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Albertson, T., Ogawa, M., Bugni, J., Hays, L., Chen, Y., Wang, Y., Treuting, P., Heddle, J., Goldsby, R. and Preston, B. (2009) DNA polymerase ε and δ proofreading suppress discrete mutator and cancer phenotypes in mice. Proceedings of the National Academy of Sciences of the United States of America, 106, 17101-17104. doi:10.1073/pnas.0907147106

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• TITLE: Implications of double-stranded DNA structure for development, cancer and evolution

  AUTHORS: Mitsuru Furusawa

  KEYWORDS: Blast; Graph Theory; Redundant Sequences; CD-HIT

  JOURNAL NAME: Open Journal of Genetics, Vol.1 No.3, December 2, 2011

  ABSTRACT: Genomes consist of DNA and the genetic information is encoded in a linear form of DNA. According to the central dogma of molecular biology, the genetic information is transcribed into mRNA, and mRNA translated into a polypeptide. Gene expression should be precisely regulated in order to create progeny. Unlike RNA, DNA has double-stranded structure. Is there any specific biological reason why DNA has evolved to possess double-stranded structure? In this presentation, biological implications of the double-stranded structure of the DNA molecule will be reviewed. In eukaryotes, it has been reported that cells might have the machinery that distinguishes one DNA-strand from the other, and that the strand-recognition mechanism might control development, cancer and evolution. Three prominent models concerning biological implications of replication of double-stranded DNA will be discussed: 1) Klar’s “somatic strand-specific imprinting and selective chromatid segregation model” for differential gene regulation, 2) Cairns’ “immortal strand inheritance model” for cancer prohibition, and 3) the “disparity mutagenesis model” for the acceleration of evolution proposed by the present author.