Without Swi6, chromosomes lag (top) because centromeres (left) but not chromosome arms (right) fall apart.


The cohesin complex acts as a glue for sister chromatids, but in some organisms most cohesin is lost from chromosome arms well before anaphase onset. Now, Robin Allshire (MRC Human Genetics Unit, Edinburgh, UK), Jean-Paul Javerzat (CNRS Institut de Biochimie et Génétique Cellulaires, Bordeaux, France), and colleagues show that Swi6, the fission yeast version of heterochromatin protein 1 (HP1), is required for the association of cohesin with centromeres. This provides one explanation for what Swi6 and heterochromatin are doing at the centromere.

“We knew before that mutants in Swi6 lost chromosomes at a high rate and displayed a high frequency of lagging chromosomes on anaphase spindles,” says Allshire. But the explanation for this defect remained unclear. Was Swi6 helping to establish kinetochore structure? Allshire says this remains a possibility, but for now he has established another explanation. Mutants lacking Swi6 maintain cohesion on chromosome arms during a mitotic block but lose cohesion at the centromeres thanks to the loss of a cohesin subunit.

Swi6 is also required for binding of cohesin near telomeres and the silent mating locus—the other heterochromatic regions in fission yeast. This suggests that kinetochore components are not necessary for Swi6-dependent cohesin loading. Only future work will show whether a direct interaction between Swi6 and cohesin is responsible for loading cohesin.▪


Bernard, P., et al. 2001. Science. 10.1126/science.1064027, http://www.sciencemag.org/cgi/content/abstract/1064027