The Golgi apparatus's layered look (top) is lost without Myt1 is (bottom).

Mitosis involves more than parceling out chromosomes. A daughter cell also inherits part of the Golgi apparatus and ER from its parent cell. Nakajima et al. reveal that a protein once thought to dictate when a cell enters mitosis helps ensure that these organelles get passed on.

Conventional wisdom about the protein Myt1 held that it works with another protein called Wee1 to delay mitosis. Evidence for that view includes the fact that the proteins phosphorylate and inhibit Cdc2, a take-charge molecule that instigates mitosis when it enters the nucleus from the cytoplasm. Moreover, previous studies of yeast and human cells showed that overexpression of Myt1 prevents mitosis.

Nakajima et al. found otherwise when they used RNAi to cut Myt1 and Wee1 levels in human cells. Although cells low on Wee1 hurried into mitosis, the loss of Myt1 had little effect on mitotic timing. But Myt1 did perform a key job, the researchers discovered. During prometaphase, the Golgi apparatus fractures into thousands of tiny vesicles, some of which travel into the daughter cell and reassemble into a new Golgi apparatus. The breakup occured in cells missing Myt1, but the reunion did not. Instead of its normal folded ribbon shape, the Golgi apparatus in postmitotic, Myt1-lacking cells consisted of clustered vesicles and short or elongated tubes. Whether these defects hamper the Golgi is not clear.

Myt1 might also get the ER back into shape at the end of mitosis. Although researchers don't know all the changes that the ER undergoes during mitosis, the network appeared abnormal in Myt1-depleted cells that had just divided, Nakajima et al. found. The tubes were thicker than usual, and the cisternae that are normally scattered around the cell concentrated at its edge. Myt1 targets the B1 and B2 cyclins, which team up with Cdc2. The researchers conclude that by blocking these Cdc2/cyclin combinations, Myt1 allows the Golgi apparatus and ER to reform as mitosis concludes.


Nakajima, H., et al.
J. Cell Biol.