A new experimental system identifies structures that help stop faulty cells from dividing.
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Abscission checkpoint bodies (green) in dividing cells with an active abscission checkpoint, arrested before severing of their intercellular bridges (magenta). Image credit: Williams et al. (CC BY 4.0)

When a cell divides, it must first carefully duplicate its genetic information and package these copies into compartments housed in the two new cells. Errors in this process lead to genetic mistakes that trigger cancer or other harmful biological events.

Quality control checks exist to catch errors before it is too late. This includes a final ‘abscission’ checkpoint right before the end of division, when the two new cells are still connected by a thin membrane bridge. If cells fail to pass this ‘no cut’ checkpoint, they delay severing their connection until the mistake is fixed.

A group of proteins called ESCRTs is responsible for splitting the two cells apart if nothing is amiss. The abscission checkpoint blocks this process by altering certain proteins in the ESCRT complex, but exactly how this works is not yet clear.

To find out more, Williams et al. imaged ESCRT factors in a new experimental system in which the abscission checkpoint is active in many cells. This showed that, in this context, certain ESCRT components were rerouted from the thread of membrane between the daughter cells to previously unknown structures, which Williams et al. named abscission checkpoint bodies. These entities also sequestered other factors that participate in the abscission checkpoint and factors that contribute to gene expression.

These results are key to better understand how cells regulate their division; in particular, they provide a new framework to explore when this process goes wrong and contributes to cancer.