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Selected nuclear LINE elements with mitochondrial‐DNA‐like inserts are more plentiful and mobile in tumor than in normal tissue of mouse and rat
Author(s) -
Hadler Herbert I.,
Devadas Krishnakumar,
Mahalingam Ravi
Publication year - 1998
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/(sici)1097-4644(19980101)68:1<100::aid-jcb10>3.0.co;2-l
Subject(s) - mitochondrial dna , nuclear dna , microbiology and biotechnology , biology , dna , carcinogenesis , restriction enzyme , mitochondrion , southern blot , cancer , genetics , gene
The nuclear DNA of normal and tumor mouse and rat tissue was examined for mitochondrial‐DNA‐like inserts by means of the Southern blot technique. The two probes were 32 P‐labeled cloned mitochondrial DNA. Kpn I, which doesn't cut either mitochondrial DNA, was one of the restriction enzymes, while the enzymes that fragment mitochondrial DNA were for mouse and rat Pst I and Bam HI, respectively. When Kpn I alone was used in the procedure a nuclear LINE family whose elements had mitochondrial‐DNA‐like insertions was selected. Such elements were much more abundant in tumor than in normal tissue. The results with Pst I alone and Bam HI alone and each combined with Kpn I indicated that there were mobile LINE elements with mitochondrial‐DNA‐like inserts in the nuclear genome of tumor. The mouse tissues were normal liver and a transplantable lymphoid leukemic ascites cell line L1210 that had been carried for 40 years. The rat tissues were normal liver and a hepatoma freshly induced by diethylnitrosoamine in order to minimize the role of 40 years of transplantation. Our unitary hypothesis for carcinogenesis of 1971, which suggested these experiments, has been augmented to include mobile nuclear elements with inserts of mitochondrial‐DNA‐like sequences. Such elements have been related to diseases of genetic predisposition such as breast cancer and Huntington's disease. J. Cell. Biochem. 68:100–109, 1998. © 1998 Wiley‐Liss, Inc.