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.

Highlights

  • The double-stranded model of DNA postulated by Watson and Crick in 1953 clearly explained how precisely equivalent daughter cells are produced when genetic material of the parental cell is replicated [1]

  • 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

  • This is because stem cells continue to replicate throughout the organisms life span

Read more

Summary

INTRODUCTION

The double-stranded model of DNA postulated by Watson and Crick in 1953 clearly explained how precisely equivalent daughter cells are produced when genetic material of the parental cell is replicated [1]. Cells that are subject to highest risk of cancer development will be stem cells This is because stem cells continue to replicate throughout the organisms life span. Organisms can produce unchanged progeny maintaining the species, and at the same time, higher mutation rates can provide raw material for accelerated evolution [4]. This idea was tested by computer simulations and proved experimentally using living organisms of Escherichia coli and Published Online November 2011 in SciRes. http://www.scirp.org/journal/OJGen. M. KLAR’S “SOMATIC STRAND-SPECIFICIMPRINTING AND SELECTIVE CHROMATID SEGREGATION MODEL (SSIS)”

Mating-Type Switching in Fission Yeasts
Support for SSIS Hypothesis
CAIRN’S “IMMORTAL STRAND HYPOTHESIS MODEL”
Computer Simulations of Disparity Mutagenesis Showing Promotion of Evolution
Acceleration of Evolution Using Living Organisms
Findings
CONCLUDING REMARKS
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call