Replication of nuclear and mitochondrial DNA in X-ray-damaged cells: evidence for a nuclear-specific mechanism that down-regulates replication.
Replication of nuclear and mitochondrial DNA in X-ray-damaged cells: evidence for a nuclear-specific mechanism that down-regulates replication.
复制标题
X 射线损伤细胞中核和线粒体 DNA 的复制:下调复制的核特异性机制的证据。
作者:
J. Cleaver
The mechanism by which X rays inhibit DNA replication has been investigated in three distinct populations of DNA molecules in human cells: (a) large chromosomal DNA, (b) a population of 50-100 10.3-kb nuclear episomal plasmids per cell, and (c) a population of about 500 16-kb cytoplasmic mitochondrial DNA molecules per cell. DNA replication was inhibited by X rays in nuclear chromosomal and plasmid DNA, but not in mitochondrial DNA. The mechanism by which ionizing radiation inhibits DNA replication must therefore be nuclear-specific and is unlikely to involve diffusible low-molecular-weight substances. Since mitochondrial DNA exists in the cell as independent 16-kb circular molecules and responds to radiation as would be expected for small targets, the implication for nuclear plasmids is that their replication is regulated by a large target. A current model for DNA replication involves the movement of DNA through replication centers made up of polymerases, helicases, and associated replication enzymes that are attached to a matrix. The difference in the response to X rays between mitochondrial DNA and nuclear plasmid DNA can be explained if nuclear plasmids are tightly associated with chromosomal DNA and attached to the matrix, and are coordinately replicated.
影响因子:
9.8
作者:
Leon N. Kapp;Robert B. Painter;Yu Lc;N. vanLoon;Richard Cw rd;Michael R. James;David Cox;J. Murnane
通讯作者:
Leon N. Kapp;Robert B. Painter;Yu Lc;N. vanLoon;Richard Cw rd;Michael R. James;David Cox;J. Murnane
影响因子:
--
作者:
D. Tapper;R. A. Etten;David A. Clayton
通讯作者:
D. Tapper;R. A. Etten;David A. Clayton
DOI:
--
发表时间:
1991
期刊:
The Journal of biological chemistry
影响因子:
--
作者:
Pettepher,CC;LeDoux,SP;Bohr,VA;Wilson,GL
通讯作者:
Wilson,GL