From error to tetraploid
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《细胞学杂志》
Shi and King started out looking for different chromosome missegregation rates in various cell lines. They noticed that the rate of missegregation was 45–166-fold higher in spontaneously arising binucleated cells than in cells with normal divisions. In time-lapse experiments, these aberrant cells did not delay in mitosis but reversed their division process just before cytokinesis completion. The thin, remaining bridge between dividing cells opened back up, yielding a binucleate cell.
Extrapolating from experiments using probes for four chromosomes, it is likely that there is a segregation error during virtually all divisions that produce new binucleates. Chromosomes were not always obstructing the division furrow, so the pair think it is possible that a dedicated signaling mechanism may detect segregation errors and put the brakes on cytokinesis.
The virtues of opting out of the diploid world depend on what happens to tetraploids. David Pellman (Harvard Medical School) has recently shown that tetraploids lacking p53 promote tumorigenesis, but tetraploids with p53 may not behave so badly. There may even, suggests King, be a pathway from tetraploids back to functional, nonaneuploid diploids. "If that were true,"
Aberrant segregation (right) yields tetraploid binucleates.
KING/MACMILLAN
he says, "there would be a full pathway for the resolution of errors."
References:
Fujiwara, T., et al. 2005. Nature. doi:10.1038/nature04217.
Shi, Q., and R.W. King. 2005. Nature. doi:10.1038/nature03958.(Anaphase is not the point of no return, )
Extrapolating from experiments using probes for four chromosomes, it is likely that there is a segregation error during virtually all divisions that produce new binucleates. Chromosomes were not always obstructing the division furrow, so the pair think it is possible that a dedicated signaling mechanism may detect segregation errors and put the brakes on cytokinesis.
The virtues of opting out of the diploid world depend on what happens to tetraploids. David Pellman (Harvard Medical School) has recently shown that tetraploids lacking p53 promote tumorigenesis, but tetraploids with p53 may not behave so badly. There may even, suggests King, be a pathway from tetraploids back to functional, nonaneuploid diploids. "If that were true,"
Aberrant segregation (right) yields tetraploid binucleates.
KING/MACMILLAN
he says, "there would be a full pathway for the resolution of errors."
References:
Fujiwara, T., et al. 2005. Nature. doi:10.1038/nature04217.
Shi, Q., and R.W. King. 2005. Nature. doi:10.1038/nature03958.(Anaphase is not the point of no return, )