文章基本信息

标题：Persistence of Thymidine Kinase Activity in Mitochondria of a Thymidine Kinase-Deficient Derivative of Mouse L Cells
本地全文：下载
作者：Barbara Attardi ; Giuseppe Attardi
期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：1972
卷号：69
期号：10
页码：2874-2878
DOI：10.1073/pnas.69.10.2874
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：The cell line LM(TK-) Cl 1D, a derivative of mouse L fibroblasts deficient in thymidine kinase (EC 2.7.1.21 ) that shows very little thymidine kinase activity in extracts of whole cells as compared to the parental line, and that does not incorporate thymidine or 5-bromodeoxyuridine into nuclear DNA, has maintained the capacity to incorporate these precursors into mitochondrial DNA at a substantial rate. The amount of [methyl-3H]thymidine incorporated into mitochondrial DNA of LM(TK-) Cl 1D cells after long-term labeling has been conservatively estimated in different experiments to be between 30 and 60% of that incorporated into mitochondrial DNA or nuclear DNA of strain A9, an L-cell derivative without any thymidine-kinase dificiency; by contrast, the incorporation of thymidine into nuclear DNA of Cl 1D cells is less than 1% of that in A9 cells. These results strongly suggest that the loss of thymidine kinase activity in the extramitochondrial compartment of LM(TK-) Cl 1D cells has not been accompanied by the loss of the mitochondria-associated enzyme activity, pointing to a different genetic or epigenetic control of the extramitochondrial and mitochondrial enzymes.
关键词：5-bromodeoxyuridine ; ethidium bromide ; mitochondrial DNA ; density gradient centrifugation