The idea that asymmetrical contraction drives cortical flow and the segregation of cell fate determinants has a long and controversial history. Earlier efforts were dogged by the transience of the flow and different results after the use of different fixation methods.
But when Munro finally had GFP-labeled myosin to work with, “the whole story unfolded in front of me,” he says. Contractile, coupled foci of cortical myosin gave way at the posterior when the sperm centrosomes approached the posterior cortex. The actomyosin network then contracted toward the anterior, taking a host of cytoskeletal proteins and anterior determinants with it.
Absence of these anterior determinants allows the PAR-2 determinant to attach to the posterior cortex, where it was needed to prevent a reverse flow of actomyosin back to the posterior. Both the PAR-2 and centrosome signal may somehow weaken or degrade parts of the actomyosin system, although the specific mechanism is a mystery.
Similar flows were seen at the 8-cell stage when cells set up PAR-based apicobasal polarity. In this case, the cue that weakens the actomyosin cortex may be basolateral contact with surrounding cells. “Any time you get differences in contractility you'll see flows in the cortex,” says Munro. “The mystery is not why do you have flows but how do you prevent flows.”