Marked chromosome areas are conserved through mitosis.


It is almost unbearable (at least for scientists) to contemplate a complete lack of order. So, it comes as some relief that chromosomes may be positioned nonrandomly in the nucleus, thus giving rise to more frequent translocations between certain chromosomes.

The seeming chaos of mitosis led most researchers to believe that any such order would have to be reestablished after each division. But now Daniel Gerlich, Roland Eils (German Cancer Research Center, Heidelberg, Germany), Jan Ellenberg (EMBL, Heidelberg, Germany), and colleagues have found that positioning is maintained through mitosis by a timing mechanism.

Congressing chromosomes make a beeline for the metaphase plate, the group found, and thus preserve information about their relative position perpendicular to the spindle axis. But congression erases information about how far the chromosomes had to travel to reach the metaphase plate. Despite this, the group found that marked territories, chromosomes or centromeres reestablished their previous geographies after mitosis. (Conflicting conclusions were recently drawn by Walter et al. in these pages.)

Chromosomes reestablished their positions by initiating anaphase separation at different times. Chromosomes that started anaphase later ended up on the side of the nucleus closest to the daughter cell. This ordering was jumbled by a heterochromatin-binding drug, so Eils suggests that chromosomes with larger regions of pericentric heterochromatin may stick to each other for longer and thus initiate anaphase later. Such a mechanism should work through multiple cell divisions.It is unlikely that the chromosomes are placed in locations with very different biochemistry: the placement is too rough, and most relevant proteins are in any case very mobile. So maybe the locations are merely a passive readout of kinetochore structure. Eils doesn't buy this argument. “I think Nature has invented this for a particular reason,” he says, “but I don't yet know what reason.” ▪


Gerlich, D., et al. 2003. Cell. 10.1016/S0092867403001892.

Walter, J., et al.
J. Cell Biol.