Sigma separation
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《细胞学杂志》
Losick/Elsevier
Symmetry can be broken in a bacterial cell by using the order of genes on the chromosome, according to Jonathan Dworkin and Richard Losick of Harvard University, Cambridge, MA.
The gene whose position is key is an antagonist to the Bacillus subtilus transcription factor F. Although F directs the process of spore formation, Losick suspected that the instability of SpoIIAB, the anti-F, might be the key to asymmetry. An exaggeration of SpoIIAB instability in the developing spore would tip the balance, but there was no clue as to how this might be achieved.
Now Dworkin and Losick show that replenishment of SpoIIAB is temporarily absent in the developing spore because an early cytokinesis leaves the chromosomal region containing the spoIIAB gene stranded in the mother cell. Only later is this part of the chromosome ferried into the spore cell.
As proof of this hypothesis, the authors demonstrate that a spoIIAB gene placednear the chromosome's origin (the first region to enter the spore) inhibits sporulation. In contrast, cells with a defective DNA translocation apparatus end up superactivating sporulation genes, presumably because the gene for anti-F never reaches the developing spore.
The anti-F does not act alone—a redundant mechanism involving a localized phosphatase is also important for formation of a spore at the pole. Dworkin says the research group is attempting to gain a better understanding not only of factors controlling the phosphatase, but of the proteins involved in determining where the initial asymmetric septum forms.
Reference:
Dworkin, J., et al. 2001. Cell. 107:339–346.
wellsw@rockefeller.edu(Delayed entry of an anti-F gene (blue) h)
Symmetry can be broken in a bacterial cell by using the order of genes on the chromosome, according to Jonathan Dworkin and Richard Losick of Harvard University, Cambridge, MA.
The gene whose position is key is an antagonist to the Bacillus subtilus transcription factor F. Although F directs the process of spore formation, Losick suspected that the instability of SpoIIAB, the anti-F, might be the key to asymmetry. An exaggeration of SpoIIAB instability in the developing spore would tip the balance, but there was no clue as to how this might be achieved.
Now Dworkin and Losick show that replenishment of SpoIIAB is temporarily absent in the developing spore because an early cytokinesis leaves the chromosomal region containing the spoIIAB gene stranded in the mother cell. Only later is this part of the chromosome ferried into the spore cell.
As proof of this hypothesis, the authors demonstrate that a spoIIAB gene placednear the chromosome's origin (the first region to enter the spore) inhibits sporulation. In contrast, cells with a defective DNA translocation apparatus end up superactivating sporulation genes, presumably because the gene for anti-F never reaches the developing spore.
The anti-F does not act alone—a redundant mechanism involving a localized phosphatase is also important for formation of a spore at the pole. Dworkin says the research group is attempting to gain a better understanding not only of factors controlling the phosphatase, but of the proteins involved in determining where the initial asymmetric septum forms.
Reference:
Dworkin, J., et al. 2001. Cell. 107:339–346.
wellsw@rockefeller.edu(Delayed entry of an anti-F gene (blue) h)