Draper G C, McLennan N, Begg K, Masters M, Donachie W D
Institute of Cell and Molecular Biology, University of Edinburgh, Edinburgh EH9 3JR, Scotland.
J Bacteriol. 1998 Sep;180(17):4621-7. doi: 10.1128/JB.180.17.4621-4627.1998.
Deletion of ftsK results in the inhibition of cell division, but this inhibition can be reversed by a plasmid carrying only the first approximately 17% of ftsK. The division block can be suppressed in most mutants by deletion of dacA, which codes for the D-alanine:D-alanine carboxypeptidase PBP5, or in all mutants by overexpression of ftsN. Overexpression of ftsK inhibits cell division and the formation of FtsZ rings. This division block is not due to the induction of either the SOS or the heat shock regulons.
ftsK的缺失会导致细胞分裂受到抑制，但这种抑制可被仅携带ftsK前约17%的质粒逆转。在大多数突变体中，通过缺失编码D - 丙氨酸：D - 丙氨酸羧肽酶PBP5的dacA可抑制分裂阻滞，或者在所有突变体中通过过表达ftsN来抑制。ftsK的过表达会抑制细胞分裂和FtsZ环的形成。这种分裂阻滞并非由SOS或热休克调节子的诱导所致。
