Abstract
SummaryDuring the first five rounds of cell division in the mouse embryo, spindles assemble in the absence of centrioles. Spindle formation initiates around chromosomes, but the microtubule nucleating process remains unclear. Here we demonstrate that Plk4, a protein kinase known as a master regulator of centriole formation, is also essential for spindle assembly in the absence of centrioles. Depletion of maternal Plk4 prevents nucleation and growth of microtubules and results in monopolar spindle formation. This leads to cytokinesis failure and, consequently, developmental arrest. We show that Plk4 function depends on its kinase activity and its partner protein, Cep152. Moreover, tethering Cep152 to cellular membranes sequesters Plk4 and is sufficient to trigger spindle assembly from ectopic membranous sites. Thus, the Plk4-Cep152 complex has an unexpected role in promoting microtubule nucleation in the vicinity of chromosomes to mediate bipolar spindle formation in the absence of centrioles.
Highlights
There are two main pathways for the assembly of meiotic or mitotic spindles
We demonstrate that Plk4, a protein kinase known as a master regulator of centriole formation, is essential for spindle assembly in the absence of centrioles
We show that Plk4 function depends on its kinase activity and its partner protein, Cep152
Summary
There are two main pathways for the assembly of meiotic or mitotic spindles. The first is the ‘‘search and capture’’ mechanism, whereby centrosome nucleated microtubules (MTs) make contact with and are stabilized by kinetochores (Kirschner and Mitchison, 1986). This pathway depends on centrosomes as the major centers for organizing MTs. Typically centrosomes comprise a pair of centrioles, surrounded by pericentriolar material (PCM; Nigg and Stearns, 2011). Polo-like kinase family member, has been established as a conserved key regulator of centriole formation (Bettencourt-Dias et al, 2005; Habedanck et al, 2005). To mediate centriole formation, Plk requires Cep152/
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