Torres Jorge Z, Bessler Jessica B, Zakian Virginia A
Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544-1014, USA.
Genes Dev. 2004 Mar 1;18(5):498-503. doi: 10.1101/gad.1154704.
Lack of the yeast Rrm3p DNA helicase causes replication defects at multiple sites within ribosomal DNA (rDNA), including at the replication fork barrier (RFB). These defects were unaltered in rrm3 sir2 cells. When the RFB binding Fob1p was deleted, rrm3-generated defects at the RFB were eliminated, but defects at other rDNA sites were not affected. Thus, specific protein-DNA complexes make replication Rrm3p-dependent. Because rrm3-induced increases in recombination and cell cycle length were only partially suppressed in rrm3 fob1 cells, which still required checkpoint and fork restart activities for viability, non-RFB rrm3-induced defects contribute to rDNA fragility and genome instability.
酵母Rrm3p DNA解旋酶的缺失会导致核糖体DNA（rDNA）内多个位点出现复制缺陷，包括复制叉屏障（RFB）处。在rrm3 sir2细胞中，这些缺陷没有改变。当RFB结合蛋白Fob1p被缺失时，RFB处由rrm3产生的缺陷被消除，但其他rDNA位点的缺陷不受影响。因此，特定的蛋白质-DNA复合物使复制依赖于Rrm3p。由于rrm3诱导的重组增加和细胞周期延长在rrm3 fob1细胞中仅得到部分抑制，而这些细胞仍需要检查点和叉形重启活动来维持生存能力，所以非RFB的rrm3诱导缺陷会导致rDNA脆弱性和基因组不稳定。
