Spindles maintain some integrity despite the loss of components specific to γTuRC.
Two complexes in cells contain γ-tubulin. The smaller complex is γTuSC, which contains γ-tubulin and two other proteins (GCP2 [Dgrip84] and GCP3 [Dgrip91]). γTuRC is composed of γTuSC, NEDD1/Dgp71WD, and three additional proteins (GCPs 4, 5, and 6).
Vérollet et al. found that depletion of any one of three γTuRC-specific proteins (Drosophila homologues of GCP4, 5, or 6) disrupted the γTuRC complex. Dgp71WD depletion did not affect complex formation, but frequently disrupted mitotic spindles. Most embryos lacking Dgp71WD were viable and appeared to survive by accumulating γ-tubulin at the centrosomes in the form of γTuSC.
Meanwhile, Haren et al. showed that NEDD1 is absolutely required for centrosomal function and for accumulation of γ-tubulin at the centrosome in mammalian cells, but not for the assembly of γTuRC. NEDD1-depleted cells resembled γ-tubulin mutants, with monopolar spindles forming in a large percentage of cells. These data agree with and extend recent work published by Lüders et al. (Nat. Cell Biol. 2005. doi:10.1038/NCB1349). Further analysis by Haren et al. demonstrated that NEDD1 is also required for duplication of the centrioles, which form the heart of the centrosome.
Why NEDD1 is essential in vertebrate cells, whereas flies can survive in the absence of Dgp71WD, may have to do with the abundance or functionality of the smaller γTuSC in flies. Despite the apparent differences, the researchers expect that ultimately the main processes involving NEDD1/Dgp71WD and γTuRC are likely to be similar between the organisms. The differences, they are finding now, may help them sort out possible models of centrosome assembly and function.
