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Weizmann Institute scientists discover a molecular security mechanism for keeping mutations in check

mes. Although this may seem paradoxical ?intuitively, more careless enzymes should mean more mutations ?each of these enzymes is tailored to deal with certain specifics types of DNA damage. This specialization is what keeps the level of mutation, and thus the cancer risk, low. But the existence of this variety of specialist enzymes implies precise regulation of the system ?otherwise copying by the careless enzymes might get out of control and lead to an unhealthy proliferation of mutations.

Prof. Livneh and his team recently discovered a security mechanism that prevents such proliferation of mutations. This mechanism allows the right enzyme to go to work at the right time, and only when it's needed. The main components in this system are the proteins p53 and p21. p53, named "molecule of the year" several years ago by Science, is well known for its central role in reining in cancer processes in the cell. In this case, the proteins seem to act as supervisors, taming the careless enzymes and keeping them in careful check. The scientists' research showed that if the functioning of p53 or its relative, p21, is harmed, the activities of the careless enzymes can go into overdrive, leading to more mutations.

The actual mechanism works with a sort of molecular clamp that holds the DNA copying enzyme onto the strand of DNA. When the enzyme encounters DNA damage, a small molecule called ubiquitin attaches to the clamp. The ubiquitin, in this case, serves to anchor replacement DNA polymerase molecules ?careless ones ?to the clamp. p53 enters the picture when it is alerted to the damage and causes p21 to be created. The p21 then acts as a sort of facilitator, helping to fasten the proper ubiquitin in place and clearing stalled DNA polymerase out of the way so its replacement can get to work. Thus, these two proteins manage to help the body's cells maintain a crucial balance, allowing them to divide and multiply while keeping the mutation rate, and therefore th
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Source:American Committee for the Weizmann Institute of Science


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