi) embryos, where PCM recruitment is efficiently blocked. CONCLUSIONS: Taken together, our results suggest that SPD-2 may link PCM recruitment and centriole duplication in C. elegans. SPD-2 shares homology with a human centrosome protein, suggesting that this key component of the C. elegans centrosome is evolutionarily conserved.
Authors: Tamara Mikeladze-Dvali; Lukas von Tobel; Petr Strnad; Graham Knott; Heinrich Leonhardt; Lothar Schermelleh; Pierre Gönczy Journal: Development Date: 2012-05 Impact factor: 6.868
Authors: Vladimir Joukov; Arcangela De Nicolo; Alison Rodriguez; Johannes C Walter; David M Livingston Journal: Proc Natl Acad Sci U S A Date: 2010-11-19 Impact factor: 11.205
Authors: Nathan Portier; Anjon Audhya; Paul S Maddox; Rebecca A Green; Alexander Dammermann; Arshad Desai; Karen Oegema Journal: Dev Cell Date: 2007-04 Impact factor: 12.270
Authors: Nathaniel Peters; Dahlia E Perez; Mi Hye Song; Yan Liu; Thomas Müller-Reichert; Cathy Caron; Kenneth J Kemphues; Kevin F O'Connell Journal: J Cell Sci Date: 2010-02-09 Impact factor: 5.285