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Scripps research team unravels new cellular repair mechanism
Date:8/6/2008

ss during the S phase, the entire process stalls.

"If either the replicating enzymes run into damage, or if there are insufficient precursors for making DNA, then this checkpoint response will be activated," says Wittenberg. "There are two aspects to this response. One is to prevent the cycle from proceeding, and the other is to prepare the cell to deal with the damage."

Wittenberg and his colleagues have found that during normal cell division, Nrm1's binding to DNA represses the activity of genes expressed during the G1 phase, in preparation for the subsequent S phase. The team has now shown that when such stalls occur, collectively referred to as DNA stress, Nrm1's repression of the G1 genes is blocked, allowing those genes to be turned back on. This presumably enables production of proteins needed to correct the problem that caused the stall.

"So, now you have cells in the S phase, which don't typically express these genes, expressing them," says Wittenberg.

The researchers were able to tease out Nrm1's specific activities through experiments where they intentionally blocked the cell cycle in yeast cells by robbing them of the precursors needed for DNA replication. They were able to show that, as a result of this induced stress, Nrm1 was chemically altered by a known checkpoint enzyme, resulting in the loss of binding to G1 genes. This resulted in expression of the G1 genes during S phase. Because those genes encode replication and repair enzymes, re-expression of the G1 genes facilitates re-starting of DNA replication.

Because the onset of cancer is so intimately tied to problems in the cell cycle, numerous cancer drugs currently under development target checkpoint mechanisms, with the goals of making cells more sensitive to chemotherapeutic agents that damage DNA, and in some cases protecting normal proliferating cells from cell cycle arrest and death. Given that, once Nrm1's human analog and its activity are id
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Contact: Keith McKeown
kmckeown@scripps.edu
858-784-8134
Scripps Research Institute
Source:Eurekalert

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