All cells are not equal, at least when it comes to the length of the cell cycle. Asymmetric distribution of two regulatory proteins in the early embryo helps create these timing differences, Rivers et al. show.
Different cell types often differ in cell cycle length. Take AB and P1, the first two cells of a worm embryo. AB completes its cycle about two minutes sooner than does P1. Researchers knew that Par proteins, which help set up the embryo's polarity, are also responsible for unequal cell cycle times. What they didn't know was how.
Rivers et al. tested whether two key proteins that control the cell cycle, cyclin E and CDC-25.1, were involved. AB and P1 harbored equal amounts of cyclin E, indicating it wasn't responsible for the timing difference. But the levels of CDC-25.1 are higher in the AB cell's nucleus, and the protein builds up faster there, suggesting it drives the asynchrony.
But what causes CDC-25.1 to accumulate in only one cell One candidate was the polo-like kinase PLK-1, which helps the human counterpart of CDC-25.1 home in on the nucleus. Rivers et al. found that at the one-celled stage, PLK-1 amasses at the anterior end, which becomes AB after the first cell division.
In turn, Par proteins seem to help set up the PLK-1 asymmetry through two other proteins, which control protein degradation. These two proteins might spur the breakdown of an unidentified inhibitor of PLK-1.