Every day, the cells in our body divide millions of times to renew themselves. Each time, the copying has to be compeleted with extreme percision. Otherwise cell deterioration and serious diseases will occur. It is no small task, however, because our body is constantly subjected to attacks from the surrounding environment as well as from the cell's own metabolic activity. Sometimes errors do happen. Fortunately, there is a mechanism to catch those errors. How does it work?

There are special proteins, named 53BP1 and RIF1, that create a 3-D scaffold around a fracture in the DNA strand. The scaffold built is much larger than the fracture itself.

Prevent deterioration

It was known before that these proteins help with neutralizing the damage. But more advanced microsopes have allowed researches to see how big the scaffold built actually is. If the fracture is the size of a pin head, the scaffold that is constructed would be the size of a basketball. This ensures not only that the area of the wound will be stabilized, but the surrounding enviroment as well. It's like putting a cast over a broken leg, that stabilizes the wound and also prevents damage from spreading to a point of no repair.

Call the helpers

The large scaffold built not only stops the spread of the fracture, but also increases the likelihood of attacting another type of protein, the "workmen" that are designed to look for scaffolds like this and rush to do the actual repair of the damage. The bigger the scaffold, the more workers will see it and come to help.

Lack of scaffolding can lead to diseases such as cancer

When scientists prevented the scaffold from been built, they observed that large parts of the neighboring chromosome rapidly fell apart. The damaged cells then attempted to create the scaffold again, but often unsuccessfully. This can explain why people who lack the scaffold building proteins are prone to diseases caused by unstable DNA.

Sources:

University of Copenhagen, the Facility of Health and Medical Sciences

Image by Zephyris, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=6285050

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