The Caenorhabditis elegans zygote rapidly establishes regional domains of partitioning defective (PAR) polarity factors along the anterior–posterior axis. Microtubules can affect this, and Seydoux and colleagues now show that this is through microtubule-mediated local protection of PAR-2. Contact of the sperm centrosome, a microtubule-organizing centre, with the posterior cell cortex triggers polarization in two ways: by initiating cortical actomyosin flow; and by recruiting PAR-2. Seydoux and colleagues find that PAR-2, which is initially excluded throughout the cortex by uniform atypical protein kinase C (aPKC) distribution, is recruited to the sperm centrosome through direct microtubule binding; this locally protects PAR-2 from aPKC-mediated phosphorylation and initiates a feedback loop in which stabilized cortical PAR-2 directly recruits PAR-1. PAR-1-mediated phosphorylation of PAR-3 then triggers exit of PAR-3–aPKC from the posterior cortex. This mechanism appears to act very early in symmetry breaking, in parallel with the effects of actomyosin flow.