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The somatic DNA strand-specific imprinting to effect gene regulation and selective chromatid segregation model was previously proposed to produce developmentally nonequivalent sister cells in mitosis. Such a mechanism might explain generation of stem-cell pattern of cell division in eukaryotes. The developmentally controlled process involves a pair of homologous chromosomes at a specific cell division to establish embryonic left-right body axis asymmetry. As a result, visceral organs in the two sides of vertebrate's body develop asymmetrically. The model was specifically proposed to explain the well-known axis randomization phenotype of the left-right dynein mutant mice where one-half of animals develop with standard visceral organ's positioning and the balance develops with the inverted arrangement. The model postulated that the specific dynein, a microtubule-based molecular motor protein, promotes the selective chromatid segregation process in mitosis. Thus, random segregation involving sister chromatids of a pair of specific chromosomes leads to axis randomization of the mutant. Moreover, the model uniquely predicts that 50 percent mutant embryos should produce symmetrical cell divisions because of random segregation; consequently, their either visceral side would develop as mirror image of the other side resulting in embryonic lethality. In view of this prediction, validity of prominent body axis-determination models is scrutinized here. Results supporting the cell-type regulated chromosome 6 and chromosome 7 selective chromatids segregation phenomenon existing in mouse cells are reviewed. Published results with the mutant mice are consistent with the chromosome segregation model for axis determination.

Support for the Selective Chromatid Segregation Hypothesis Advanced For the Mechanism of Left-Right Body Axis Development in Mice