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Molecular gate that could keep cancer cells locked up
Date:7/31/2014

They found that if they blocked one specific interface, between MCM2 and MCM5, DNA could not enter. A small molecule called rapamycin brings the linkages together; such a molecular switch can be used to control DNA entry to the MCM ring and subsequent DNA replication. "Both in the context of our in vitro and in vivo experiments, we showed that opening of the MCM2/MCM5 interface is essential for helicase loading onto DNA," explains Christian.

"The field has known for a while that DNA can pass into the MCM2-7 ring, but has never been sure which MCM subunits are used for regulated helicase loading. By designing an elegant experiment, the Speck laboratory has now shown once and for all that the MCM2-5 is the only DNA entry point," says collaborator Huilin Li at BNL.

In eukaryotes, the MCM2-7 helicase forms a double hexamer (with another MCM2-7 unit) when it is loaded onto DNA. In this study, the group also settled the longstanding dispute surrounding whether the helicase is actually loaded as a single hexamer, which then dimerises, or is loaded as a dimer at the offset. They concluded that the helicase is in fact loaded as a single hexamer before forming a double hexamer.

In a successful collaboration that harnesses the electron microscopy expertise at BNL with the chemical biology and genetic expertise at the MRC Clinical Sciences Centre, the study addresses key questions detailing the processes involved in DNA replication. "Our work is aimed at understanding the molecular mechanism of DNA replication at a fundamental level. Yet our findings could also have important implications, possibly pointing to new ways to fight cancer, because DNA duplication is a prime target to inhibit cancer cell growth," says Christian.


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Contact: Christian Speck
christian.speck@imperial.ac.uk
44-208-383-3387
MRC Clinical Sciences Centre
Source:Eurekalert  

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